Apple scab is caused by a fungus Venturia inaqualis, which overwinters in infected leaves on the orchard floor. Mating among different strains of the fungus occurs shortly after leaf fall and spores develop in the fallen leaves during the winter. Spring rains cause spores to be forcibly discharged. Spores continue to mature and are discharged over a period of 5-9 weeks. If the surface of apple tissue is wet and temperatures are suitable, the spores germinate and penetrate the cuticle and outer layers of the plant, causing an infection. The fungus grows beneath the cuticle and eventually ruptures it and forms dark green lesions. Masses of spores are produced asexually within the lesions and become detached during rain. Water splashes and redistributes these spores, causing secondary infections. Each leaf scab lesion is capable of producing 50,000-100,000 spores. Assuming 50,000 leaves per tree have 2% scab infection, about 50 million spores would be present on a single tree. One spore can cause an infection. Infections early in the season can kill tissues near the fruit surface and the fruit develops unevenly as uninfected portions continue to grow. Cracks appear in the skin and flesh and the fruit may become deformed. Heavily infected fruit fall from the tree resulting in yield losses. Scab lesions on harvested apples result in a lower price for growers since the commercial tolerance for scab damage approaches zero.
“Apple scab [Venturia inaequalis (CKE.) Winter] is one of the most important diseases of apple, causing considerable losses every year in many countries. Crop losses in the Netherlands caused by apple scab would be about 80% if no control measures were taken; therefore, 15-22 conventional spray applications per season are used to prevent apple yield loss under Dutch weather conditions.”
Authors: Holb, I. J., et al.
Affiliation: Department of Plant Protection, Centre of Agricultural Sciences, Debrecen University.
Title: Summer epidemics of apple scab: the relationship between measurements and their implications for the development of predictive models and threshold levels under different disease control regimes.
Source: Journal of Phytopathology. 2003. 151:335-343.