UBC Math Bio Seminar: Marjolein Toorians

Biodiversity loss worldwide coincides with an increase in epidemics. This loss of species and reassembly of species communities is thought to be connected to disease transmission via two, opposing, theories: (1) the dilution effect predicts that high species richness can buffer diseases, and therefore higher host diversity lowers disease prevalence or outbreak potential (R0); (2) the amplification effect states that more host diversity creates more opportunity for disease transmission, increasing disease prevalence. Both theories are predicated by the mode of disease transmission, and the abundance and disease competence of hosts in the community. Defining host competence is complex, but as research shows that more closely related species have a higher probability of sharing a pathogen, I assumed host competence is determined by phylogeny. To elucidate the mechanisms underlying dilution and amplification effects, I explored the role of host phylogenetic structure on disease outbreak, using epidemiological models that assume the probability of transmission co-varies with the phylogenetic distance between hosts. I composed a multi-host SI model using host phylogeny as a proxy for probability of disease-sharing, and show that even when host species richness has an amplifying effect on disease outbreak potential, it is possible to observe a phylogenetic dilution effect: more phylogenetically diverse host communities have a reduced R0 compared to phylogenetically clustered communities. I applied this model to an empirical system, bovine Tuberculosis in South Africa, using camera-trap data to infer host contact-rates, which, combined with the phylogenetic host structure, informs transmission rates between species. I show here that the effect of host phylogenetic structure, and the phylogenetic position of the reservoir host (African Buffalo, Syncerus caffer) is more important than contact structure in determining disease outbreak potential, assuming transmission is scaled by the phylogenetic distance between the reservoir (donating) and receiving host. This applied model suggests that bovine Tuberculosis dynamics are primarily driven by intraspecific transmisson within the reservoir host. This work contributes to the disease-diversity debate, and reveals how host phylogenetic community structure may be an important mechanism underlying the disease-outbreak potential.