SUMMARY Plasmopara viticola epidemics on grapevines are caused by both primary and secondary infections that overlap for part of the season. To date, this complexity has not been incorporated into models for grape downy mildew infection forecasting. 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. Van der Plank’s logis- tic equation was integrated with a time step of 1 day; the resulting rates of disease increase were calculated separately for primary and secondary infections, then linked together. Key model parameters included oospore density and development, infection efficiency for primary infections, ability of the lesions to repro- duce asexually, infection efficiency for secondary infec- tions, and carrying capacity of the host leaves. Model structural adequacy procedures (MSA) were used to es- timate model parameters, and the model outputs were compared with real data not used in model develop- ment and parameterization. Data used for validation were taken from published studies of 23 vineyards, where lesions had been previously genetically analyzed and distinguished as primary (caused by singleton geno- types) 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. Key words: polycyclic diseases, primary and second- ary infections, model, grapevine, downy mildew. Corresponding author: V. Rossi Fax: +39.0523.599256 E-mail: vittorio.rossi@unicatt.it INTRODUCTION Many polycyclic fungal pathogens exhibit polymor- phism in their spore forms, with sexual and asexual re- production. Forms associated with sexual reproduction often serve to bridge adverse and/or non-host periods and are usually responsible for primary infections. Dis- persal units associated with asexual reproduction form a secondary inoculum that is responsible for the succes- sion of infection cycles during the host growing season (Agrios, 1988). These two kinds of spores often have different ecological requirements and have different epi- demiological characteristics (Rapilly, 1991). Downy mildew epidemics on grapevine, caused by the oomycete Plasmopara viticola Berl. et de Toni, are typical examples of polycyclic diseases caused by pathogens with dimorphic reproductive forms, i.e., with both sexual and asexual spores, which cause primary and secondary infec- tions, respectively. Oospores are the sexual spores (Wong et al., 2001) that form within the affected leaf tissue from grape ripening until leaf fall. These spores survive through the winter in the leaf litter or in the soil (Galbiati and Longhin, 1984; Gehmann, 1987). Oospores are the sole relevant source of inoculum for primary downy mildew infections (Galbiati and Longhin, 1984). They germinate gradually during the next spring (Park et al., 1997; Rossi et al., 2008a) and also during the spring(s) that follow (Kennelly et al., 2007). Germinating oospores form sporangia, which release zoospores. These zoospores are dispersed by rain splashes from the soil to the grape plants. Once deposited on the leaves, zoospores cause primary infections, and initial disease symptoms are visible as lesions in the form of “oil spots”. After a period of latency, the pathogen repeatedly pro- duces sporangia on lesions (Kennelly et al., 2007) that are dispersed in the vineyard onto new host tissues. Sporan- gia contain asexually produced zoospores, which cause secondary infections. Lesions actively contribute to the epidemic for an infectious period before becoming old and sterile (Kennelly et al., 2007). In the traditional concept of the pathogen life cycle, a downy mildew epidemic begins with a relatively small number of germinating oospores, and the explosive in- crease of the epidemic is ensured by massive clonal mul- Journal of Plant Pathology (2009), 91 (3), 615-627 Edizioni ETS Pisa, 2009 615 MODELLING THE DYNAMICS OF INFECTIONS CAUSED BY SEXUAL AND ASEXUAL SPORES DURING PLASMOPARA VITICOLA EPIDEMICS V. Rossi 1 , S. Giosuè 2 and T. Caffi 1 1 Istituto di Entomologia e Patologia Vegetale, Università Cattolica del Sacro Cuore, Via E. Parmense 84, 29422 Piacenza, Italy 2 Horta s.r.l., spin off dell’Università Cattolica del Sacro Cuore, Via E. Parmense 84, 29422 Piacenza, Italy