Fig. 3. Oospore formation in sunflower tissue. Left: clusters of oospores of different developmental stages still hulled by the oogonium and adjacent Antheridium (fluorescence microscopy after staining with resorcin). Right: young intercalary oogonium with attached antheridium. Bar equals 20 µm.
Oospores are assumed to be the source of primary infection for biotrophic oomycetes living on seasonal plants, but the mode of infection through oospores has not been investigated in many species. Studies on the germination of oospores in the Albuginomycetidae are yet limited to a single taxon, Albugo candida (DeBary, 1983; Vanterpool, 1953; Verma and Petri, 1975). Oospores of P. helianthicola, when placed in water on agar plates or on microscopic slides, formed vesicle-like structures, germ sporangia or in some cases just germ tubes (Fig 4). This process started after about 24h and within two weeks, approximately 40% of the oospores had germinated. The release of zoospores was not observed. Between oospore formation in the sunflower tissue and their germination, no dormancy or period of vernalization was necessary. The infectivity of the oospores was shown by placing them onto the apical bud of sunflower seedlings in the same way as described for inoculation with zoosporangia. The infection became visible after two weeks, when the typical pustules with zooporangia developed on leaves. Attempts to infect seedlings through the roots failed. This parallels the results observed in infection experiments with zoosporangia and suggests, that both types of spores depend on stomata to enter the host tissue before establishing a primary haustorium. For the primary infection of sunflower in the field through soil-borne or seed-borne oospores we assume, that the inoculum must reach the above ground plant parts either at an early stage of seedling development or possibly through water splash when rain drops hit the soil.
The site of primary infection is not necessarily close to the area on which first symptoms become visible through the formation of the typical blisters. Recent experiments employing a PCR-based detection system for P. helianthicola revealed that the pathogen can live asymptomatically in areas outside the chlorotic leaf lesions (Spring et al, 2011). The latter obviously develop only when mass propagation with mitotic zoosporangia starts