SYMP 6-2 - Mammalian host traits and species contributions to disease transmission

Tuesday, August 9, 2011: 8:25 AM
Ballroom G, Austin Convention Center
M. Andrea Previtali, Departamento de Ciencias Naturales, Facultad de Humanidades y Ciencias, Universidad Nacional del Litoral, Santa Fe, Argentina, Felicia Keesing, Program in Biology, Bard College, Annandale-On-Hudson, NY and Richard S. Ostfeld, Cary Institute of Ecosystem Studies, Millbrook, NY
Background/Question/Methods

In multi-host disease systems, different hosts have different impacts on pathogen proliferation and transmission.  Attempts to link aspects of the host community (e.g., species richness or composition) with disease transmission have relied on inductive study designs: only when each species’ role in disease transmission is described can the aggregate effect of a community be induced.   Potentially, this slow and inefficient process could be improved by identifying traits that predict species-specific roles.  We have begun to seek host traits that might underlie variation in species’ contributions to Lyme disease risk

In the case of Lyme disease, the host species most efficient at transmitting Borrelia burgdorferi to ticks tend to have high population densities, smaller body sizes, and faster pace of life than species with lower reservoir competence. We hypothesized that these fast-living species are competent reservoirs because they rely on cheap, broad immune defenses, whereas slower-living species have low reservoir competence owing to specific but expensive immune defenses.  To assess immunological strategies we captured wild individuals of several mammalian host species, collected a blood sample, and measured bacterial killing capacity (BKC).

Results/Conclusions

We found strong differences between males and females within host species, the direction of which depended on the species. We also found significant individual variation in BKC. To ask which species-specific traits best explained interspecific variation, we replaced the species identity with life-history traits.  We found that body mass was better at explaining species differences than lifespan or densities. However, the predictive power of body mass was much lower than that of species identity, indicating that this trait is related to but not able to fully capture the mechanisms by which these species differ in their innate immune function. For a trait-based disease ecology to thrive, traits that faithfully predict species-specific roles must be identified and the underlying mechanisms uncovered.

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