Effects of habitat fragmentation on choke disease (Epichloë bromicola) in the grass Bromus erectus

Authors

  • Kathleen Groppe,

    1. Botanisches Institut der Universität Basel, Hebelstrasse 1, CH-4056 Basel,
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  • Thomas Steinger,

    1. Botanisches Institut der Universität Basel, Hebelstrasse 1, CH-4056 Basel,
    2. Institut für Umweltwissenschaften, Universität Zürich, Winterthurerstrasse 190, CH-8057 Zürich,
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  • Bernhard Schmid,

    1. Botanisches Institut der Universität Basel, Hebelstrasse 1, CH-4056 Basel,
    2. Institut für Umweltwissenschaften, Universität Zürich, Winterthurerstrasse 190, CH-8057 Zürich,
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  • Bruno Baur,

    1. Botanisches Institut der Universität Basel, Hebelstrasse 1, CH-4056 Basel,
    2. Department of Integrative Biology, Section of Conservation Biology (NLU), University of Basel, St Johanns-Vorstadt 10, CH-4056 Basel, Switzerland
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  • Thomas Boller

    1. Botanisches Institut der Universität Basel, Hebelstrasse 1, CH-4056 Basel,
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B. Schmid, Institut für Umweltwissenschaften, Universität Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland (e-mail:bschmid@uwinst.unizh.ch).

Summary

  • 1 The fungal endophyte Epichloë bromicola causes choke disease on Bromus erectus, thereby suppressing maturation of host inflorescences. We conducted a 3-year field experiment to investigate the effects of small-scale habitat fragmentation on the occurrence of choke disease in three calcareous grasslands in the Swiss Jura Mountains, where, overall, 4.3% of all flowering tillers had diseased inflorescences.
  • 2 The number of diseased B. erectus plants (presumed genets), the number of tillers with diseased inflorescences, and the number of tillers with healthy inflorescences were counted over 3 years, but healthy tillers could not be allocated to particular genets. Each of 12 blocks contained one large (4.5 × 4.5 m), one medium (1.5 × 1.5 m) and two small (0.5 × 0.5 m) fragments and corresponding control plots. The percentage of tillers in the plots that were infected but did not show disease symptoms (asymptomatic plants) was estimated in the final year of the study using a diagnostic polymerase chain reaction. On average 1.7% of all tillers without disease symptoms were infected.
  • 3 There were significantly more diseased plants in fragment than in control plots, particularly in small fragment plots or in the third year of the study, indicating that disease incidence in the host plant increased after fragmentation if assessed at the level of the genet population. This was probably due both to a switch of genets from the asymptomatic to the symptomatic state and to increased horizontal transmission of the disease in fragments.
  • 4 The increase in the number of flowering tillers with diseased inflorescences was outweighed by that in the number of tillers with healthy inflorescences. Disease incidence was therefore decreased by fragmentation if assessed at the level of the host flowering tiller population. The effect on healthy plants was probably due to beneficial abiotic edge effects following fragmentation.
  • 5 Plot size affected fragmentation response, with the largest increases in small, followed by medium and large fragments. Similarly, the strength of fragmentation responses increased through time over the 3-year study period.
  • 6 Significant site to site and year to year variation in the number of diseased plants and in the number of tillers with diseased inflorescences suggested that separate experiments with replication within site and year would have yielded a series of interesting but individually different results. Only by repeating the experiments at several sites and over several years was it possible to obtain the general results reported in the previous points.

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