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Significance of leaf infection by Botrytis cinerea in stem rotting of tomatoes grown in non-heated greenhouses

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Abstract

The most serious symptom of Botrytis cinerea in tomatoes grown in greenhouses is stem rotting. Lesions on the stem may result from direct infection or from progression of the rot along infected leaves, until infection approaches the stem. In a set of experiments conducted in commercial greenhouses, an experimental greenhouse and growth chambers, the significance of the two types of stem infections was studied. In non-heated greenhouses most of the stem lesions originated from progression of the pathogen along infected petioles. The rate at which B. cinerea had progressed on infected petioles was 0.3–0.5 cm/day, an average of ca. 6 weeks was needed for a leaf infection to approach the stem. Application of Trichoderma harzianum T39 extended this time by 1–2 weeks and application of chemical fungicides by 3 weeks. Influence of the environment on the progression of B. cinerea along infected petioles was then determined. Within range of 5–30 °C, the higher the temperature, the more rapid was the rate of disease progression. The fungus progressed more rapidly on tomato petioles incubated at high vapour pressure deficit (VPD) rather than at low VPD. The source-sink relationship of the plant governed the rate of B. cinerea progression along the petioles as well: it was more rapid when the source was restricted (by shading) and slower when the sink was restricted (by removal of flowers and small fruits). The possibility that sanitation of infected leaflets would reduce the incidence of stem rotting was examined in two experiments. In plots not treated with a fungicide, the sanitation treatment substantially decreased the incidence of stem lesions and this treatment was as effective as weekly application of chemical fungicides.

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Shtienberg, D., Elad, Y., Niv, A. et al. Significance of leaf infection by Botrytis cinerea in stem rotting of tomatoes grown in non-heated greenhouses. European Journal of Plant Pathology 104, 753–763 (1998). https://doi.org/10.1023/A:1008690925443

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