Direct and indirect effects of viral pathogens and the environment on invasive grass fecundity in Pacific Coast grasslands
Article first published online: 12 AUG 2009
© 2009 The Authors. Journal compilation © 2009 British Ecological Society
Journal of Ecology
Volume 97, Issue 6, pages 1264–1273, November 2009
How to Cite
Seabloom, E. W., Borer, E. T., Jolles, A. and Mitchell, C. E. (2009), Direct and indirect effects of viral pathogens and the environment on invasive grass fecundity in Pacific Coast grasslands. Journal of Ecology, 97: 1264–1273. doi: 10.1111/j.1365-2745.2009.01550.x
- Issue published online: 13 OCT 2009
- Article first published online: 12 AUG 2009
- Received 2 June 2009; accepted 1 July 2009 Handling Editor: Jeremy Burdon
- Avena fatua;
- Bromus hordeaceus;
- community ecology;
- disease ecology;
1. Pathogens can have strong effects on their hosts and can be important determinants of biological invasions. In natural systems, host–pathogen interactions may be mediated by direct environmental effects on pathogen communities and host fitness.
2. While environmental mediation of host–pathogen interactions has been investigated experimentally and at single sites, there have been few studies tracking pathogen effects on lifetime host fecundity across large naturally occurring environmental gradients.
3. If environmental factors directly mediate both pathogen transmission and host fecundity, laboratory and local-scale studies may not predict pathogen effects across large spatial scales.
4. Here we investigate the relationship between host fecundity and infection by a suite of RNA viral pathogens, by surveying two invasive annual grasses at 18 locations along a 1200-km latitudinal gradient on the west coast of North America.
5. Infected hosts of both species had 28–30% lower fecundity than uninfected hosts in our field surveys. However, the correlation of reduced fecundity to infection arose from indirect effects of the environment on both host fecundity and pathogen prevalence, rather than direct effects of the pathogen on the host. Pathogen prevalence was highest at sites where uninfected hosts had lowest fecundity.
6. Synthesis. In past experimental inoculations, virus infection reduced fecundity of these host species. Against this background, the results of our geographic-scale survey demonstrate the challenges not only of inferring cause from correlation, but also of extrapolating from local studies and experimental inoculations to larger spatial scales. Our results highlight a need for experimentally manipulating infection across environmental gradients. Such an integrated approach would allow quantification of the fitness impacts of infection, even when the environment directly affects both prevalence and host fecundity.