The life history of Anisogramma anomala (Pk.) E. Müller (Diaporthaceae) and its pathological and epidemiological association with Corylus avellana L. Public Deposited

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  • Eastern Filbert Blight, caused by Anisogramma anomala (Peck) E. Miller, was first discovered in the Pacific Northwest in 1974. Orchard experiments suggest that the fungus completes its life cycle in two years. Infection takes place from mid-January to May, mainly through mite-galled-buds infested with an Eriophyid mite, Phytocoptella avellanae Nal. Ascospores are presumed to be the only infectious propagules since no conidial stage has been observed during the four years of investigation. After a latency period of 12-16 months, the fungus can be detected in the primary phloem and vascular cambium and later penetrates deep into the xylem. Stromata are initiated during May as indicated by a somatic pressure cushion which gradually crushes and splits the bark to expose the ectostroma. Dense aggregates of smaller fungal cells arise deep within the endostroma in 2-3 layers forming primordia. The primordia consist of an "outer coil" of filamentous hyphal cells terminated by a non-functional trichogyne, surrounding an "inner coil" of more isodiametric ascogenous cells. The centrum arises from this "inner coil" as a loose clump of ascogenous cells which lack croziers. Mononucleate asci arise from these ascogenous cells near the end of July. Meiosis occurs from mid-July through August and each ascus cleaves eight unequally two-celled hyaline ascospores. A. anomala causes a simple interest type of disease during a single season but is considered a compound interest type in longstanding orchards. Disease severity, measured as the percent of plant surface attacked, was evaluated for individual cankers, for individual trees and for orchards as a whole. Disease increase was found to be r=0.265, r=1.084 and r=1.240 units/year respectively. The disease spread south from the original focus which was determined to be a group of five orchards, in the northwest quadrant of the diseased area. Spread of inoculum over long distances is infrequent. Therefore, established secondary foci to the south are more likely to be the source of inoculum to nearby orchards and pose the greatest threat of spread into orchards further south in the main filbert growing areas of Oregon. Various inoculation methods were tested on several filbert tissues. Hypodermic infiltration of ascospores into mite-galled-buds and into healthy non-infested buds, proved to be the only successful inoculation methods giving 46.5 and 29.0 percent infection respectively. There was a general increase in percent infection as inoculation dates approached the natural infection period which was determined to extend from February through May and to correlate with the duration of rainfall during the same season. Ascospores were recovered continuously from each of ten different exposure periods from 26 November to 3 April. Spore release is thought to be at least six months in duration extending well beyond the spore trapping dates, and thus lasts longer than the natural infection period. Heaviest discharge was recorded during periods of constant wetting of the stromata. Free moisture on the stromata induces inoculum discharge which is further dispersed by rain splash. Natural infection occurs when the inoculum is washed between the scales of P. avellanae infested buds. Hypodermic infiltration of ascospores into mite-free-buds also resulted in a substantial percent infection. Following infection there is normally a 12-16 month latency period for symptom expression. Under greenhouse conditions symptoms developed within six months of inoculation. Culture isolation taken from diseased and healthy filbert twigs resulted in a substantial recovery of Phomopsis sp., from 36.4 to 93.2 percent. Therefore although Phomopsis was isolated from cankered tissue it is unlikely that it is more than an epiphyte.
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