The disease cycle begins in early spring, when cool temperatures and abundant moisture promote the release of sexual spores (ascospores) from overwintering structures (pseudothecia) found in the debris at the base of previously-infected trees.
Moisture is a critical factor in the development of the disease as rainfall not only triggers the release of ascospores, but also facilitates the infection of new hosts by helping the spores adhere to and germinate on the healthy tissue of new hosts.
Following their dissemination, ascospores are transported to the surfaces of newly-emerged leaves and blossoms by wind and splashing water.
The tissue is then penetrated either directly with a germ tube or indirectly using an appressorium, thus initiating a new infection.
Shortly after penetration, light-green, irregularly shaped lesions develop on infected foliar tissue and gradually darken, expand, and pucker as the infection progresses.
Lesions on fruit are black or brown and irregularly shaped, with older fruit lesions causing the underlying tissue to become dry, corky, and eventually disfigured by splitting.
Within 10 days of infection, asexual conidia will develop on the darkened lesions and allow for the establishment of secondary infections in healthy leaf and fruit tissue.
Under optimal conditions, this cycle may repeat every 1–2 weeks during the growing season.
At the end of the season, heavily-infected fruit and foliage fall from the canopy, allowing for the development of pseuothecia, which serve as a source of primary inoculum for the next spring.
The disease cycle begins in early spring, when cool temperatures and abundant moisture promote the release of sexual spores (ascospores) from overwintering structures (pseudothecia) found in the debris at the base of previously-infected trees. Moisture is a critical factor in the development of the disease as rainfall not only triggers the release of ascospores, but also facilitates the infection of new hosts by helping the spores adhere to and germinate on the healthy tissue of new hosts. Following their dissemination, ascospores are transported to the surfaces of newly-emerged leaves and blossoms by wind and splashing water. The tissue is then penetrated either directly with a germ tube or indirectly using an appressorium, thus initiating a new infection. Shortly after penetration, light-green, irregularly shaped lesions develop on infected foliar tissue and gradually darken, expand, and pucker as the infection progresses. Lesions on fruit are black or brown and irregularly shaped, with older fruit lesions causing the underlying tissue to become dry, corky, and eventually disfigured by splitting. Within 10 days of infection, asexual conidia will develop on the darkened lesions and allow for the establishment of secondary infections in healthy leaf and fruit tissue. Under optimal conditions, this cycle may repeat every 1–2 weeks during the growing season. At the end of the season, heavily-infected fruit and foliage fall from the canopy, allowing for the development of pseuothecia, which serve as a source of primary inoculum for the next spring.
Apple scab