How do changes in biodiversity influence disease?
Disease emergence and biodiversity loss are two of the most pressing environmental challenges of the modern era. Each is driven predominantly by human-mediated alterations in the environment. Although changes in biodiversity and infectious diseases have often been studied separately, the importance of interactions between them has received comparatively little attention. Under what circumstances will disease epidemics drive species losses? And, reciprocally, can higher levels of biodiversity reduce parasite transmission (i.e., the dilution effect) or lead to increases in infection (i.e., the amplification effect)? Through what ecological mechanisms and at what magnitude relative to other pathways known to affect parasite spread, such as changes in host density?
The project
We use a combination of field surveys, laboratory manipulations, and large-scale experiments to understand the links among biodiversity, community composition, and infectious disease risk. While a common approach to studying the relationship between biodiversity and disease is test for bivariate correlations between species richness and some metric of disease or infection, this simplified strategy fails to recognize the dynamic nature of most diseases. Many infections vary strongly both spatially and temporally, and the large number of response variables related to ‘disease risk’ can lead to conflicting or confusing results. We have been using trematode parasites to study these questions in more detail, includingÌýSchistosoma mansoniÌý(the causative agent of human schistosomiasis) andÌýRibeiroia ondatraeÌý(the causative agent of amphibian malformations). Results from both laboratory- and more complex mesocosm experiments indicate that higher levels of host diversity can reduce transmission of both parasites (i.e., the dilution effect), but that such patterns depend critically on the order and pattern of host community assembly. Mechanisms that mediate the relationship between diversity and infection include variation in host competence, the presence of non-competent ‘decoy’ hosts, predators that consume parasites or alter host exposure to infection, and interactions between coinfecting parasites.
Using field data from simple pond ecosystems, our findings highlight the importance of identifying potential links between the order of species assembly and a given host’s competence to support an infection. In cases in which the most widespread and abundant hosts are also the most competent, with subsequent colonizers functioning as lower competence hosts, the transmission potential of the community will decrease predictably with increased diversity (Johnson et al. 2013, 2024). This can happen, for instance, when tradeoffs between immune defenses and colonization ability occur among ‘fast’ vs. ‘slow’ species (e.g., Johnson et al. 2012). However, whether this pattern is common remains unclear, particularly given how little we know about host competence, host assembly, and transmission for many multi-host infections. We are currently working to expand this research to a wider range of host and parasites systems with the aim of advancing our understanding of how and when biodiversity can protect against disease threats.
Project publications
Johnson, P. T. J., Stewart Merrill, T. E., Dean, A. D. and A.ÌýFenton (2024). Diverging effects of host density and richness across biological scales drive diversity-disease outcomes. Nature CommunicationsÌý15:1937. .Ìý
Koprivnikar, J., Thieltges, D. W., and P. T. J. Johnson (2023). Consumption of trematode parasite infectious stages: from conceptual synthesis to future research agenda. Journal of Helminthology 97: E33. .Ìý
Stewart Merrill, T., Calhoun, D. M. and P. T. J. Johnson (2022).ÌýBeyond single host, single parasite interactions: quantifying competence for complete multi-host, multi-parasite communities.ÌýFunctional EcologyÌý36: 1845-1857.Ìý.Ìý
Hobart, B. K., Moss, W. E., McDevitt-Galles, T., Stewart Merrill, T. and P. T. J. Johnson (2022).ÌýIt's a worm-eat-worm world: consumption of parasite free-living stages protects hosts and benefits predators.ÌýJournal of AnimalÌýEcologyÌý91: 35-45. Ìý.Ìý
McDevitt-Galles, T., Carpenter, S., Koprivnikar, J. and P. T. J. Johnson (2021). How predator and parasite size interact to determine consumption of infectious stages.ÌýOecologiaÌý197:551-564. .Ìý
Johnson, P. T. J., Calhoun, D. M., Riepe, T. B., and J. KoprivnikarÌý(2019). Community disassembly and disease: realistic -- but not randomized -- biodiversity losses enchance parasite transmission.ÌýProceedings of the Royal SocietyÌýB:Ìý286.Ìý.Ìý
Johnson P. T. J., Wood, C. L., Joseph, M. B., Preston, D. L., Haas, S. E., and Y. P. Springer (2016). Habitat heterogeneity drives the host diversity-begets-parasite diversity relationship: evidence from experimental and field studies.ÌýEcology LettersÌý19: 752-761.ÌýÌý
Johnson, P. T. J., De Roode, J. C. and A. Fenton (2015). Why infectious disease biology needs community ecology.ÌýScienceÌý349: 1259504.Ìý
Johnson, P. T. J., Ostfeld, R. S. and F. Keesing (2015). Frontiers in research on biodiversity and disease.ÌýEcology LettersÌý18: 1119-1133.Ìý
Orlofske, S. A., Jadin, R. C. and P. T. J. Johnson (2015). It's a predator-eat-parasite world: how characteristics of predator, parasite and environment affect consumption.ÌýOecologiaÌý178: 537-547.Ìý
Orlofske, S. A., Jadin, R. C., Hoverman, J. T. and P. T. J. Johnson (2014). Predation and disease: understanding the effects of predators at severalÌýtrophic levels on pathogen transmission.ÌýFreshwater BiologyÌý59: 1064-1075.Ìý
Johnson, P. T. J., Preston, D. L., Hoverman, J. T., and K. L. D. Richgels (2013). Biodiversity decreasesÌýdisease through predictable changes in host community competence.ÌýNatureÌý494: 230-234.Ìý
Orlofske, S. A., Jadin, R., Preston, D. L., and P. T. J. Johnson (2012). Parasite transmission in complex communities: predators and alternative hosts alter pathogenic infections in amphibians.ÌýEcologyÌý93: 1247-1253.Ìý
Johnson, P. T. J., Rohr, J. R., Hoverman, J. T., Kellermanns, E., Bowerman, J. and K. B. Lunde (2012). Living fast and dying of infection: host life history drives interspecific variation in infection and disease risk.ÌýEcology LettersÌý15: 235-242.Ìý
Johnson, P. T. J., Preston, D. L., Hoverman, J. T., Henderson, J. S., Paull, S. H., Richgels, K. L. D. and Redmond, M. D. (2012). Species diversity reduces parasite infection through cross-generational effects on host abundance.ÌýEcologyÌý93: 56-64.Ìý
Johnson, P. T. J., Dobson, A., Lafferty, K. D., Marcogliese, D., Memmott, J., Orlofske, S., Poulin, R., and D. W. Thieltges (2010). When parasites become prey: ecological and epidemiological significance of eating parasites.Ìý Trends in Ecology & EvolutionÌý25: 362-371.Ìý
Johnson, P. T. J., and D. W. Thieltges (2010). Diversity, decoys and the dilution effect: how ecological communities affect disease risk.ÌýÌýJournal of Experimental BiologyÌý213: 961-970.Ìý
Johnson, P. T. J., Lund, P. J., Hartson, R. B., and T. P. Yoshino (2009).Ìý Community diversity reducesÌýSchistosoma mansoniÌýtransmission and humanÌýinfection risk.ÌýProceedings of the Royal Society of London, Series BÌý276: 1657-1663.Ìý
Johnson, P. T. J., Hartson, R. B., Larson, D. J. and D. R. Sutherland (2008). Linking biodiversity loss and disease emergence: amphibian community structure determines parasite transmission and pathology.ÌýEcology LettersÌý11: 1017-1026.Ìý