General Disease Ecology

Collaborators: Wayne Getz (UC Berkeley), Jamie Lloyd-Smith (UCLA)

Much of my work has focused on where the general principles of disease dynamics in humans may, or may not, be applicable to wildlife species. The primary differences I have focused on are: smaller group sizes, more limited movement among groups, periodic breeding, and density dependence. First, we investigated the role of host social structure on disease invasion using empirical behavior data and simulation models. That work revealed a key interaction between the infectious period of the parasite and the host social structure. In particular, diseases with acute infectious periods perceive a more sparsely connected host social structure than chronic pathogens. We began with the specific case of African buffalo and developed what may be the first empirically-derived dynamic social network model of a disease in a wildlife host. We then generalized these results to a range of different pathogens using a metapopulation model with mechanistic host movement . We found that R0, the net reproductive number of a disease, fails as a predictor of pandemics in spatially structured populations. R*, the group-based equivalent of R0, is far superior in systems where host groups are small because it accounts for the movement of the disease among groups rather than individuals within a group. In a review of the wildlife disease literature, my collaborators and I looked for evidence supporting population thresholds for disease persistence in wildlife species. We found that the evidence was generally weak, that theoretical models suggest gradual changes rather than sharp thresholds, and that density dependent processes may lead to increasing the probability of disease persistence when host densities are reduced.



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