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Steve Chaplin
IU Communications

Last modified: Thursday, March 29, 2012

Evolving to become more susceptible to disease? 'Yes,' finds research from Indiana lakes

Ecology, often human-influenced, drives epidemic size; species evolutionary paths follow

March 29, 2012

BLOOMINGTON, Ind. -- New research at a series of Indiana lakes has produced a surprising result at the intersection of the ecology and evolution of disease. During disease outbreaks, host populations can evolve to become more resistant to their deadly parasites -- or they might instead evolve to become more susceptible to these very same parasites. The key factor determining these opposing outcomes: the size of the disease outbreaks.

Sick Daphnia

Two Daphnia dentifera, left and right, infected with the fungus Metschnikowia bicuspidata, surround an uninfected host. Darker areas exhibit the location where fungal spores have collected.

Print-Quality Photo

"It's a pretty amazing result that hosts can evolve to become more susceptible to parasites that ultimately kill them, but it does make sense if hosts trade off resistance to infection with capacity to make more offspring," said Spencer R. Hall, an associate professor in the Indiana University College of Arts and Sciences' Department of Biology and co-author of the research to be published Friday, March 30, in Science. "Sometimes the genotypes that make more babies are overall more fit, even if they become more readily infected. This tradeoff helps to explain our results."

With assistance from Indiana's Division of Forestry and Division of Fish and Wildlife, researchers quantified epidemic size of the yeast parasite Metschnikowia bicuspidata in seven lakes in Greene and Sullivan counties in Indiana. To explain variation in epidemic size among lakes, they accounted for differences in ecological factors known to influence disease: overall productivity (phosphorus and nitrogen amounts) and fish predation. Then, to quantify evolutionary response of hosts, they also measured susceptibility of genotypes of the zooplankton Daphnia dentifera before and after epidemics started.

"The evolutionary paths of the Daphnia in the lakes correlated with the ecologically driven variation in epidemic size in the lakes," Hall noted.

That's important, he said, because it also suggests that anthropogenic influences that tilt predation pressure and the productivity of ecosystems in one direction or another may influence the evolution of host-parasite interactions.

"What we showed here was that ecological context -- how productive the lakes were and how much predation hosts experienced in them -- influenced the size of yeast parasite epidemics. Size of the epidemics then determined the evolutionary responses of the Daphnia to the parasite," Hall said.

Three lakes with low fish predation and high nitrogen content -- Island, Midland and Scott -- experienced large yeast outbreaks. In these lakes, the host populations became dominated by more resistant genotypes as epidemics waned. This result makes evolutionary "common sense."

Yeast Spores

Scanning electron microscope image of masses of cylindrical fungal spores collected within the body of a Daphnia.

Print-Quality Photo

The opposite was true in Canvasback, Downing and Hale lakes. There, epidemics remained small due to high predation pressure and low nitrogen levels. At the end of the epidemics in these lakes, Daphnia populations were dominated by genotypes that were more susceptible to infection. This result was much more surprising, although the researchers know that more susceptible genotypes typically produce more offspring, thus allowing them to increasingly dominate through time. (Daphnia in the seventh lake, Beaver Dam, showed no significant change in disease susceptibility, although there was a trend toward Daphnia showing increased disease resistance).

Hall said that in an age where genomics and immunology have become such a strong focus in disease biology, it remains vitally important to recognize that ecological context strongly shapes evolutionary outcomes during disease epidemics. As this research progresses, those outcomes may become increasingly predictable in the future.

"Anthropogenic manipulation of ecosystems, such as culling of predators or eutrophication, can noticeably boost disease prevalence. These factors can also profoundly influence genetic composition of hosts, a less visible but still important consequence," he said.

Lead author on the paper is Meghan A. Duffy of Georgia Institute of Technology, with Hall, IU Bloomington biology Ph.D. student David J. Civitello, Jessica Housley Ochs and Rachel M. Penczykowski, also of Georgia Tech, and Christopher A. Klausmeier of Michigan State University as co-authors. Hall and Duffy have collaborated on ecology and infectious disease research since working together in 2003 at Michigan State's W.K. Kellogg Biological Station.

"We also have to thank Indiana's Department of Natural Resources and specifically Steve Siscoe at the Division of Forestry's Greene-Sullivan State Forest and Ron Ronk at the Division of Fish and Wildlife's Minnehaha Fish and Wildlife Area. They make it possible for us to work on public lands," Hall said.

The research was funded by the National Science Foundation and the James S. McDonnell Foundation.

For more information or to speak with Hall, please contact Steve Chaplin, IU Communications, at 812-856-1896 or Tweeting IU science news: @IndianaScience

"Ecological Context Influences Epidemic Size and Parasite-Driven Evolution," published March 30, 2012, in Science. (Abstract only for non-subscribers).