Dilution and ash weathering are the most important processes controlling the ion chemistry of lakes in the Mount St. Helens blast zone. Gibbs' models indicated total dissolved solids were decreasing as a result of dilution from high precipitation and runoff and the lakes plot in the rock weathering dominated region. Plots of theoretical dilution curves indicated a decline in ion concentrations as a result of dilution. Ion concentrations followed the exponential decline predicted by the dilution curve, although concentrations were higher than predicted by the curve. Increased concentrations were a result of the rapid weathering of ash in basins and on lake bottoms. Rapid weathering of ash in lake watersheds and on lake bottoms continues to influence the ionic concentrations of the lakes. In general, sodium and potassium have declined at a much faster rate than calcium or magnesium. Slower relative declines in concentrations of calcium and magnesium were a result of more rapid rate of leaching of calcium and magnesium from the ash. Ash in the watersheds will continue to be a major contributor to the overall ion chemistry of the lakes until such time as the watersheds are stabilized by vegetation and a permanent soil layer. Ash on lake bottoms will be unavailable as sources of ionic constituents when it becomes buried within deep sediment layers. Ion concentrations observed in study lakes affected by the eruption were similar to those observed in control lakes with few exceptions. Although ion concentrations in affected lakes have declined to values observed in control lakes, most were at higher concentrations than the regional means. Several functions of the ion chemistry were used to correlate planktonic community structure to lake ion chemistry. The data suggested ion chemistry was not influencing biological community structures as no patterns emerged. Analysis of diatom populations with respect to monovalent:divalent cation ratios showed no correlation.

I investigated effects of environmental change on disease, and effects of disease on ecosystems, using a freshwater zooplankton host and its fungal parasite. This research involved lake surveys, manipulative experiments, and mathematical models. My results indicate that ecosystem characteristics such as habitat structure, nutrient availability, and quality of a host’s resources (here, phytoplankton) can affect the spread of disease. For example, a survey of epidemics in lakes revealed direct and indirect links between habitat structure and epidemic size, where indirect connections were mediated by non-host species. Then, in a mesocosm experiment in a lake, manipulations of habitat structure and nutrient availability interactively affected the spread of disease, and nutrient enrichment increased densities of infected hosts. In a separate laboratory experiment, poor quality resources were shown to decrease parasite transmission rate by altering host foraging behavior. My experimental results also suggest that disease can affect ecosystems through effects on host densities and host traits. In the mesocosm experiment, the parasite indirectly increased abundance of algal resources by decreasing densities of the zooplankton host. Disease in the experimental zooplankton populations also impacted nutrient stoichiometry of algae, which could entail a parasite-mediated shift in food quality for grazers such as the host. Additionally, I showed that infection dramatically reduces host feeding rate, and used a dynamic epidemiological model to illustrate how this parasite-mediated trait change could affect densities of resources and hosts, as well as the spread of disease. I discuss the implications of these ecosystem–disease interactions in light of ongoing changes to habitat and nutrient regimes in freshwater ecosystems.