Linking aggregation patterns to pathogen seroprevalence: Are there multiple ways to be dense and spread disease?

Background/Question/Methods

To understand the relationship between host density and parasite transmission it is important to measure host density at a scale relevant to transmission. Among social species it is often assumed that transmission increases with increasing group size, but this may not be the case for species whose aggregation patterns vary across space and time. Under these circumstances, there may be more than one way to be dense and spread disease which could have direct effects on successful disease control strategies. To examine this issue, we studied elk (Cervus canadensis) aggregation patterns and brucellosis in the Greater Yellowstone Area, where previous studies suggest the disease may be increasing. We hypothesized that rates of increasing brucellosis would be more associated with the frequency of large groups, but we examined whether other measures of density would also explain rising seroprevalence. We measured elk density and group size across multiple spatial and temporal scales using three years of aerial flights over 10 regions. We used Bayesian hierarchical models and 21 years of serologic data to estimate rates of increase in brucellosis seroprevalence among the 10 regions, and we examined the linear relationships between these estimated rates of increase and seven measures of elk aggregation.

Results/Conclusions

All measures of aggregation were positively related with one another, but we observed some high density populations with smaller group sizes and vice versa. Brucellosis seroprevalence increased over time in eight regions (e.g., one region showed an estimated increase from 0.015 in 1991 to 0.26 in 2011), and these rates of increase were positively related to all measures of aggregation. The relationships between aggregation and rates of increase in seroprevalence were weaker when the analysis was restricted to only areas where brucellosis was present for at least two years. Our findings suggest that (i) most reasonable measures of host aggregation had similar utility to predict changes in seroprevalence over time, (ii) these patterns may have been influenced by the effects of aggregation on disease-establishment within a population, and (iii) group size did not explain brucellosis increases any better than density, even though elk populations were structured by grouping throughout the transmission period. Finally, disease control strategies aimed at reducing either the total number of individuals or the size of the largest groups may not effectively reduce transmission for social species with complex aggregation patterns.