Epidemics caused by Plasmopara viticola on grapevines are caused by both primary and secondary infections that overlap for a part of the season. To date, this complexity has not been incorporated into models for grape downy mildew. A conceptual model was developed that links the quantitative aspects of both sexual and asexual stages of the P. viticola life cycle in a biologically coherent framework. Vanderplank’s logistic equation was integrated with a time step of 1 day; the resulting rates of disease increase were separately calculated for primary and secondary infections and linked together. Key model parameters included oospore density and development, infection efficiency for primary infections, ability of the lesions to reproduce asexually, infection efficiency for secondary infections, and carrying capacity of the host leaves. The model structural adequacy procedures (MSA) were used to estimate model parameters, and the model outputs were compared with real data not used in model development and parameterization. Real data were taken from published studies of 23 vineyards, where lesions had been previously genetically analyzed and distinguished as primary (caused by singleton genotypes) and secondary (caused by clonal genotypes). The 23 vineyards had experienced epidemics characterised by a low to high level of clonality. The estimated model parameters were biologically plausible and consistent with previous knowledge, and the model accurately mimicked the variability of the 23 real epidemics. The model represents a coherent mathematical structure for developing a simulator for downy mildew epidemics in the vineyard.
|Numero di pagine||13|
|Rivista||Journal of Plant Pathology|
|Stato di pubblicazione||Pubblicato - 2009|
- downy mildew
- polycyclic diseases
- primary and secondary infections