Virulent parasites can depress the densities of their hosts. Taxa that reduce disease via dilution effects might alleviate this burden. However, ‘diluter’ taxa can also depress host densities through competition for shared resources. The combination of disease and interspecific competition could even drive hosts extinct. Then again, genetically variable host populations can evolve in response to both competitors and parasites. Can rapid evolution rescue host density from the harm caused by these ecological enemies? How might such evolution influence dilution effects or the size of epidemics? In a mesocosm experiment with planktonic hosts, we illustrate the joint harm of competition and disease: hosts with constrained evolutionary ability (limited phenotypic variation) suffered greatly from both. However, populations starting with broader phenotypic variation evolved stronger competitive ability during epidemics. In turn, enhanced competitive ability—driven especially by parasites— rescued host densities from the negative impacts of competition, disease, and especially their combination. Interspecific competitors reduced disease (supporting dilution effects) even when hosts rapidly evolved. However, this evolutionary response also elicited a potential problem. Populations that evolved enhanced competitive ability and maintained robust total densities also supported higher densities of infections. Thus, rapid evolution rescued host densities but also unleashed larger epidemics.
|Original language||English (US)|
|Journal||Proceedings of the Royal Society B: Biological Sciences|
|State||Published - Dec 6 2017|
Bibliographical noteFunding Information:
Data accessibility. All data are available on Dryad Digital Repository http://dx.doi.org/10.5061/dryad.tm041 . Authors’ contributions. A.T.S., S.R.H., C.E.C. and M.A.D. designed the study. A.T.S. led trait measurements, assisted by J.L.H. and S.R.H. A.T.S, J.L.H. and M.S.S. sampled the mesocosm experiment. A.T.S. led DNA extractions (assisted by J.L.H.) and genotyping (assisted by M.S.S. and C.E.C.). A.T.S. conducted statistical analyses and wrote the first draft of the manuscript. All authors contributed to revisions. Competing interests. We declare we have no competing interests. Funding. This work was supported by NSF DEB 1120316, 1353749, 1354407, 1353806, and 1406846, as well as NSF DUE 1129198. Acknowledgements. A.T.S. was supported by the NSF GRFP. O. Schmidt assisted with trait measurement assays, and S. Duple assisted with the mesocosm experiment. C. Holmes and P. Lee assisted with geno-typing conducted at the W.M. Keck Center for Comparative and Functional Genomics (University of Illinois at Urbana-Champaign).
This work was supported by NSFNational Science Foundation DEB 1120316, 1353749, 1354407, 1353806, and 1406846, as well as NSFNational Science Foundation DUE 1129198.
© 2017 The Author(s) Published by the Royal Society. All rights reserved.
- Dilution effect
- Disease ecology
- Eco-evolutionary dynamics
- Friendly competition
- Rapid evolution