Fact Sheet FS512
Botrytis blossom blight, also referred to as twig blight or gray mold, is a fungal disease that can infect the twigs, leaves, blossoms, and berries of highbush blueberries. The common name of this disease is determined by the infection site and/or timing (i.e., twig blight refers to twig infections and gray mold refers to the color of post-harvest berry infections). Botrytis cinerea is the primary causal organism of Botrytis blossom blight in New Jersey, but infections can be less commonly caused by other species such as B. pseudocinerea. The host range of this pathogen is broad, including small berry crops such as raspberries, grapes, strawberries, vegetable crops and many ornamental plants.
Botrytis blossom blight is infrequent and unpredictable on blueberry in New Jersey, even though the pathogen is abundant. In other growing regions, this disease is more common, especially in the cooler, wetter growing regions where it is devastating if left uncontrolled. In New Jersey, the pathogen frequently affects strawberries and some cane fruits. As is the case with many fungal pathogens, climatic factors are closely associated with the severity of the disease.
Diagnosis
Symptoms of Botrytis blossom blight include dead, necrotic blossoms (Fig. 1A) that may cause water-soaked areas to form on berries (Fig. 1B). Under wet, cool conditions, the symptoms will expand to the entire flower cluster, killing the blossoms and calyx as well as the supporting stems (Fig 1A, C). Fruit can begin rotting before ripening, eventually causing necrotic, shriveled berries (Fig. 1C). The leaves will also develop brown lesions when infected blossoms drop on the leaf surface (Fig. 1D) whereas twig lesions develop when infections progress from infected blossoms back into the woody tissues. Grayish spores form in masses on the blossoms and calyces (Fig. 1E, F). Spores can be seen on the dying blossoms, calyx, and shriveled berries. B. cinerea also produce hardy, blackened structures called sclerotia that survive the winter season in soil or attached to plant stems (Fig. 1G).
Life Cycle
Spores of the fungus, B. cinerea, are introduced into the field at the beginning of each season in many ways. The pathogen can be introduced to blueberry fields from other crops via airborne spores. In a field that was previously infected, the pathogen may develop from overwintering structures. Dead plant debris and sclerotia can serve as an inoculum source and location for the pathogen to overwinter. Wet, foggy conditions with temperatures between 16 °C (61 °F) and 20 °C (68 °F) are ideal for infection to occur. Older, weak, or damaged tissue is more susceptible to infection than newer, healthy tissue. Blossoms are often the first part of the plants to be symptomatic, especially during seasons with poor or slow pollination.
Slow pollination occurs when conditions affect pollinator activity, such as rain or cold and following frost events that damage flowers. This results in senescing petals that remain attached to the plant. These petals are susceptible to infection and lead to berry infections (See Fig. 1). Conidiation, or the production of asexual spores, leads to the infection's further spread on other tissues such as twigs, leaves, and berries. These spores are spread naturally through wind or rain events, or by humans conducting various agricultural activities in the production area.
Predisposing Factors
In general, B. cinerea is a weak, opportunistic pathogen. It typically infects tissue that is already senescing or diseased, where it then spreads to healthier plant tissue. Despite its weak nature, there has been fungicide resistance discovered in multiple strains of B. cinerea, leading to difficulties managing the fungus. Additionally, B. cinerea is often prevalent as the spores are often airborne throughout the environment, including cropping systems and post-harvest conditions.
A variety of factors can predispose highbush blueberries to Botrytis blossom blight. Frost damage can injure or kill emerging buds at the beginning of the growing seasons, leaving the tissue vulnerable to infection (Fig. 2). Water stress may also weaken plant defenses leading to greater incidences of B. cinerea. Phytotoxicity caused by pesticide applications may also lead to injured or dead tissue that is easily infected. As mentioned before, poor pollination can prolong the bloom period, causing older, senescing blooms still attached to the plant to become susceptible. Finally, pre-existing infections of other diseases such as Phomopsis canker and twig blight and blueberry scorch virus (BIScV) can leave highbush blueberries susceptible to other pathogens and encourage opportunistic co-infections of B. cinerea and the pre-existing pathogen.
Management
Fungicide applications are important in highbush blueberry production, however implementing cultural practices in a management program is an essential first step as fungicides can be expensive and not sustainable if solely relied on. When planting new fields, low lying areas are not ideal as they may experience longer frosts or fog. Row and plant spacing and pruning methods can affect plant ventilation between and within plants. These cultural methods can help reduce the risk of Botrytis by allowing bushes to dry out more quickly. Pruning out dead canes and twigs removes potential inoculum sources in the field.
Before applying fungicides, it is important to ask the following questions:
If no in-bloom fungicide applications were used and the climatic conditions are conducive, the risk of Botrytis blossom blight increases. For fungicide recommendations, refer to the current edition of the Commercial Blueberry Pest Control Recommendations for New Jersey.
References
November 2024
Copyright © 2024 Rutgers, The State University of New Jersey. All rights reserved.
For more information: njaes.rutgers.edu.
Cooperating Agencies: Rutgers, The State University of New Jersey, U.S. Department of Agriculture, and Boards of County Commissioners. Rutgers Cooperative Extension, a unit of the Rutgers New Jersey Agricultural Experiment Station, is an equal opportunity program provider and employer.