Biology of Fungal Canker Diseases of Sweet Cherry in California
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Biology of Fungal Canker Diseases of Sweet Cherry in California

Abstract

Calosphaeria canker caused by Calosphaeria pulchella, Cytospora or Leucostoma canker caused by Cytospora sorbicola, and Eutypa dieback caused by Eutypa lata are the main canker diseases of sweet cherry in California commercial orchards and a limiting factor to orchard productivity and longevity. It was understood that pruning wounds serve as the primary avenue of infection for these fungal canker pathogens; however, very little is known about the other infection courts of Cal. pulchella, Cyt. sorbicola and E. lata. Thus, this present study was undertaken to identify common infection courts other than pruning wounds for fungal canker pathogens affecting sweet cherry. This was determined by assessing the field incidence of canker pathogens in the wood below pruning wounds, in buds, fruiting spurs and unpruned apical shoots exhibiting dieback symptoms. This work was supplemented by assessing the susceptibility of naturally occurring wounds such as leaf scars, bud scale scars, and harvest wounds on fruiting spurs to the three major canker pathogens of sweet cherry. Additionally, little is known about the effects of temperature and season on the biology of these three pathogens (except for E. lata). Therefore, the second objective of this study were to ascertain their optimal temperatures for spore germination and mycelial growth in vitro among temperatures 5, 10, 15, 20, 25, 30, 35, and 40°C. The third objective of this study supplements the second objective by comparing the susceptibility of pruning wounds to infection by Cal. pulchella, Cyt. sorbicola and E. lata made in summer and winter. Our survey revealed disease incidences of Cal. pulchella and Cyt. sorbicola to be as high as 20% and 35%, respectively, in shoot tips and up to 19.4% and 26.7%, respectively, in declining spurs. Additionally, harvest wounds of fruiting spurs were shown to be highly susceptible to canker infection by the three pathogens with 60% recovery for Cyt. sorbicola, and 42.5% for Cal. pulchella and E. lata. The optimal temperatures for spore germination were estimated to be 29.15°C for Cal. pulchella, 26.95°C for Cyt. sorbicola, and 22.85°C for E. lata; and optimal temperatures for mycelial growth were estimated to be 27.2°C, 23.85°C and 22.5°C, respectively. In field experiments, average recovery of Cal. pulchella was significantly greater from pruning wounds made in summer than that of winter with 84.6% and 10.7% recovery, respectively. The average recovery of E. lata from pruning wounds made in winter was 92.8%, which was significantly greater than that of summer with 80% recovery. Overall, our findings demonstrated that summer pruning of sweet cherry in California poses greater risks of infection by Cal. pulchella. In contrast, winter pruning poses greater risks of infection by E. lata. This study represents new knowledge on the seasonal susceptibility of pruning wounds of sweet cherry to canker infection by Cal. pulchella and Cyt. sorbicola. Additionally, this study provided new information on additional infection courts of major canker pathogens of sweet cherry in California. Since distinct cherry canker pathogens vary in their seasonal infectivity, synchronizing maintenance pruning with low periods of inoculum pressure will be critical for canker disease management in sweet cherry orchards.

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