Research in the Strauss lab is conceptually motivated by questions in community and/or disease ecology. We work in both aquatic and terrestrial ecosystems, and we strive to tackle our questions through a combination of field studies, experiments, and mathematical models. Several current projects in the lab include:
- The thermal community ecology of disease
- Disease in an ecosystem context
- Mysterious microsporidians
- Harmful algal blooms
- Pathogen interactions
The thermal community ecology of disease
Disease dynamics in populations of hosts can be shaped by interactions of hosts with their predators, their competitors, and their resources. However, it is unclear how these community drivers of disease might change in warmer or cooler environments. For example, predators can reduce infection prevalence in populations of their prey according to the ‘healthy herds hypothesis.’ Therefore, if predators are better adapted to warmer environments than their prey, then warming could intensify these inhibitory effects of predators on disease. Similarly, competitors can inhibit transmission of parasites in host populations and drive ‘dilution effects’: patterns that link higher biodiversity with lower disease risk in a focal host population. If competitors are better adapted to warmer environments than hosts, then warming could increase the relative abundance of competitors over hosts, strengthen dilution effects, and mitigate outbreaks of disease. We are beginning to explore these hypotheses and other related ideas within the theme of the ‘thermal community ecology of disease.’ The Daphnia-Metschnikowia is perfect for tackling these questions, since it enables both parameterization of general mechanistic models and empirical tests at mesocosm scales, both along thermal gradients.
left: The host Daphnia dentifera infected by the fungus Metschnikowia bicuspidata. The first and third hosts are infected (notice the darker coloration due to fungal spores filling the host’s haemolymph). right: Mesocosm experiments that manipulate temperature (using giant water baths and water chillers/heaters) and community composition (e.g., presence of parasites, competitors, and/or predators).
Disease in an ecosystem context
Ecosystem models describe fluxes and pools of elements, while epidemiological models track susceptible and infected hosts. Because of these different currencies, ecosystem ecologists rarely ask how infections alters ecosystem processes, and disease ecologists rarely ask how elemental ratios shape disease dynamics. We are striving to bridge this gap between disease and ecosystem ecology in both aquatic and terrestrial ecosystems. In terrestrial grasslands, we are interested in how the availability of nutrients affects the growth of fungal pathogens on plants, and reciprocally how infections alter rates of photosynthesis and tissue chemistry of hosts. In aquatic mesocosms, we are investigating how epidemics in consumer populations (i.e., Daphnia) redistribute biomass across trophic levels and alter community-level rates of primary productivity and respiration. We are tackling these projects with both mathematical models and mesocosm experiments.
left: Sampling disease damage in the BioCON global change experiment at Cedar Creek Ecosystem Reserve, with Hajira, Katie, and Rachel. center: An aquatic mesocosm experiment with clear differences in primary productivity (i.e., greenness) right: Sampling the Georgia Piedmont Prairie site of DRAGNet, a globally distributed experiment in grasslands, with Katie and Jordan.
Mysterious microsporidians
Populations of zooplankton in ponds and reservoirs near Athens, GA are frequently infected by a relatively unknown group of microsporidian parasites. Preliminary sequencing has revealed at least four taxa of parasite that infect at least six species of host, including several species of Daphnia and other related Cladocerans. The parasites nearly or completely sterilize hosts (depending on host species) and infection prevalence can reach 70%. We are hoping to learn more about this mysterious group of parasites and its impacts on host communities and pond ecosystems. Key outstanding questions include how the parasite is transmitted, why infection prevalence peaks in springtime, how other members of pond communities shape the timing and severity of outbreaks, how these outbreaks impact the likelihood of harmful algal blooms, and why coinfections between multiple parasite taxa seem relatively common even in short-lived hosts.
left: Populations of Daphnia ambigua are heavily infected by the microsporidians Pseudoberwaldia daphniae and Conglomerata obtusa in early spring. Infected hosts appear darker in the center of their bodies. center: Daniel samples local ponds for communities of zooplankton and their parasites. right: Outbreaks of the microsporidians can reach up to 70%, like in this population of Daphnia laevis.
Harmful algal blooms
Harmful algal blooms form when toxin-producing phytoplankton – typically cyanobacteria – reach high densities. These events are increasing worldwide due to a complex combination of warmer temperatures, increased nutrient pollution, and more frequent extreme weather events. Communities of zooplankton grazers may be able to inhibit algal blooms via top-down control – at least under certain conditions. However, zooplankton might also increase the likelihood of blooms because grazing can shift the composition of phytoplankton communities away from “good” algae and towards large, inedible, toxin-producing species. We are interested in how zooplankton grazers (and potentially their parasites!) impact the timing and severity of harmful algal blooms in ponds and reservoirs in the Southeast. We are exploring these questions with field surveys and are planning corresponding lab and mesocosm experiments.
left: Daniel and Kate prepare to sample at VIP pond, including assessment of the zooplankton and phytoplankton communities. top right: sampling out on the water. bottom right: Zooplankton differ substantially in body size, like these larger Daphnia and smaller Ceriodaphnia. Body size may be related to ability of zooplankton to inhibit harmful algal blooms.
Pathogen interactions
Coinfections occur when a single host individual is infected by more than one species of parasite or pathogen. Coinfections are important because they often increase disease severity, alter the course of epidemics, and drive evolution of pathogen populations. In a coinfected host, pathogens can interact with one another either antagonistically (e.g., via competition for shared space or resources) or synergistically (e.g., by weakening hosts or distracting host immune function). We are interested in how these interactions shape the assembly of pathogen communities and likelihood of coinfection. We are also investigating how these interactions might differ across environmental gradients or within different ecological communities. So far we have focused these questions on the grass host tall fescue, which is frequently infected by a suite of fungal foliar pathogens in local populations around Athens.
left: Growing fescue hosts in the greenhouse with and without a vertically transmitted endophyte, the mutualist Epichloe. center: Measuring length and scoring leaves for fungal damage after transplanting hosts into a field experiment. right: Disease damage on the host big bluestem (Andropogon gerardii). The large splotches show damage caused by the fungal rust pathogen Puccinia andropogonis; the smaller black dots are likely caused by a second fungal foliar pathogen.