COS 44-3
Host abundance thresholds to pathogen invasion in a Daphnia-microparasite system

Tuesday, August 12, 2014: 2:10 PM
Regency Blrm E, Hyatt Regency Hotel
Tad A. Dallas, Odum School of Ecology, University of Georgia, Athens, GA
John M. Drake, Center for the Ecology of Infectious Diseases, University of Georgia, Athens, GA

A common theoretical threshold in disease ecology is the critical community size, referring to the minimum number of susceptible individuals in a population necessary for a pathogen to invade. Efforts to identify this threshold in field populations have been hampered by demographic stochasticity, complex population structures, and limited replication. However, this threshold remains an important quantity to disease ecology, and can used to inform vaccination or culling efforts. Recent microcosm work has suggested that there may also be an upper threshold in host density, where the pathogen cannot invade as a result of scaling of host foraging rate and transmission rate with host abundance. Here, we examined microcosm populations of Daphnia dentifera across a range of densities (20 - 640 hosts * L-1) to determine the potential for lower and upper thresholds to the invasion of a free-living fungal pathogen. Populations were monitored for 56 days for changes in host density and pathogen prevalence. Analytical expressions for the pathogen invasion threshold (R0 > 1) were obtained from a SI model with free-living pathogen, parameterized with experimental data.


Distinct waves of infection were observed in microcosm populations, beginning with primary infections, which caused a secondary infection peak after the death and spore release of hosts infected with primary infections. We found evidence for a lower threshold to pathogen invasion (between 80 and 160 hosts * L-1), but no evidence for an upper limit to pathogen invasion. After one infection cycle, infection prevalence monotonically increased with host abundance, suggesting that there is no upper threshold to pathogen invasion. When considering the entire epidemic course, the area under the infection curve and maximum prevalence was lower in the highest host density treatment (640 hosts * L-1). This suggests that high host density may not impede the invasion of a pathogen, but may reduce total epidemic size. Altogether, we provide empirical evidence and support from a theoretical model for the presence of a lower threshold to pathogen invasion.