Publication details


Biodiversity is declining dramatically. Meanwhile, disease risk of infectious disease in human, wildlife and livestock is undergoing an increase. Several studies showed that a change in biodiversity can impact disease risk. One hypothesis, the dilution effect, suggests that a loss in species richness can increase disease risk as competent species are more likely to remain when incompetent species go locally extinct. However, the generality of the dilution effect is debated. For example, the direction of the relationship between disease risk and biodiversity depends on the different measurements of disease risk (e.g., infection prevalence and the density of infected animals), the spatial scale of observation, and the disease transmission type (i.e., density vs. frequency dependent).

The objective of this thesis is to advance the understanding of the relationships between disease risk and biodiversity. My results give new insights into these relationships. My findings suggest that the commonly used species richness is not a good indicator of disease risk, and that assemblage composition (i.e., abundance and relative abundance of species) and structure of wildlife assemblages (i.e., functional diversity and phylogenetic diversity) are more important than species richness in affecting disease risk. I used species evenness to measure the assemblage composition, and showed that species evenness was a better indicator of disease risk than species richness, as evenness also contains information on the relative differences in species’ abundances, and these abundances are positively correlated with contact rates among hosts. My results also highlight the importance of the distribution of functional traits (e.g., body mass) in the species assemblage, as body mass can be correlated to the species’ competence to pathogens. I also studied the role of phylogenetic relatedness in the relationships between disease risk and biodiversity, and showed that if the species in an assemblage are closely related, especially among competent hosts species, the assemblage is expected to have a higher disease risk. So, phylogenetic relationships within local assemblages can help us to better understand why a loss in species richness can either positively or negatively affect disease risk. To conclude, my study highlights the importance of composition and structure of local assemblages (i.e., evenness, functional diversity, phylogenetic relatedness) on disease risk, and suggests that future studies should look beyond species richness when studying relationships between biodiversity and disease risk.