Susceptibility of almond leaf to Coryneum blight, and evaluation of helicopter spray applications for disease control

Ogawa, J. M.; Yates, W. E.; Kilgore, Wendell W.

doi:10.3733/hilg.v35n19p537

Cited by 3 publications

(2 citation statements)

References 2 publications

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“…The disease is routinely controlled using fungicides (Aldrich et al 1974;Leupschen et al 1968;Ogawa et al 1964). In Washington, fungicides are applied without regard to prevailing meteorological conditions.…”

Section: Introductionmentioning

confidence: 99%

Influence of temperature and wetness period on infection of cherry and peach foliage byWilsonomyces carpophilus¹

Grove¹

2002

Canadian Journal of Plant Pathology

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The effects of temperature and wetness duration on infection of sweet cherry (Prunus avium L.) and peach (Prunus persica L.) by Wilsonomyces carpophilus (Lev.) Adaskaveg, Ogawa & Butler were determined under controlled conditions. Young foliage of cherry seedlings and peach trees was inoculated with a conidial suspension of W. carpophilus and subjected to wetness periods of 0-24 h at temperatures of 5-30°C. On cherry, disease severity increased with wetness duration at each temperature tested, e.g., at 15°C, severity increased from no lesions at wetness durations < 1 h to 0.1, 1.9, 6.8, and 9.1 lesions/cm 2 after 6, 12, 18, and 24 h, respectively. After 24 h of wetness, the maximum disease severity of 10.5 lesions/cm 2 was obtained at 20°C. Although severity values were different, the general responses to temperature and wetness period were similar on peach. Multiple-regression equations using temperature and wetness duration as independent variables adequately described infection of cherry and peach foliage. The incubation period on cherry was 2, 2, and 3 d at 5, 15, and 25°C, respectively, while the latent period was 6 d at 15-25°C.

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Section: Introductionmentioning

confidence: 99%

Influence of temperature and wetness period on infection of cherry and peach foliage byWilsonomyces carpophilus¹

Grove¹

2002

Canadian Journal of Plant Pathology

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“…Numerous studies of shot hole and W carpophilus have been made and include studies on the biology of the fungus and disease (Wilson 1937;Jaunch 1940), epidemiology (Shaw et al 1990;Adaskaveg et al 1990b), survival (Highberg and Ogawa 1986), host range of the fungus (Smith and Smith 1942;Zafar and Sufi 1972;Ahmed 1973), effects of the disease on yield reduction of almond (Highberg and Ogawa 1986), and disease control (Ogawa et al 1959;Luepschen et al 1968;Aldrich et al 1974;Teviotdale et al 1989). Few studies, however, have been conducted on conidial morphology and germination of the fungus or the host -pathogen interaction of this disease.…”

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confidence: 97%

Conidial morphology, host colonization, and development of shot hole of almond caused by Wilsonomyces carpophilus

Adaskaveg¹

1995

Can. J. Bot.

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Morphology and ultrastructure of shot hole disease of almond infected by conidia of Wilsono~rzyces carpophilus were examined using light, scanning, and transmission electron microscopy. The multicelled conidia of the fungus were thick-walled and darkly pigmented. The conidial wall was multilayered and mainly consisted of an electron-dense, outer-wall layer and an electron-translucent, inner-wall layer. Septa of conidia were also multilayered. An electron-translucent zone separated the electron-dense, septa-wall layers of adjacent cells, and this zone extended to the inside of the outer-wall layer of a conidium. Conidia lacked true septa (distoseptate) and germinated by rupturing the outer-wall layers. Germination hyphae penetrated indirectly through stomata or directly through the cuticle into leaf tissue from appressoria that were produced terminally or on lateral branches of germ tubes. An extracellular mucilaginous matrix was commonly observed around hyphae and germ tubes in contact with leaf surfaces. Within leaf tissue, hyphae ramified throughout intercellular spaces and degraded cell walls of epidermal cells apparently without cuticle degradation. Diseased host tissue was tan brown and collapsed; ultrastructurally, diseased leaf cells were reduced in size, nonvacuolated, and had disrupted chloroplasts. A healthy host tissue response, adjacent to an infection site on leaves of potted plants, was the formation of a wound periderm. Within 10-14 days after an infection period (16 h of wetness), the periderm became a lignified-suberized barrier at 15°C or a suberized abscission layer at 22°C based on the histological stains Safranin 0 , Sudan 111, and Sudan Black. At lS°C, no abscission occurred and meristematic cells remained isodiametric but their walls became suberized and lignified, whereas cells adjacent to diseased tissue became lignified. At 22"C, abscission occurred as cells adjacent to diseased tissue became vacuolated, enlarged, and suberized. Subsequently, the epidermis ruptured and the enlarged cells separated along the middle lamella to form an abscission layer. Hyphal growth was limited to the boundaries of the walled-off diseased tissue. Under favorable environmental conditions, hyphae replaced host epidermal cells and aggregated above the palisade layer to form pulvinate sporodochia. Sporodochia consisted of hyphae, numerous sympodially developing conidiogenous cells, and conidia that ruptured the host cuticle.

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