Since 2001, Oregon nurseries, Christmas tree plantations, and other sites have been surveyed for the federally regulated pathogen Phytophthora ramorum. Host plants at each site were visually surveyed for disease symptoms and symptomatic tissues tested in the laboratory by isolation onto a selective medium and by a polymerase chain reaction (PCR) assay. In 2002 and 2003, we detected PCRpositive plants that later proved to be infected with another Phytophthora, suggesting there are limitations to the PCR assay tested. In 2003, P. ramorum was detected for the first time in Viburnum, Pieris, Rhododendron, and Camellia plants in six nurseries. All infected and neighboring plant materials were destroyed by incineration and the nurseries and surrounding environs subsequently surveyed for the pathogen. Phytophthora ramorum was not detected, indicating the pathogen was successfully eradicated. Accepted for publication 10 February 2004. Published 9 March 2004.
Phytophthora ramorum, the cause of sudden oak death in California and Oregon coastal forests and ramorum blight in European nurseries and landscapes (1), was detected in six Oregon nurseries in Jackson, Clackamas, and Washington counties from May to June 2003. The pathogen was isolated from: Viburnum bodnantense ‘Dawn’, V. plicatum var. tomentosum ‘Mariesii’, Pieris japonica × formosa ‘Forest Flame’, P. japonica ‘Variegata’ and ‘Flaming Silver’, P. floribunda × japonica ‘Brouwer's Beauty’, Camellia sasanqua ‘Bonanza’ and other cultivars, C. japonica, and Rhododendron × ‘Unique’. Samples of symptomatic tissues were plated on a Phytophthora-selective medium (PARP) and tested by polymerase chain reaction (PCR) (3). All samples positive for P. ramorum with PCR yielded P. ramorum isolates in culture. The isolates have the European genotype, mating type A1, except for the Camellia spp. isolates, which have the North American genotype, mating type A2 (2). Isolates are deposited in the American Type Culture Collection. Koch's postulates for this pathogen have been completed on V. bodnantense and C. japonica (1). To confirm pathogenicity on the new hosts, isolates from V. plicatum var. tomentosum ‘Mariesii’, Pieris × ‘Forest Flame’, Pieris × ‘Brouwer's Beauty’, and P. japonica ‘Variegata’ and ‘Flaming Silver’ were used to inoculate healthy plants of the same cultivars. For isolates from Rhododendron × ‘Unique’ and C. sasanqua ‘Bonanza’, pathogenicity was tested on Rhododendron × ‘Nova Zembla’ and C. sasanqua ‘Sutsugekka’ and ‘Kanjiro’. Three to five plants of each cultivar were inoculated and three to five were noninoculated. Zoospore inoculum was prepared on dilute V8 agar for one isolate from each host. Foliage of plants growing in 10-cm pots was dipped for 5 sec in a zoospore suspension (3 × 104 zoospores per ml) or sprayed to runoff with a hand mister (6 × 104 zoospores per ml). Control plants were dipped in or sprayed with sterile water. C. sasanqua plants were also inoculated by placing 6-mm mycelial plugs on individual leaves that had been wounded by piercing with a pin. Control leaves were wounded but not inoculated. Foliage was enclosed in plastic bags to retain humidity and the pathogen, and plants were incubated in a locked growth chamber (21 to 23°C). After 21 days, plants were examined for symptoms, and isolations onto PARP were made. All inoculated plants showed foliar symptoms, and P. ramorum was consistently isolated from inoculated plants, but not from asymptomatic control plants. On Rhododendron × ‘Nova Zembla’, nearly all leaves were wilted and dead, as were terminal buds and stems. Pieris spp. cultivars exhibited leaf and stem necrosis and defoliation. On V. plicatum var. tomentosum ‘Mariesii’, necrotic leaf lesions and defoliation of the lower leaves were observed. On C. sasanqua, necrotic lesions developed only on wounded leaves inoculated with mycelial plugs; these leaves abscised. Our results confirm the pathogenicity of Oregon nursery isolates of P. ramorum on V. plicatum var. tomentosum ‘Mariesii’, P. japonica × formosa ‘Forest Flame’, P. japonica ‘Variegata’ and ‘Flaming Silver’, P. floribunda × japonica ‘Brouwer's Beauty’, C. sasanqua and Rhododendron and complete Koch's postulates for several new hosts. References: (1) J. M. Davidson et al. Online publication. doi:10.1094/PHP-2003-0707-01-DG. Plant Health Progress, 2003. (2) E. M. Hansen et al. Plant Dis. 87:1267, 2003. (3) L. M. Winton and E. M. Hansen. For. Pathol. 31:275, 2001.
Barley yellow dwarf viruses (BYDVs) continue to cause losses California cereal production. In some parts of the USA, native grasses have been implicated as reservoirs of BYDVs. This study examines the potential of native and irrigated pasture grasses as sources of BYDV inoculum in California. The effects of both natural and natural plus supplemental inoculum were examined in field trials over two growing seasons using a completely randomized design. Results were assessed by enzyme-linked immunosorbent assay (ELISA) and verified with controlled greenhouse vector transmission trials. Thirty-seven of 56 species of cool-season grasses were infected by either PAV, MAV, or RPV isolates of the BYDVs. Of the BYDV-infected grasses, only 38% displayed symptoms typically seen in infected oat (Avena sativa L.) and barley (Hordeum vulgare L.), while the others were asymptomatic. None of the plants from seven species of Leymus, nor plants from the majority of Elymus and Elytrlgia species, had detectable BYDV infections, even though they supported aphid vector populations. A survey of common grasses from irrigated pastures showed that plants from 6 of 10 species were infected by either the PAV, MAV, or RPV isolates of BYDVs. The incidence of MAV, PAV, and RPV BYDVs were roughly equivalent for the cool-season grasses, but were highly skewed toward PAV in the irrigated pasture survey. Both cool-season and irrigated warm-season pasture grasses have the potential to serve as BYDV reservoirs in California. T HE BYDVs are common and widespread pathogens of grain and grass forage crops (Oswald and Houston, 1953; Bruehl, 1961; Plumb, 1983). The BYDVs are taxonomically separated by various characteristics such as vector transmissibility, serotype, and host ultrastructural reactions, and are designated as the PAV, MAV, SGV, RPV, and RMV types or groups (Rochow, 1984). Various BYDVs have the capacity to infect many small grains, including rice (Oryza sativa L.), corn (Zea mays L.) and many noncultivated gramineous species (Slykhuis, 1967;
Hop powdery mildew (HPM) was first observed in commercial hop (Humulus lupulus L.) fields in Washington State on 10 June 1997 near Toppenish in the Yakima Valley. The disease appeared throughout the valley in 1997; by mid-July, scattered fields throughout the Yakima growing area reported HPM. Approximately 2,000 of 30,000 acres in production were not harvested in 1997 due to HPM. The pathogen apparently perennated in buds, and flagshoots originating from infected buds were observed during March and April 1998 at various locations throughout the Yakima Valley. During the 1999 growing season, the majority of hop acreage in Washington State was affected, and most fields planted to susceptible cultivars contained at least one infected plant. HPM was initially discovered in southern Idaho during early July 1998, in two adjacent fields of hops in Canyon County. HPM was found ≈644 km (400 miles) north in another hop-growing region of Idaho, Boundary County, during mid-July 1998. HPM eventually was observed in more than 20 Idaho hop fields. The initial discovery of HPM in Oregon's Willamette Valley was made during late-July 1998, in two neighboring hop fields. By the end of the growing season, HPM was observed in nine commercial fields representing 3.7% of the hop production acreage in Oregon. Affected cultivars include Brewer's Gold, Chinook, Cluster, Columbus/Tomahawk, Eroica, Fuggle, Galena, Golding, Liberty, Olympic, Perle, Symphony, Tettnanger, Willamette, and Zeus. Infected basal leaves of bines had small whitish circular spots on adaxial surfaces. In some cases, blisters preceded direct observation of the fungus. Cones also were infected, appearing stunted and malformed. The pathogen usually was visible on infected cones but sometimes was found only under overlapping bracts. Cleistothecia have not been observed in the field to date. Conidia were transferred to leaf disks (12 mm diameter) excised from greenhouse-grown cv. Galena hop plants. Inoculated leaf disks were incubated on moistened filter paper in glass petri dishes at 20°C with illumination provided for a 12 h day by two cool-white fluorescent bulbs. HPM lesions with chains of unicellular, barrel-shaped conidia (30 to 36 × 15 to 18 μm) were visible within 7 days. The causal agent was identified as Sphaerotheca macularis (Wallr.:Fr.) Lind (synonym S. humuli (DC.) Burrill) on the basis of conidial shape and size as well as host range (1). Reference: (1) D. J. Royle. 1978. Powdery mildew of the hop. Pages 381–409 in: The Powdery Mildews. D. M. Spencer, ed. Academic Press, New York.
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