Botrytis cinerea is ubiquitous in the orchard being present as sclerotia in soil on plant debris, weeds, grass mowings, windbreak trees, mummified fruits and bark.
- In wet, windy, weather at most times of the year the sclerotia sporulate and the spores (conidia) are spread by wind and rain.
- At blossom time spores will infect dying blossom and remain as latent infections in the remains of the flower parts still attached to the developing fruits, or become established as latent infections in the calyx.
- Occasionally the fungus continues to develop and form a small rot or blemish around the calyx.
- This does not usually progress far and then dries forming the dry-eye rot lesion.
- Usually though the fungus does not start to rot fruit from these blossom infections until the fruit has been in store for several months, usually December onwards.
- Then the fungus will invade the fruit at the calyx end forming the typical calyx end rot with irregular fingers of rotting spreading down from the calyx.
- Once developed the fungus can spread to healthy fruit in the bin by contact spread, forming large nests of rotted fruit. Research has shown that most apples become symptomlessly infected with Botrytis during flowering.
- However, not all infected fruit subsequently rot in store.
- The factors that affect development of Botrytis eye rot in store are not fully understood.
- Controlled atmosphere storage, especially low oxygen, appears to encourage rot development but further research is needed to determine other factors that may be involved.
Botrytis may also act as a wound pathogen, where it behaves more like Penicillium rot.
- Fruit becomes infected via wounds sustained during harvesting and handling, particularly from Botrytis spores contaminating drench tanks and water flumes on grading machines.
- Botrytis that invades via wounds starts rotting immediately in store and the rot readily spreads to healthy fruit in the bin causing extensive nesting of rots.