97th ESA Annual Meeting (August 5 -- 10, 2012)

COS 131- - The population dynamics of pathogens and social groups

Thursday, August 9, 2012: 11:10 AM
D139, Oregon Convention Center
Andy Dobson, Ecology and Evolutionary Biology, Princeton University, Princeton, NJ
Background/Question/Methods

Social groups naturally divide many host populations into metapopulations.  This population structure presents a twin challenge to pathogens: how do they transmit themselves between social groups whose territorial behavior may minimize contacts between groups?  Simultaneously, the pathogens have to persist in any individual group until opportunities for transmission between groups arise.  I will present some models for pathogens in social groups that quantify the tradeoffs between social contact and disease transmission.  The viability of any social group is dependent upon having enough breeding individuals, as well as younger animals that play a major role in catching and subduing prey; these details are captured in a ‘within-group’ component of the model.  The groups of prey hunt prey and this is included in the ‘between group’ dynamics of the model.  Initially we explore the dynamics of an SI type pathogen, such as mange, we then extend the model and consider an SIR pathogen, such as canine distemper, that creates immunity to re-infection.  The models parameters are derived from published studies of Yellowstone wolves and wild dogs in the Serengeti.

Results/Conclusions

The models suggest that pathogens reduce both the size of social groups and the number of social groups living in an ecosystem.   Groups tend to collapse when pathogen reduce the number if individuals that hunt and provide food for the year’s pups; this creates a disease driven Allee effect that can cause local extinction.  However, if prey dynamics are included in the model, the increases in prey abundance that occur when the number of predator group declines can ultimately lead to a buffering of the Allee effect and the presence of the pathogen causes the tritrophic system to settle to a state of increased prey abundance, reduced predator density and endemic disease. The models are broadly applicable to pathogens of social carnivores and primates.   The metapopulation dynamic behavior of the models will be compared with published data collected from long-term studies and with more detailed simulation models that explicitly examiner how  within group dynamics  of the pathogen modify the factors that ultimately determine social group size and composition.