Apple Anthracnose Life Cycle and Disease Cycle

Apple anthracnose [caused by Neofabraea malicorticis (H.S. Jacks) anamorph Cryptosporiopsis curvispora (Peck)] is a fungal disease that impacts apple production. The pathogen produces cankers on trees as well as a rot on the fruit known as ‘Bull’s-eye rot’. The cankers cause severe damage to trees, can kill newly planted trees, and is limiting long-term orchard productivity in western Washington and in regions with similar climates. Growers in northwest Washington have reported removing 2-5% of trees each year and in some cases entire orchard blocks due to apple anthracnose canker. Research on apple anthracnose canker is limited and current apple anthracnose management recommendations are for Bull’s-eye rot on the fruit, not for the canker stage of the disease on trees. Thus, no effective control program exists for apple anthracnose canker. In western Washington infection appears to occur in late fall but disease progression ceases in the winter. In spring, the fungus resumes growth resulting in canker expansion and new infections may also occur. Cankers become fully mature by mid-spring (March – May), and in summer (June – August) conidia are produced on the mature cankers and are dispersed by heavy rains and wind, causing new infections to surrounding trees and fruit. To better understand the epidemiology of this disease and the elements of an effective management plan, a controlled inoculation study was conducted in a screen house at Mount Vernon, WA. The treatments are designed to elucidate the necessity of wounding for infection and if Bordeaux mixture [copper sulfate (CuSO₄) and calcium hydroxide (Ca (OH)₂)] a common fungicide used in the orchards can prevent infection with or without wounding. The five treatments include: 1) Bordeaux mixture, wounding, inoculation; 2) Bordeaux mixture, no wounding, inoculation; 3) wounding, inoculation; 4) inoculation only; 5) control (no treatment). Treatments were applied 25 Nov. 2015 to 2 year-old ‘Tompkins King’ apple trees, and after one month trees were observed every 2 weeks for symptom development. A canker was first observed 9 weeks after inoculation on, 27 Jan. 2016 in treatments 1 and 2. On 27 Feb., 13 weeks after inoculation, a canker appeared in all treatments excluding the control. Canker size ranged from 0.02 to 0.24 and infection occurred regardless of wounding and Bordeaux mixture. Small streaks of diseased tissue expanding from the wounded/inoculated area were observed only in treatment 3, suggesting that Bordeaux mixture may prevent disease progression when wounding occurs.