coexistence remain relatively unexplored. However, it is important to understand coexistence as it has significant consequences for resistance management. For example, the survival of even a small sensitive population under treatment will enhance the post treatment recovery of sensitivity. All current spray technologies are imperfect and result in an incomplete coverage of fungicide to the host crop. Here we use modelling to examine whether this spatial heterogeneity in spray coverage can facilitate the coexistence of resistant and sensitive strains. We extend the model by Gubbins & Gilligan (1999) to incorporate incomplete spray coverage and explicitly model the dynamics of the spores within the resulting heterogeneous system. By accounting for the dynamics of the limited supply of susceptible host tissue and its effect on the competition between strains, we show that spray heterogeneity per se does not facilitate coexistence but that the outcome depends on the trade-off between the fitness cost to resistance and the effectiveness of the fungicide. In addition we find that the maximum density of healthy host tissue is attained when there is coexistence of pathogen strains.
Studies investigating the biology and epidemiology of Rhynchosporium secalis (leaf blotch of barley)
James Fountaine1, Bart Fraaije1, Elaine Ward1, Naomi Pain2, Sarah Perfect2 and Michael Shaw3
1 Plant-Pathogen Interactions Division, Rothamsted Research, Harpenden, Hertfordshire, UK, AL5 2JQ, 2 Syngenta, Jealotts Hill Research station, Bracknell, Berkshire, UK, RG12 6EY, 3 Department of Agricultural Botany, University of Reading, PO Box 221, Reading, UK, RG6 6AS
Leaf blotch, caused by Rhynchosporium secalis, is the most important disease of barley in the UK. Very little is known about the primary infection and subsequent, spatial and temporal distribution of this disease within a field-grown commercial crop. This study is primarily focused on the development of natural epidemics of leaf blotch in winter barley. PCR techniques and visual assessments were used to study epidemics of R. secalis in commercially available cultivars throughout three growing seasons. Results using multiplex PCR showed that R. secalis was present in both resistant and susceptible cultivars. A real-time PCR assay was developed and used to quantify the amount of disease in different cultivars of winter barley. There was generally good correlation between visual assessments and real-time PCR using TaqMan probes. Some resistant cultivars showed no sign of symptoms but R. secalis could be detected by PCR. Since there are two opposite mating types in populations of R. secalis, the production of ascospores could be an important source of primary inoculum. However, no ascospores were detected by PCR using tapes from a Burkard spore trap. Results (from 2004) show that seed-born infections are an important source of primary inoculum and can explain the spatio-temporal development of epidemics. A better understanding of epidemic development will allow more precise targeting of fungicides and curtail the potential for fungicide resistance development.
Modelling stem canker on winter oilseed rape
Konstantina Papastamati1,2, Frank van den Bosch1, and Mike Jeger2 1Biomathematics Unit, Rothamsted Research, Harpenden AL5 2JQ, Herts; 2Dept Agricultural Sciences, Imperial College at Wye, Wye, Ashford, Kent TN25 5AH.
Stem canker (Leptosphaeria maculans) is an economically important disease affecting winter oilseed rape in the UK. The dynamics of the disease are driven by weather variables, as temperature and leaf wetness are important for infection to occur (West et al., 1999). The initial phase of infection (caused by air-borne ascospores) happens in autumn and it is followed by four phases: period to lesion appearance, asymptomatic systemic growth along the petiole, latent infection of the stem and stem canker development (Hammond and Lewis, 1986). The rosette stage is critical in understanding the mechanism of the initial infection process because the development of phoma lesions during autumn/winter and the stem cankers in spring are related (Sun et al., 2000). A mechanistic model is developed to understand how the pathogen reaches the stem after it has successfully infected leaves during autumn. The model estimates the production of new and healthy leaf area, infected leaf area (symptomless), visible phoma lesion area and probability of the stem getting infected, using real ascospore counts and leaf wetness estimated by an oilseed rape-specific wetness model. The model was extended for treated plants assuming different fungicide types (protective, curative or complete) and time of application. The model predicts phoma and expected stem canker incidence well and suggests more than one treatments with a curative or complete fungicide, first applied in November/December or in October in case of early phoma epidemics. These results agree with previous field studies and the model could be used for evaluation of fungicide spray programs. This is the first mechanistic model to be developed for phoma and stem canker and it can aid in the development of forecasting schemes due to its biological reality and good performance.