Fungicide Sensitivity of Pythium spp. Associated with Cavity Spot of Carrot in California and Michigan

The identity of 172 isolates of Pythium spp. from cavity spot lesions on carrot produced in California and Michigan was determined, and their sensitivity to three fungicides was examined. Pythium violae accounted for 85% of California isolates, with P. irregulare, P. dissotocum (the first report as a carrot pathogen in the United States), P. ultimum, and P. sulcatum making the balance. P. sulcatum, P. sylvaticum, and P. intermedium were the most commonly recovered (85%) species in Michigan; others from Michigan included P. intermedium, P. irregulare, and an unclassified strain, M2-05. On fungicide-amended media, 93% of isolates were sensitive to mefenoxam (inhibition of mycelial growth was >60% at 10 μg active ingredient [a.i.]/ml); however, two of five isolates of P. irregulare from California were highly resistant (≤60% inhibition at 100 μg a.i./ml); about half of the isolates of P. intermedium and P. sylvaticum and a single isolate of P. violae were highly or intermediately resistant to mefenoxam (>60% inhibition at 100 μg a.i./ml, or ≤60% inhibition at 10 μg a.i./ml). P. dissotocum, P. irregulare, P. sulcatum, M2-05, and three of seven isolates of P. intermedium were insensitive to fluopicolide (effective concentrations for 50% growth inhibition [EC50] were >50 μg a.i./ml), while P. sylvaticum, P. ultimum, P. violae, and some isolates in P. intermedium were sensitive (EC50 < 1 μg a.i./ml). All isolates were sensitive to zoxamide (EC50 < 1 μg a.i./ml). Sensitivity baselines of P. violae to zoxamide and fluopicolide were established.

A comparative study of carrot root tissue colonization and cell wall degradation by Pythium violae and Pythium ultimum, two pathogens responsible for cavity spot

The process of infection of carrots by Pythium violae and Pythium ultimum, two causes of cavity spot, is described. The first species causes limited root necrosis, the second progressive root rot. Colonization by both species was intracellular and limited within the tissues. Modes of cell wall degradation were studied by staining (PATAg test) and labeling techniques. Pectins were labeled with monoclonal antibodies and cellulose with an exoglucanase-gold complex. Cell wall polysaccharides were degraded differently by the two species. Pythium violae was responsible for degradations, which could be noticeable, especially for high methylesterified pectins, but which occurred after colonization and were localized near the hyphae. The conservation of integrity of diseased tissue was apparently due to the absence of degradation away from the hyphae. In contrast, P. ultimum was responsible for more extensive degradation of pectins and cellulose, which occurred at a relatively greater distance from the hyphae. Degradation of pectins was always more rapid in the cell walls than in the intercellular junctions. This phenomenon led to loss of tissue integrity and could explain the tissue maceration caused by P. ultimum infection. These differences in infection process are discussed in connection with the enzymic potential for degradation of cell wall polysaccharides.Key words: Daucus carota L., Pythium, pectin, cellulose, cytochemistry.