Environmental drivers of vector-borne disease
Anthropogenic environmental change is pervasive, rapid, and multifaceted. Climate change, human population growth and urbanization, land use change, and species invasions and extinctions are reshaping ecological communities and with them, infectious disease dynamics. Our work investigates the environmental drivers of disease, including climate, land use, and human interactions with the environment in a variety of mosquito-borne diseases. We are studying impacts of climate and socio-economic factors on arboviruses like dengue, chikungunya, and Zika in Kenya, Ecuador, and Costa Rica (in collaboration with Desiree LaBeaud, Eric Lambin, Anna Stewart Ibarra, Sadie Ryan, Taylor Ricketts, Matías Piaggio, and others, funded by the Stanford Woods Institute for the Environment – Environmental Ventures Program). We are also investigating the impacts of deforestation on malaria in the Amazon (in collaboration with Andy MacDonald, Lisa Mandle, and others at the Natural Capital Project, funded by the Moore Foundation). Images: Erin Mordecai & Chris Anderson.
Effects of temperature on vector-transmitted diseases
Mosquitoes and other biting insects transmit many of the most important, devastating, and neglected human infectious diseases, including malaria, dengue, chikungunya, and West Nile virus. Because these disease vectors are small-bodied and cold-blooded they are sensitive to environmental temperature. As a result, climate change is likely to shift the global distribution of these vector-borne diseases. We have used laboratory data and a mathematical model to show that thermal responses of traits involved in malaria transmission are nonlinear, and that the resulting optimum temperature for malaria transmission is just 25°C. The model allows us to make nuanced predictions about where climate change may most impact malaria transmission. In a new project funded by the National Science Foundation Ecology and Evolution of Infectious Diseases Program, we are working to predict thermal responses in 13 vector-borne diseases, to map these predicted changes, and to estimate their uncertainty using mathematical models and Bayesian statistics. Our work will also explore local thermal adaptation in two key mosquito species that transmit dengue, chikungunya, Zika, and yellow fever viruses: Aedes aegypti and Aedes albopictus. Collaborators include Leah Johnson, Sadie Ryan, Krijn Paaijmans, Samraat Pawar, Kevin Lafferty, Jason Rohr, Van Savage, Matt Thomas, Anna Stewart Ibarra, Courtney Murdock, and others. Images: Erin Mordecai & Krijn Paaijmans.
Pathogen impacts on plant communities
Parasitism is one of the most common strategies of life on earth, and natural plant communities host a huge diversity of pathogens. Our work examines feedbacks between pathogen and host communities in California grasslands and other systems. We are growing fungal pathogens of native and exotic grasses in culture to identify the pathogen community in this vast and heavily invaded ecosystem. In tandem, we are experimentally measuring pathogen impacts on plant competition and other demographic rates. Combined with mathematical models, this work will help us understand how pathogens affect the composition of plant communities. We are particularly interested in how generalist pathogens that can be transmitted between host species may indirectly modify competition. In California grasslands, where native and exotic grasses compete intensely and share pathogens, disease may be a major driver of coexistence and competitive exclusion. This work takes place in the amazing and beautiful Jasper Ridge Biological Preserve, just seven miles from Stanford University main campus. Images: Erin Mordecai.
Maintenance of parasite diversity
Parasites live in diverse communities, competing for host resources. What mechanisms allow all these parasites to coexist? We have studied how several life history tradeoffs may promote parasite coexistence. In California salt marshes, we have shown that a competition – colonization tradeoff promotes coexistence for trematode parasites, but that other mechanisms may also contribute. In grasslands, we have shown that competing viruses coexist by coinfecting host plants and via a tradeoff between transmission efficiency and the ability to use multiple vector species. In fungi infecting native and exotic wild grasses in California, we have shown that pathogens infect multiple grass species and have minor effects on host fitness, in stark contrast with their close relatives--wheat pathogens like Parastagonospora nodorum and Pyrenophora tritici-repentis--which are extremely host-specialized and damaging. We're now investigating the possibility that the diversity of natural grasslands maintains pathogen host generality and low virulence by preventing aggressive, host-specific lineages from rising to dominance. Images: Erin Mordecai.