This dissertation research contributes to understanding the role of fungal community succession in chestnut blight cankers on American chestnut trees and interactions between the chestnut blight pathogen, Cryphonectria parasitica, virulence-altering hypoviruses, and secondary fungal invaders. Hypoviruses infect the pathogen mycelium directly and are known to decrease pathogen virulence (i.e. hypovirulent). These viral infections can slow pathogen growth, decreasing the rate of canker expansion and lowering the probability of girdling. Secondary fungi also invade the expanding canker and may antagonize C. parasitica and reduce pathogen growth. The main objectives of this research are: (i) describe the spatial and temporal dynamics of the fungal community within cankers from six American chestnut populations from 2012-2016 and correlate with the severity of cankers and the likelihood of girdling; (ii) assess the ability of different fungal taxa, isolated from low severity cankers, to inhibit the growth of virulent and hypovirulent forms of C. parasitica in dual culture tests; and (iii) evaluate the combined effect of fungal antagonism and a hypovirus on canker expansion rates with treatment of experimental cankers.The spatial distribution of virulent and hypovirulent C. parasitica and non-C. parasitica fungi within a canker differed from the spatial structuring we predicted and resembled a mosaic. Fungal communities within cankers were unstable. The fungal community structure in one year was classified differently the next year. There was a net shift of the community toward abundant non-C. parasitica fungi in cankers on surviving stems but were not associated with higher stem survivorship compared to cankers with abundant hypovirulent C. parasitica. Cankers on surviving trees containing hypovirulence consistently were invaded by non-C. parasitica fungi and are associated with declining survivorship over time. Fungal invasion may facilitate canker expansion through greater inhibition of hypovirulent C. parasitica relative to the virulent form of the pathogen, allowing virulent C. parasitica to escape hypovirus infection and resume rapid canker expansion. Commonly occurring fungi in chestnut blight cankers, including Trichoderma, may inhibit the hypovirulent C. parasitica more than virulent C. parasitica based on dual culture testing. Inoculations at the margin of experimental cankers on American chestnut stems using hypovirulent C. parasitica were effective at slowing canker expansion. However, inoculations of potentially antagonistic fungi such as Trichoderma did not reduce the rate of canker expansion. Applying antagonistic fungi to the inner area of a canker may offset the influence of hypovirulent C. parasitica.This work investigates the fungal community within chestnut blight cankers and the role it plays in canker expansion and stem girdling. Although Trichoderma is noted as a biological control agent in other plant-pathogen systems, it may be too inhibitory of hypovirulent C. parasitica, which is known to slow canker expansion and delay tree girdling. The presence of invading fungi into the canker does not seem to slow canker expansion and may prevent dissemination of hypovirulent C. parasitica in a canker and a forest.
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