Emerging infectious diseases and animal social systems

Abstract

Emerging infectious diseases threaten a wide diversity of animals, and important questions remain concerning disease emergence in socially structured populations. We developed a spatially explicit simulation model to investigate whether-and under what conditions-disease-related mortality can impact rates of pathogen spread in populations of polygynous groups. Specifically, we investigated whether pathogen-mediated dispersal (PMD) can occur when females disperse after the resident male dies from disease, thus carrying infections to new groups. We also examined the effects of incubation period and virulence, host mortality and rates of background dispersal, and we used the model to investigate the spread of the virus responsible for Ebola hemorrhagic fever, which currently is devastating African ape populations. Output was analyzed using regression trees, which enable exploration of hierarchical and non-linear relationships. Analyses revealed that the incidence of disease in single-male (polygynous) groups was significantly greater for those groups containing an average of more than six females, while the total number of infected hosts in the population was most sensitive to the number of females per group. Thus, as expected, PMD occurs in polygynous groups and its effects increase as harem size (the number of females) increases. Simulation output further indicated that population-level effects of Ebola are likely to differ among multi-male-multi-female chimpanzees and polygynous gorillas, with larger overall numbers of chimpanzees infected, but more gorilla groups becoming infected due to increased dispersal when the

Host–pathogen evolutionary signatures reveal dynamics and future invasions of vampire bat rabies

“…This study shows that contrasting host and pathogen genetic markers with different inheritance modes provides a framework to begin to evaluate sex-biased pathogen dispersal. Other approaches, such as theoretical modeling of pathogen transmission within host contact networks, incorporate similar concepts, but typically lack corresponding data from pathogens to verify how host dispersal heterogeneity affects disease spread, require extensive field datasets on host contacts, and offer limited guidance for managing pathogens emerging at the landscape level (17,24). Identifying the sex responsible for pathogen spread carries practical implications for the prevention and control of VBRV because blocking viral movement between colonies is predicted to cause viral extirpation (10).…”

Infectious disease and group size: more than just a numbers game

“…(c) Theoretical model of disease spread Our theoretical model was constructed as a modification of a meta-population model used previously to study the spread of socially transmitted infections [57] and cultural traits [58]. The model was implemented in MATLAB version R2013b.…”

Competing pressures on populations: long-term dynamics of food availability, food quality, disease, stress and animal abundance

“…Rates of discovery [11] and emergence of infectious diseases appear to be accelerating [12][13][14], though some of this is likely based on increased sampling effort and improved diagnostics techniques; also, some of these diseases may cause pathology, whereas others may not. For example, within the past decade in one small area of Kibale National Park, Uganda, our research group has discovered distinct simian pegiviruses in three species of wild monkeys [15], a new SIV lineage in red-tailed guenons (Cercopithecus ascanius) [16], and novel delta-lenti-and spuma-retroviruses [17], just to name a few.…”