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Latent infections of apricot fruit with Monilinia fructicola were initiated by inoculation at shuck fall and 43 and 63 days after shuck fall. The fungus entered via the stomata and penetrated a guard cell through the thin walled region at the stomatal pore. The fruit tissue responded by death of cells around the point of infection, suberization of walls of surrounding living cells and accumulation o phenolic compounds in cells up to 20 distant. Periderm developed around lesions formed at shuck fall but was absent from those formed 65 days later. When the fruit ripened, approximately 100 days after shuck fall, viable hyphae in latent infections escaped from the lesions by growing out between the cuticle and epidermis or just below the epidermal cells. Outbreak was more efficient from later inoculations and only a small proportion of latents initiated at shuck fall became invasive.