Anthracnose, caused by Colletotrichum acutatum and C. gloeosporioides, is a major fungal disease of olive in many countries. In Spain, the disease has been associated only with a characteristic rot and mummification of mature fruit. The purpose of this study was to determine whether C. acutatum could infect other plant tissues that may serve as sources of inoculum for anthracnose epidemics. Inoculations of young plants or detached leaves and field observations demonstrated that flowers and immature olive fruit are susceptible to the pathogen. Flower infection caused blight of inflorescences and infection of developing fruit. Immature fruit were infected in all phenological stages, although infection remained latent for 7 to 8 months, until the onset of fruit ripening. Fruit susceptibility increased and latent period decreased with maturity. Fruit were required for symptom development on inoculated plants. Plants without fruit were infected but they did not show any disease symptoms. Only plants with rotten fruit developed leaf wilting and branch dieback symptoms several weeks later. These results, together with the low level of pathogen isolation from affected leaves and branches and the toxicity of sterile fungal extracts to olive cuttings, suggest that a toxic substance produced by C. acutatum in rotten fruit may account for this syndrome. Both disease syndromes, fruit rot and branch dieback, developed in several olive cultivars, which were equally susceptible to the pathogen. However, olive cultivars differed in their response to flower and fruit infection. Latent infection of developing fruit during the spring may permit survival of the pathogen during the hot and dry summer and serve as an inoculum source for anthracnose epidemics that develop on ripening fruit in autumn.

The influence of temperature, wetness duration, and planting density on infection of olive fruit by Colletotrichum acutatum and C. simmondsii was examined in laboratory and field experiments. Detached olive fruit of 'Arbequina', 'Hojiblanca', and 'Picual' were inoculated with conidia of several isolates of the pathogen and kept at constant temperatures of 5 to 35°C in humid chambers. Similarly, potted plants and stem cuttings with fruit were inoculated and subjected to wetness periods of 0 to 48 h. Infection occurred at 10 to 25°C, and disease severity was greater and the mean latent period was shorter at 17 to 20°C. Overall, C. acutatum was more virulent than C. simmondsii at temperatures <25°C. When temperature was not a limiting factor, disease severity increased with the wetness period from 0 to 48 h. Disease severity was modeled as a function of temperature and wetness duration; two critical fruit incidence thresholds were defined as 5 and 20%, with wetness durations of 1.0 and 12.2 h at the optimum temperature. In the field, anthracnose epidemics progressed faster in a super-high-density planting (1,904 olive trees/ha) than in the high-density plantings (204 to 816 olive trees/ha) and caused severe epidemics in the super-high-density planting even with the moderately resistant Arbequina. Data in this study will be useful for the development of a forecasting system for olive anthracnose epidemics.

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