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The initial symptom is usually a dark-brown, sunken lesion which eventually may girdle the stem just above soil level (Jones, 1991). Secondary cankers may develop later, higher up the stem. The soft, outer diseased tissue contains numerous conidiomata and, in damp conditions, conidia are extruded in slimy pink masses (Holliday and Punithalingam, 1970).
Avoid wounds and high rates of watering. Remove diseased plants. Debris from the previous season's crop should also be removed and destroyed. In glasshouses the humidity should be kept below 90% RH and the temperature above 15°C (Verhoeff, 1962; Fagg and Fletcher, 1987; van Steekelenburg, 1988). Solarization of soil and of the reed canes (Arundo donax) or Eucalyptus stakes used to support tomatoes reduces disease incidence (Besri, 1983; Cartia, 1989; Besri, 1991).
Resistance to D. lycopersici on F3- and Bc1-lines from interspecific crosses of L. esculentum with L. hirsutum and with L. hirsutum f. glabratum is not monogenic and is inherited in a dominant fashion (Boukema, 1982). Tomato grafting on the hybrid KNVF has shown resistance to D. lycopersici (Ginoux et al., 1978) but there is no tomato cultivar with complete resistance to the disease (Fagg and Fletcher, 1987).
Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:
D. lycopersici occurs sporadically in Europe and New Zealand. Modern techniques used in tomato production (culture in nutrient solutions and rockwool) have eliminated soil as a source of inoculum and have, therefore, reduced disease incidence. Despite this, localized outbreaks do occur: in one glasshouse in West Sussex, UK, 105 basal lesions (affecting 12% of the tomato plants) were recorded in June 1985, 6 months after the plants were established on rockwool (Fagg and Fletcher, 1987).