Developmental Histopathology of Cankers Incited by Hypovirulent and Virulent Isolates ofEndothia parasiticaon Susceptible and Resistant Chestnut Trees

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Abstract
The histopathology of canker development on blight-resistant Chinese chestnut [Castanea mollissima] and blight-resistant and blight-susceptible American chestnut [C. dentata] was examined after wounding plus inoculation with virulent (V) or hypovirulent (H) isolates of E. parasitica. Bark lesions or wounds were delimited initially by a zone of lignified tissue forming 8-10 days after inoculation in all host-treatment combinations, which halted advance of individual hyphae. Wound periderm formation began immediately adjacent to this lignified zone 10-14 days after inoculation. Wound periderm formation began at the deepest point of a wound or canker and progressed outward to the bark surface. The development of wound periderm was affected by its orientation in bark tissues and was disrupted by growth of mycelial fans. Otherwise, there were no differences in rate or extent of wound periderm formation among host-treatment combinations. Superficial cankers were formed in resistant trees by V E. parasitica, or in susceptible trees by H E. parasitica. This occurred when slow-growing mycelial fans expanded through outer regions of bark, where wound periderm had not formed or had not developed fully. The lignified zone and developing wound periderm in the susceptible host were penetrated by mycelial fans of the V isolate at 18 days and by mycelial fans of the H isolate at 28 days. In the 2 resistant hosts, mycelial fans of V but not H E. parasitica sometimes formed and grew after 30 days. Physical pressure probably played a role in the growth of mycelial fans. Mycelial fan penetration halted wound periderm development because host tissues were killed; individual hyphae or fans killed host cells before touching them.

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