Stegophora ulmea

Stegophora ulmea infects all Ulmus species and Japanese zelkova.[2] It is most virulent on American white elm, Ulmus Americana[1]. Other elms it is known to infect include:[1]

• Ulmus alata (winged elm)
• Ulmus carpinifolia (European field elm)
• Ulmus crassifolia (cedar elm)
• Ulmus glabra (Wych elm)
• Ulmus hollandica (Dutch elm)
• Ulmus japonica (Japanese elm)
• Ulmus laciniata
• Ulmus laevis (European white elm)
• Ulmus parvifolia (Chinese elm)
• Ulmus procera (English elm)
• Ulmus pumila (Siberian elm)
• Ulmus serotina
• Ulmus thomasii (rock elm)
• Ulmus rubra (slippery elm)
• Zelkova serrata

Stegophora ulmea is characterized by chlorotic yellow spots 1 millimeter in diameter with a black center that develop early in the spring.[1][2][4] They darken and become raised. The black center can increase to occupy the entire chlorotic area.[4] The black spots can become about 5 millimeters in diameter.[1] As the season continues, the tissue around the original spot may become necrotic.[4] In severe cases of the disease there is premature shedding of leaves, blight of young leaves and shoots, and complete defoliation early in the fall.[1] Fruits that are infected become crumpled.[1] Infection of mature trees is rarely fatal.[1][2]

In the spring, new leaves are infected with ascospores which develop from the survival structure, perithecia, found in leaf debris.[1] It is thought that inoculum from overwintered buds can also result in infection.[1][4] The perithecia are the structure in which S. ulmea survives the winter. Ascospore release is synchronized with the foliar development of the elms.[4] Ascospores commonly infect lower leaves and leaves near the bud.[1] A period of wetness and dryness with a temperature over 7 degrees Celsius is required before ascospores are released.[1] The ascospores disperse through the air and have the potential to travel over long distances.[1] Acervuli develop in the center of the lesions.[1] Acervuli can release macroconidia, which are white.[1] They mature 10–20 days after infection.[1] During spring and early summer, the macroconidia act as a secondary inoculum. This is the asexual part of S. ulmea’s life cycle.[1] Water is necessary for the dispersal of the macroconidia.[1] Microconidia are produced in the lesions during midsummer.[1] They act as spermatia in the sexual stage of the S. ulmea’s life cycle.[1] During late summer and fall perithecia, the sexual structure, begins to develop.[1]

Sanitation, or removal all leaf debris seems to be the best method of control.[1] In commercial growing arenas, it is suggested that overhead watering should not be used, because it helps spread the pathogen.[1] Resistance greatly varies between species.[1] U. thomasfi seems to be the most resistant.[4] The majority of elms seem to be tolerant.[4] A dominant gene conferring resistance to U. parvifolia was discovered, though it did not provide absolute resistance.[5] There is currently no information about fungicides used to control this disease.[1] This disease is not typically fatal and is not actively addressed.[3] Aeration seems to moderately reduce growth and sporulation.[6] Cool temperatures and high humidity enhance the disease, so avoidance of these conditions will decrease the prevalence of disease.

• Index Fungorum
• USDA ARS Fungal Database