Determine the importance of Monilinia fructicola apothecia as a source of primary inoculum in stonefruit orchards in the San Joaquin Valley.|
Study the conditions that favor the stromatization of mummified fruit by M. fructicola that enhance the production of apothecia capable of initiating blossom infections in the spring.
Determine the importance of thinned fruit as a source of inoculum during the season; and whether thinned fruit can become stromatized, overwinter, and produce apothecia in the spring.
Apothecia of the brown rot pathogen, Monilinia fructicola, of stone fruit were commonly observed in February and March in commercial orchards during a disease survey and in experimental orchards where stonefruit mummies were added. Several millions of ascospores can be released by each apothecium at the beginning of the season. Conidial sporulation of M. fructicola was not observed either on mummified fruit, peduncles, or blighted flowers and twigs. Mummies, however, produced conidia under laboratory conditions. Blossom blight was less severe in research plots where mummies were removed than when mummies were left on the ground. Subsequently, preharvest fruit brown rot was also less severe in plots where mummies were completely removed than where infected fruit were left on the ground. A similar relationship was observed for postharvest fruit brown rot in both 1995 and 1996. In addition, preharvest fruit brown rot was reduced in plots where the orchard floors were disced, herbicides were applied to berms in the tree rows, and mummies were removed in comparison with plots where no till, no herbicide, and no removal of mummies were practiced. These results suggest that apothecia can function as a main source of primary inoculum for initiating brown rot epidemics in stonefruit orchards of the San Joaquin Valley; and that blossom blight and fruit rot can be reduced by removing mummies from orchard floors or by preventing the development of apothecia after discing and/or applying herbicides during winter.|
Apothecia were produced in February and early March from stromatized mummies that were placed in the orchard soil only in October, November, or December. Stromatized mummies placed in the field in August/September and January/February did not produce apothecia, presumably because they did not have the proper conditions for apothecia development. Apothecia were never produced from nonstromatized or fresh fruit mummies, and laboratory results confirmed these field studies. Therefore, growers who knock infected fruit to the ground before October (preferentially immediately after harvest) can break the life cycle of the brown rot fungus by preventing fresh mummies to become stromatized and by subjecting the mummies under conditions favorable to destruction.
Field fruit brown rot was less severe in plots where thinned fruit were removed than where thinned fruit were not removed and where the thinned fruit were added in five orchards in both 1995 and 1996. Postharvest brown rot was also less severe in treatment plots, from one nectarine orchard in 1996, where thinned fruit were completely removed than where thinned fruit were not removed. No difference was observed in both pre and postharvest brown rot of fruit from treatment plots where thinned fruit were racked from "dry" berms into "wet" irrigation drenches than when thinned fruit was left untouched in two nectarine orchards. Our results suggest that thinned fruit can function as a significant source of secondary inoculum for M. fructicola and brown rot disease can be reduced by destroying thinned fruit.