Exploring the Separate and Interactive Effects of Pesticides and Parasites on Amphibians
In the Anthropocene, amphibians must not only cope with natural stressors but also a suite of human-made stressors that have been experienced relatively recently within their evolutionary history. Because it has become increasingly common for natural and anthropogenic stressors to co-occur in aquatic ecosystems, the study of their separate and combined effects on ecosystems and their component species is increasingly necessary. This is especially important for amphibians, which have experienced global declines and can be highly sensitive to both natural and anthropogenic stressors. Pesticides and parasites are two commonly co-occurring stressors that can have complex individual and synergistic detrimental effects in amphibian populations. Here, I conducted three studies to broadly assess the separate and interactive effects of pesticides and parasites on amphibians. More specifically, I explored: 1) the underlying physiological mechanism allowing amphibians to induce increased tolerance to a pesticide within a single generation, 2) the effects of exposure timing to two functionally similar cryptic parasite species on infection outcomes, and 3) population-level variation in susceptibility to parasites and whether prior exposure to pesticides influenced the outcome of host-parasite interactions. First, to test the hypothesis that induced pesticide tolerance is the result of a generalized stress response, I exposed tadpoles to an anthropogenic stressor (sublethal pesticide dose), a natural stressor (cues from a caged predator), or a simulated stressor via exogenous exposure to the stress hormone corticosterone (CORT). I then exposed the larvae to a lethal carbaryl treatment to assess how the stressor exposures influenced survival. I found that prior exposure to exogenous CORT and predator cues induced tolerance to a lethal concentration of carbaryl, providing evidence that pesticide tolerance can be induced by a generalized stress response both in the presence and absence (exogenous CORT) of specific cues. Second, I explored how the timing of host exposure to two co-occurring cryptic echinostome species influences infection outcomes. I found that echinostome infection success in larval anurans can differ significantly based on the parasite species makeup, density, and exposure timing. I also found that priority effects can occur even between functionally similar cryptic species, with an early exposure to Echinoparyphium lineage 3 reducing the infection success of Echinostoma trivolvis three days later. Finally, I assessed the influence of pesticide exposure on host-parasite interactions and population-level variation in these responses. This was accomplished by exposing wood frog larvae from eight populations to one of two treatments (a sublethal carbaryl concentration or a pesticide-free control) followed by controlled parasite exposures to either echinostome trematodes or ranavirus. Then, I assessed how pesticide exposure influenced infection loads, infection prevalence, and survival in each population. I found significant population-level variation in infection outcomes. Interestingly, however, I found no significant effects of pesticide exposure on disease outcomes. Together, these three studies demonstrate the wide-ranging and surprising outcomes that can result from interactions among and between natural and anthropogenic stressors.