Herbicides in the environment alter infection dynamics in a microbial host–parasite system

Authors

  • Silke Van den Wyngaert,

    Corresponding author
    1. Institute of Integrative Biology, ETH Zürich, Zürich, Switzerland
    Current affiliation:
    1. Department of Biology, Laboratory of Aquatic Biology, Kortrijk, Belgium
    • Aquatic Ecology, Eawag, Duebendorf, Switzerland
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  • Alena S. Gsell,

    1. Department of Aquatic Ecology, Netherlands Institute of Ecology, Wageningen, The Netherlands
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  • Piet Spaak,

    1. Aquatic Ecology, Eawag, Duebendorf, Switzerland
    2. Institute of Integrative Biology, ETH Zürich, Zürich, Switzerland
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  • Bas W. Ibelings

    1. Aquatic Ecology, Eawag, Duebendorf, Switzerland
    2. Institute of Integrative Biology, ETH Zürich, Zürich, Switzerland
    3. Department of Aquatic Ecology, Netherlands Institute of Ecology, Wageningen, The Netherlands
    4. Institut F.-A. Forel, Université de Genève, Versoix, Switzerland
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For correspondence. E-mail silke.vandenwyngaert@kuleuven-kulak.be; Tel. (+32) 56 24 60 59; Fax (+32) 56 24 69 99.

Summary

Parasites play an important role in the regulation of host population growth. How these ubiquitous stressors interact with anthropogenic stressors is less often studied. In a full factorial experiment we explored the independent and combined effects of the widely used herbicide diuron and a chytrid parasite on the fitness of genetically different monoclonal diatom populations. Furthermore, we evaluated how herbicide exposure influenced infection dynamics, parasite fitness and the impact of infectious disease on host populations. We found no evidence of host genetic variation for diuron sensitivity and parasite resistance. Instead, host population phenotype was a decisive factor in controlling parasite growth. Although herbicide exposure initially posed a constraint on disease transmission, it enhanced the spread of disease over time. Consequently, the nature of the parasite–toxicant stressor interaction shifted from antagonistic (on exponential host growth) towards additive (on final uninfected host density). We conclude that herbicide exposure can modify infection dynamics and impact of disease on host populations through the complex interplay between host and parasite growth dynamics and host population phenotype.

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