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1
Austin, Roy L. "Family Environment, Educational Aspiration and Performance in St. Vincent." Review of Black Political Economy 17, no. 3 (January 1989): 101–22. http://dx.doi.org/10.1007/bf02901104.
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Father-absence occurs with unusual frequency among people of African descent in the Caribbean. Yet concern over possibly harmful effects of this condition to children and society which is most obvious in the United States is not informed by scientific findings from this region. The present study yielded no evidence that father-absence retards the aspiration or performance of secondary school students in St. Vincent, West Indies, although twelve different groupings of the available cases were analyzed. Findings from this and some American studies suggest that father-absence is not harmful if it is not strongly condemned by the culture with which youths identify.
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Ambrey, Christopher L., Cameron Parsell, Melanie Spallek, and Richard N. S. Robinson. "An Investigation Into Repeat Requests for Charity: Evidence From the St Vincent de Paul Society Queensland, Australia." Nonprofit and Voluntary Sector Quarterly 48, no. 1 (August 22, 2018): 91–107. http://dx.doi.org/10.1177/0899764018794300.
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In advanced industrialized economies, charitable organizations work alongside formal social services provided through welfare states to assist people living in poverty. The work of charities with socially and economically marginalized people, however, often takes place in the absence of robust evidence about what impact charity has on people’s lives. This study draws on a large administrative database to investigate what determines repeat requests for charity and how people may achieve dignity. Our findings show that frequent residential address changes seem to make people more reliant on charity, whereas the more time spent with people receiving charity significantly decreases repeat requests for charity. We propose that the provision of charity can be an opportunity to promote connectedness.
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Holcomb, G. E. "First Report of Petunia Blight Caused by Choanephora cucurbitarum in the United States." Plant Disease 87, no. 6 (June 2003): 751. http://dx.doi.org/10.1094/pdis.2003.87.6.751c.
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A blight (wet rot) of petunia (Petunia ×hybrida Hort. Vilm.-Andr.) was observed in a wholesale propagation nursery in Baton Rouge, LA in September 2002. The grower reported that plants wilted and then completely rotted. The disease occurred during a period of hot, humid, and cloudy weather. Approximately 100 flats of flowering-age plants of cvs. Rose and White Madness were destroyed. No fungal sporulation was noticed on dead plants, but occasional strands of white mycelium were observed. The grower's use of azoxystrobin, iprodione, and thiophanate methyl plus mancozeb fungicides during current and past outbreaks of this disease did not prevent disease spread, but disease activity stopped after temperature and humidity dropped in early October. A fungus that produced white aerial mycelia that later developed light yellow areas and also black aerial spore masses was consistently isolated from diseased tissue placed on acidified potato dextrose agar (APDA). The fungus was identified as Choanephora cucurbitarum (Berk. & Ravenel) Thaxt. on the basis of cultural and morphological characteristics (3). Sporangiola were ellipsoid, pale brown to reddish brown with distinct longitudinal striations and measured 15 to 20 × 9 to 14 μm. Sporangiospores were broadly ellipsoid, pale brown to reddish brown, indistinctly striate with fine, hyaline polar appendages, and measured 16 to 34 × 7 to 12 μm. Spore measurements were within the range previously given for C.cucurbitarum (3). Pathogenicity tests were performed by misting a mixture of sporangiola and sporangiospores (25,000 to 70,000 per ml of water taken from 7- to 10-day-old cultures grown on APDA) on flowering-age petunia plants (cvs. Rose Madness, White Madness, and Dreams Pink). Tests were repeated twice. Inoculated plants and uninoculated control plants (2 to 4 of each treatment in each test) were held in a dew chamber at 28°C for 48 h and then moved to a greenhouse. Within 48 h after inoculation, plants developed water-soaked lesions on flowers, leaves, and stems, then wilted and rotted. Uninoculated plants remained disease free except for several that developed disease symptoms in the first test, apparently from the presence of natural inoculum on healthy-appearing plants that were obtained from the nursery where the disease was found. Koch's postulates were completed by reisolation of the pathogen from diseased inoculated plants. C. cucurbitarum (1) and C. infundibulifera (Curr.) Sacc. (2) have been reported to cause flower blight of petunia in the United States and whole plant blight (wet rot) of petunia in Japan (4). To our knowledge, this is the first report of C. cucurbitarum causing whole plant blight of petunia in the United States. References: (1) M. L. Daughtrey et al. Choanephora wet rot of poinsettia. Page 15 in: Compendium of Flowering Potted Plant Diseases. The American Phytopathological Society, St. Paul, MN, 1995. (2) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (3) P. M. Kirk. Mycological Paper 152:1, 1984. (4) J. Takeuchi and H. Horie. Jpn. J. Phytopathol. 66:72, 2000.
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Tsahouridou, P. C., and C. C. Thanassoulopoulos. "First Report of Hendersonula toruloidea as a Foliar Pathogen of Strawberry-tree (Arbutus unedo) in Europe." Plant Disease 84, no. 4 (April 2000): 487. http://dx.doi.org/10.1094/pdis.2000.84.4.487c.
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During spring 1997 and 1998 in the area of Chalkidiki, in northern Greece, leaves of wild strawberry-tree (Arbutus unedo) were heavily spotted. Small, necrotic brown spots with light gray centers appeared on leaves, and when intense spotting was present, strong defoliation was observed. Isolations from leaves on potato dextrose agar consistently yielded a fungus that was identified as Hendersonula toruloidea (2). Pathogenicity tests on wild strawberry-tree plants were performed, yielding symptoms identical to those originally observed, and H. toruloidea was isolated consistently from inoculated leaves. No cankers appeared on the twigs of the plants, which is a consistent symptom caused by this fungus on strawberry-tree in the United States. Leaf spotting caused by H. toruloidea has been observed in Musa and Rhus spp. (1). This is the first report of H. toruloidea causing leaf spotting and defoliation of strawberry-trees in Europe. References: (1) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN. (2) R. M. Nattrass. Br. Mycol. Soc. Trans. 18:189, 1945.
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Seebold, K. W., D. B. Langston, R. C. Kemerait, and J. E. Hudgins. "First Report of a Leaf Spot and Stem Canker Caused by Myrothecium roridum on Watermelon in the United States." Plant Disease 89, no. 3 (March 2005): 342. http://dx.doi.org/10.1094/pd-89-0342a.
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Myrothecium roridum Tode:Fr, pathogenic to a number of cucurbit species, causes fruit rots, cankers on crowns and stems, and leaf spots. Hosts include cantaloupe and honeydew (Cucurbita melo) and cucumber (Cucumis sativus) (1,3). In June 2004, following a period of heavy rainfall, numerous round-to-oblong, brown lesions with concentric rings were observed on leaves of watermelon (Citrullus lanatus) cv. Desert King at the Blackshank Farm in Tifton, GA. Disease was localized in the field and severity was low (<5% of leaf area affected). No symptoms were observed on fruit. Sections of tissue were removed from the margin between healthy and diseased tissue and plated on acidified, 25% potato dextrose agar (aPDA). A small plug of agar and mycelium were removed from colonies that emerged from lesions and were transferred to aPDA. Isolated colonies were characterized by a white, floccose mycelium with concentric, dark green-to-black rings of sporodochia bearing viscid masses of conidia. Conidia were cylindrical with rounded ends and measured 6 to 8 × 1.5 to 2.5 μm. The features of the fungus were consistent with the description of Myrothecium roridum (1,2). Pathogenicity tests were conducted in a temperature-controlled greenhouse. Twenty-five watermelon plants (cv. Desert King) were inoculated with a conidial suspension of M. roridum (5 × 105 conidia per ml) plus 0.1% vol/vol Tween 20. Inoculum was applied on leaves and stems until runoff with a hand-held mister, and plants were placed in a dew chamber for 72 h. Ten plants were sprayed with sterile, distilled water to serve as controls. Inoculated and noninoculated control plants were removed from the dew chamber and maintained at 25 to 28°C. Symptoms appeared 8 days after inoculation and were characterized by round, dark lesions with concentric rings; noninoculated plants were symptomless. Sections of symptomatic tissue were plated, and M. roridum was reisolated. Although M. roridum is a common pathogen of melons and cucumber, to our knowledge, this is the first field report of a leaf spot caused by M. roridum on watermelon in the United States. No further occurrences of the disease on watermelon have been observed in Georgia since the initial discovery of M. roridum in 2004; however, losses could be potentially severe if widespread infection of fruit were to occur. References: (1) B. D. Bruton. Crater Rot. Pages 49–50 in: Compendium of Cucurbit Diseases. T. A. Zitter et al., eds. The American Phytopathological Society, St. Paul, MN, 1996. (2) M. B. Ellis. Page 552 in: Dematiaceous Hyphomycetes. CAB International, Wallingford, UK, 1971. (3) D. F. Farr et al. Page 809 in: Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989.
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Hernández, J. R., M. E. Palm Hernández, and T. Tidwell. "First Report of Puccinia vincae on Vinca spp. in California." Plant Disease 86, no. 1 (January 2002): 75. http://dx.doi.org/10.1094/pdis.2002.86.1.75b.
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In 2000, chlorotic leaves with inconspicuous leaf spots were observed on several Vinca major L. and V. minor L. plants in a 0.8-ha area in Woodside, CA. In August 2001, 80 to 90% of the plants were symptomatic. Uredinia measuring 2 to 3 × 1 mm were present on the lower surface of leaves. Urediniospores were ellipsoidal to oblong, 27 to 36 × 17 to 27 μm, with cinnamon-brown walls 1 to 2 μm thick, echinulate, and with three or four equatorial or slightly supraequatorial germ pores. Telia were produced in the uredinia. Teliospores were 1-septate, ellipsoidal to clavate, slightly constricted at the septum, and 34 to 45 × 19 to 30 μm. Teliospore walls were chestnut brown, 1.5 to 2.5 μm thick, and verrucose, with the verrucae sometimes in longitudinal lines. One germ pore covered by a hyaline papilla was present in each cell, at the apex in the upper cell and adjacent to the short, hyaline pedicel in the lower cell. The rust was identified as Puccinia vincae Berk. (1). P. vincae is widespread in Europe on Vinca species and is common on V. major in the eastern United States, Washington, and Idaho (2). To our knowledge, this is the first report of P. vincae on V. major in California (vouchers BPI 841363, 841364) and on V. minor in the United States (voucher BPI 841365). References: (1) J. C. Arthur. Page 324 in: Manual of Rusts in the United States and Canada. Purdue Research Foundation, Lafayette, IN, 1934. (2) D. F. Farr et al. Pages 35 and 916 in: Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN, 1989.
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Newcombe, G. "Southerly Extension of Poplar Leaf Blight (Linospora tetraspora) in the Pacific Northwest." Plant Disease 82, no. 5 (May 1998): 590. http://dx.doi.org/10.1094/pdis.1998.82.5.590b.
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Poplar leaf blight caused by Linospora tetraspora G. E. Thompson (Ascomycetes, Valsaceae) is widespread on Populus balsamifera in Canada from Quebec to British Columbia (1). The only United States records of this northerly fungus are from Vermont, Wisconsin, and Alaska (1,2). There are no records of this fungus on the Pacific Coast south of British Columbia, despite the presence of susceptible hosts (i.e., Populus trichocarpa and its hybrids). However, in September of 1997, the disease was observed in a hybrid poplar plantation at latitude 47.9°N and longitude 122.1°W near Snohomish, Washington. Blight affected the lower crown of trees in their second year of growth. Leaf lesions, with their characteristic black stromata, were easily distinguished from symptoms of other diseases. Some individual lesions of L. tetraspora affected entire leaf laminae, but there appeared to be little premature defoliation at the time of observation. Populus trichocarpa × P. deltoides hybrids were more commonly blighted than were P. trichocarpa × P. maximowiczii hybrids (i.e., 13/18 clones affected versus 4/11, respectively). A voucher specimen was deposited in the Herbarium at the Pacific Forestry Centre (DAVFP 25289). References: (1) M. E. Barr. Mycol. Mem. No. 7:130, 1978. (2) D. F. Farr. et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN.
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Putnam, M. L. "First Report of Leaf Blight and Stem Dieback of St. John's-Wort Caused by Diploceras hypericinum in Oregon." Plant Disease 84, no. 11 (November 2000): 1250. http://dx.doi.org/10.1094/pdis.2000.84.11.1250b.
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St. John's-wort, Hypericum perforatum L., was formerly considered a noxious weed in the Pacific Northwest and is now grown commercially for its medicinal properties. In May 1999, plants from a 5-ha field in Jefferson County, OR, were observed with yellowing leaves and stem dieback. Lower leaves showed marginal necrosis or circular, expanding, uniformly brown, unremarkable leaf lesions that appeared randomly over the lamina and consumed from a quarter to nearly the entire leaf area. Remaining leaf tissue was chlorotic, and affected leaves eventually abscised. Infection of the stems resulted in girdling lesions 0.5 to 1.0 cm in length that caused chlorosis, wilting, and eventual dieback of tissues distal to the lesion. Diploceras hypericinum (Cesati) Diedicke was sporulating on affected stems and leaves. The fungus was isolated from surface-disinfested tissue onto 1.5% water agar. A single-spore isolate was used to inoculate 10-month-old plants raised from seed in sand. Spores from 6-week-old cultures grown on 50% potato-dextrose agar were harvested, suspended in phosphate buffer with 0.2% gelatin (PBG), and sprayed onto three plants using a DeVilbiss atomizer. Inoculum concentration was 7 × 103 and 3 ml per plant were used (plants were 8 to 10 cm tall). Three control plants were sprayed with sterile PBG. Inoculated and control plants were separately bagged to retain moisture and maintained at 22 to 25°C. Four days later, inoculated plants exhibited leaf spots similar to those originally observed, followed by stem dieback. D. hypericinum was isolated from all inoculated plants but not from control plants. The known distribution of D. hypericinum is France, Germany, Portugal, Sweden, Greece, and Ontario, Canada (1,2). This is the first report of D. hypericinum causing leaf blight and stem dieback of St. John's-wort in the United States. References: (1) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN. (2) T. R. Nag Raj. 1993. Coelomycetous Anamorphs with Appendage-bearing Conidia. Mycologue Publications, Waterloo, Canada.
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Paulitz, T. C., F. Dugan, W. Chen, and N. J. Grünwald. "First Report of Pythium irregulare on Lentils in the United States." Plant Disease 88, no. 3 (March 2004): 310. http://dx.doi.org/10.1094/pdis.2004.88.3.310a.
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In late June and early July 2002, stunted, chlorotic, and partially defoliated lentils (Lens culinaris Medik.) were observed throughout the lentil-growing areas of eastern Washington. These symptoms were investigated in two fields near Garfield, WA and one field near Genesee, ID. Cv. Mason was more affected than cv. Brewer. Roots were dry and brittle with black discoloration in some cases. Isolates of Fusarium oxysporum and F. solani were obtained from washed roots plated on water agar, but they were nonpathogenic in greenhouse testing in pasteurized field soil and peat-based growing mixes. On 21 April 2003, volunteer lentils growing in the same fields showed symptoms of root rot, and Pythium oospores were observed in the roots. Pythium spp. were isolated by using a selective medium (2). Oospores were aplerotic, intercalary, 12.6 to 21 μm long × 11.2 to 18.2 μm wide, mostly smooth, and often formed in chains. Isolates resembled P. paroecandrum Drechs. and P. irregulare Buisman on the basis of morphological characters (3), but DNA sequences of the internal transcribed spacer region were closer to P. irregulare on the basis of a comparison with a worldwide database of Pythium sequences (C. A. Lévesque, personal communication). Isolates were deposited with the USDA-ARS Western Regional Plant Introduction Station, Pullman, WA. Four hyphal-tip isolates were tested in the greenhouse with inoculum grown in autoclaved sandy loam amended with 1% ground rolled oats. Experiments were performed twice in Thatuna silt loam, first in pasteurized and then in nonpasteurized soil. Inoculum was added to the soil at 500 CFU/g, and seeds were planted on the same day. Each isolate was tested on cvs. Brewer and Mason, with five replicates per treatment. Plants were grown in 4- × 20.5-cm plastic tubes (two plants per tube) for 1 month at 16 to 22°C and supplemented with 14 h of light per day. P. irregulare was reisolated from infected roots in both experiments. Damping-off, stunting, chlorosis, and root rot were observed in the Pythium-inoculated treatments, which corresponded to symptoms observed in the field in 2002. In pasteurized soil, only one isolate reduced the whole, dry, plant weight of Brewer, but the other three isolates reduced the dry weight of Mason. All isolates reduced the root dry weight of Mason in natural soil, but only two isolates reduced the root dry weight of Brewer. To our knowledge, Pythium spp., but not P. irregulare, have been reported previously from lentils (1). P. irregulare also causes root rot on winter wheat, which is rotated with lentils, and this pathogen likely causes yield reduction in both crops. References: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (2) S. M. Mircetich and J. M. Kraft. Mycopathol. Mycol. Appl. 50:151, 1973. (3) A. J. van der Plaats-Niterink. Stud. Mycol. 21:1, 1981.
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Briere, S. C., and G. D. Franc. "First Report of Leaf and Stem Rust Caused by Puccinia sherardiana on Sphaeralcea grossulariaefolia in North America and S. munroana in Wyoming." Plant Disease 82, no. 7 (July 1998): 831. http://dx.doi.org/10.1094/pdis.1998.82.7.831a.
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Diseased samples of globe mallow, Sphaeralcea grossulariaefolia and S. munroana, were submitted by an ornamental seed producer in Wyoming to our Extension Plant Pathology Laboratory in July 1997. Dark brown, amphigenous telia surrounded by chlorotic halos were present on both foliage and stems. Mean teliospore dimensions observed were 30.8 × 44.8 μm. The teliospores germinated readily on water agar at 20°C and formed basidiospores within 24 h. Aecia and uredinia were not found. Based on characteristics mentioned above, this fungus was identified as Puccinia sherardiana Körn (1). This microcyclic rust was previously described on 12 other Sphaeralcea spp. plus other plant species in the Malvaceae family (1,2). Stem and foliar symptoms were reproduced in a greenhouse on 8-week-old plants of S. grossulariaefolia and S. munroana. These plants were inoculated with teliospores removed from the original diseased plant material. Immediately after inoculation, plants were misted and placed in plastic bags and incubated for 36 h at 100% relative humidity and 20°C. Plants continued growth with natural lighting and with day and night temperatures of 20 and 15°C, respectively. Symptoms developed within 12 days with initial telia rupturing the host epidermis 13 days after inoculation. Telia were examined microscopically to complete Koch's postulates. References: (1) J. C. Arthur. Manual of Plant Rusts in United States and Canada. Hafner Pub., 1962. (2) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. American Phytopatholical Society, St. Paul, MN, 1989.
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Sconyers, L. E., R. C. Kemerait, J. H. Brock, R. D. Gitaitis, F. H. Sanders, D. V. Phillips, and P. H. Jost. "First Report of Phakopsora pachyrhizi, the Causal Agent of Asian Soybean Rust, on Florida Beggarweed in the United States." Plant Disease 90, no. 7 (July 2006): 972. http://dx.doi.org/10.1094/pd-90-0972a.
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Phakopsora pachyrhizi Syd. & P. Syd., which causes Asian soybean rust (SBR), was observed on Florida beggarweed, Desmodium tortuosum (Sw) DC., in Attapulgus, GA during late October and early November 2005. Tan to brown lesions (<1.0 mm in diameter) consistent with symptoms of SBR (2) were observed on older leaves of several plants collected near an SBR-infected soybean trial. Dissection (40 to 60×) and compound microscopy (×200 to 400) revealed conical pustules and ellipsoid, echinulate urediniospores (average size 15 × 20 μm) on the abaxial leaf surface. Polymerase chain reaction (PCR) (primers Ppm1 and Ppa2) (1) was conducted on four samples to confirm identification of P. pachyrhizi or P. meibomiae. Three were positive for P. pachyrhizi, and one was negative for both species. Using morphology and real-time PCR, SBR was confirmed as P. pachyrhizi by the USDA/APHIS in Beltsville, MD. Six noninfected Florida beggarweed plants were transplanted to pots during December 2005 and grown at 22 to 24°C in a greenhouse. On 11 January 2006, a water suspension of urediniospores collected from SBR-infected soybeans (1 × 105 spores per ml) was spray inoculated on all leaves to almost runoff and incubated for 48 h in a plastic humidity chamber. Lesions, pustules, and urediniospores consistent with SBR (2) were observed on 3 February 2006. A PCR assay was conducted on six samples from the infected greenhouse plants and all were positive for P. pachyrhizi. Florida beggarweed is widespread in the southern United States and may serve as an additional overwintering source for P. pachyrhizi and a potential inoculum source for the soybean crop. References: (1) R. D. Fredrick et al. Phytopathology 92:217, 2002. (2) J. B. Sinclair and G. L. Hartman. Soybean rust. Pages 25–26 in: Compendium of Soybean Diseases. 4th ed. G. L. Hartman et al., eds. The American Phytopathological Society, St. Paul, MN, 1999.
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French, J. M., R. A. Stamler, J. J. Randall, and N. P. Goldberg. "First Report of Phytophthora nicotianae on Bulb Onion in the United States." Plant Disease 95, no. 8 (August 2011): 1028. http://dx.doi.org/10.1094/pdis-01-11-0048.
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Phytophthora nicotianae (synonym P. parasitica) Breda de Haan was isolated from recently harvested onion bulbs (Allium cepa) in cold storage from a commercial field in southern New Mexico. Deteriorating, water-soaked tissue from the center of four bulbs was plated onto water agar and incubated at room temperature. After 72 h, cultures of Phytophthora (identified by the presence of coenocytic hyphae and papillate sporangia) were isolated and transferred to V8 agar amended with ampicillin (250 mg/liter), rifampicin (10 mg/liter), and pimaricin (0.2% wt/vol). Isolates were identified as P. nicotianae based on morphological characteristics and DNA analysis. Sporangia were sharply papilliate, noncaducous, and ovoid to spherical. The average sporangium size was 45.9 × 39.9 μm with a length-to-width ratio of 1.15. Clamydospores, both terminal and intercalary, were spherical to ovoid and averaged 37.2 × 35.2 μm (2). PCR from whole-cell extracts was performed on four cultured isolates from the infected onion tissue using previously described primers ITS4 and ITS6, which amplify the 5.8S rDNA and ITS1 and ITS2 internal transcribed spacers (1,4). A band of approximately 890 bp was amplified and directly sequenced (GenBank Accession No. HQ398876). A BLAST search of the NCBI total nucleotide collection revealed a 100% similarity to multiple P. nicotianae isolates previously sequenced (1). To confirm the pathogenicity of the isolates, onion seedlings were inoculated with 25 ml of P. nicotionae zoospore solution (15,000 zoospores/ml). Necrosis of leaf tissue and seedling death was observed 5 days postinoculation. P. nicotianae was reisolated from the infected onion seedlings and the ITS region was sequenced to confirm its identity. P. nicotianae was previously reported in bulb onion from Australia, Taiwan (Formosa), and Zimbabwe (Rhodesia) (2). P. nicotianae was reported on bunching onions (A. fistulosum) in Hawaii in 1989 (3). Onions are an important crop in New Mexico with a total production value of 47 million dollars in 2008 (NM Agriculture Statistics 2008). This discovery of a potentially significant postharvest disease poses a threat to the onion industry in New Mexico. To our knowledge, this is the first report of P. nicotianae in bulb onion in the United States and the first report of P. nicotianae in New Mexico on any crop. References: (1) D. E. L. Cooke and J. M. Duncan. Mycol. Res. 101:667, 1997. (2) D. C. Erwin and O. K. Ribeiro. Page 56 in: Phytophthora Diseases Worldwide. The American Phytopathological Society, St Paul, MN, 1996. (3) R. D. Raabe et al. Information Text Series No. 22. University of Hawaii. Hawaii Inst. Trop. Agric. Human Resources, 1981. (4) T. J. White et al. Page 315 in: PCR Protocols: A Guide to Methods and Applications. M. A. Innis et al., eds. Academic Press, San Diego, 1990.
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Garibaldi, A., A. Minuto, D. Bertetti, and M. L. Gullino. "First Report of Powdery Mildew Caused by Oidium Subgenus Pseudoidium on Salvia scabra in Italy." Plant Disease 88, no. 6 (June 2004): 682. http://dx.doi.org/10.1094/pdis.2004.88.6.682c.
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Salvia scabra Thunb. is grown and used on the Italian Riviera as a potted plant and used in gardens. During the spring of 2003, severe outbreaks of a previously unknown powdery mildew were observed in a collection of Salvia spp. maintained at an experimental station at Albenga (northern Italy). Powdery mildew was observed only on S. scabra. Leaves were covered with white exophytic mycelia on both surfaces. As the disease progressed, infected leaves turned yellow and died. Conidia were single, hyaline, cylindric, and measured 21.3 to 35.5 × 12.5 to 22.5 μm (average 28.2 × 18.4 μm). Observations made with a light microscope revealed that foot cells were cylindric and appressoria lobed. Cleistothecia were not observed. The pathogen was identified as Oidium subgenus Pseudoidium (1,2), and pathogenicity was confirmed by gently pressing diseased leaves onto mature leaves of healthy, 40-day-old S. scabra plants. Five plants of S. scabra were used as replicates. Noninoculated plants served as controls. Inoculated and noninoculated plants were maintained in a growth chamber at 20°C. After 5 days, typical symptoms of powdery mildew developed on inoculated plants. Noninoculated plants did not show symptoms. To our knowledge, this is the first report of the presence of powdery mildew on S. scabra in Italy as well as in the world. Erysiphe polygoni DC. (Oidium subgenus Pseudoidium) and E. cichoracearum DC. (Oidium subgen us Reticuloidium) were previously reported as causal agents of powdery mildew on other species of Salvia (S. officinalis and S. sclarea) (3,4). Specimens of this disease are available at the DIVAPRA Collection at the University of Torino. References: (1) R. Belanger et al., eds. The Powdery Mildew A Comprehensive Treatise. The American Phytopathological Society, St Paul, MN, 2002. (2) U. Braun. Nova Hedwigia. 89:700, 1987. (3) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St Paul, MN, 1989. (4) A. Pisi and M. G. Bellardi. Inf. Fitopatol. 48(10):57, 1998.
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Elmore, W. C., M. D. Gooch, and C. M. Stiles. "First Report of Gaeumannomyces graminis var. graminis on Seashore Paspalum in the United States." Plant Disease 86, no. 12 (December 2002): 1405. http://dx.doi.org/10.1094/pdis.2002.86.12.1405b.
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Gaeumannomyces graminis var. graminis is an ectotrophic, root-infecting fungus found on some warm-season turfgrass species (1). A sample of seashore paspalum (Paspalum vaginatum) exhibiting rotted roots and stolons was taken from dying patches of turf in a home lawn in Hernando County, FL, and submitted to the Florida Extension Plant Disease Clinic, Gainesville, in October 2001. The lawn had been established within the previous year. Strongly lobed hyphopodia typical of G. graminis var. graminis (3,4) were present on diseased roots and stolons, and no other fungal plant pathogens were detected in the sample. Diseased roots and stolons with lobed hyphopodia were surface-sterilized and placed on one-quarter-strength potato dextrose agar (PDA) amended with rifampicin and streptomycin. One isolate produced structures characteristic of G. graminis var. graminis (3,4), including dark, strongly lobed hyphopodia, and perithecia and ascospores in PDA after incubation. The isolate (PDC 2965) was grown on a sterile ryegrass seed substrate at 25°C for 4 weeks to produce inoculum (2). The isolate was used to inoculate pots of ‘Sea Isle 1’ seashore paspalum grown in sterile soil from sprigs. An inoculum layer, 1 to 2 cm deep, was placed 2 to 4 cm below each sprig and covered with an overlay of sterile soil prior to sprigging (2). Following 4 weeks of plant growth in a greenhouse, dark, necrotic lesions appeared on leaf bases. Very dark lesions developed on roots, and brown runner hyphae and strongly lobed hyphopodia were observed on root and shoot tissues. Selected pieces of symptomatic root and shoot tissue were surface-sterilized and placed on PDA. One week later, dark mycelia and deeply lobed hyphopodia were observed growing from roots and shoots on the PDA. After 1 month, black, flask-shaped perithecia, 156 to 234 μm in body width, developed in cultures. Hyaline, filiform, septate ascospores ranged from 75 to 100 μm (mean = 89 μm; n = 250) long and were approximately 2.5 μm wide. Hyphopodia, perithecia, and ascospores were characteristic of G. graminis var. graminis (3,4). To our knowledge, this is the first report of take-all root rot disease due to G. graminis var. graminis on seashore paspalum in the United States. References: (1) L. E. Datnoff et al. Plant Dis. 81:1127, 1997. (2) M. L. Elliott. Plant Dis. 79:699, 1995. (3) M. L. Elliott and P. J. Landschoot. Plant Dis. 75:238, 1991. (4) P. J. Landschoot. Taxonomy and biology of ectotrophic root-infecting fungi associated with patch diseases of turfgrasses. Pages 41–71 in: Turfgrass Patch Diseases. B. B. Clarke and A. B. Gould, eds. American Phytopathological Society, St. Paul, MN, 1997.
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Garibaldi, A., A. Minuto, and M. L. Gullino. "First Report of Sclerotinia sclerotiorum on Calendula officinalis in Italy." Plant Disease 85, no. 4 (April 2001): 446. http://dx.doi.org/10.1094/pdis.2001.85.4.446c.
Full textAbstract:
Pot marigold (Calendula officinalis) has recently become popular as a potted ornamental plant in Italy. During the spring 1999, a sudden wilt of 120 day-old plants was observed in the Albenga region of Northern Italy, an area of intensive floriculture production. Initial symptoms included stem necrosis at the soil line and yellowing and tan discoloration of leaves. As stem necrosis progressed, infected plants wilted and died. Necrotic tissues resulted, covered with whitish mycelium that produced dark, spherical (2- to 6-mm diameter) sclerotia. Sclerotinia sclerotiorum was consistently recovered from symptomatic stem sections surface disinfested 1 min in 1% NaOCl and plated on potato dextrose agar (PDA), amended with 100 ppm streptomycin sulfate. Pathogenicity of three isolates was confirmed by inoculating 90-day-old pot marigold plants grown in containers. Inoculum that consisted of wheat kernels infested with mycelium and sclerotia was placed on the soil surface around the base of previously wounded or non-wounded plants. Non-inoculated plants served as controls. All plants were kept outdoors where temperatures ranged between 8 and 16°C, under 50% shade and were maintained moist. Inoculated plants developed symptoms of leaf yellowing, followed by wilt within 7 days, while control plants remained symptomless. Sclerotia developed on infected tissues and S. sclerotiorum was reisolated from inoculated plants. This is the first report of stem blight of C. officinalis caused by S. sclerotiorum in Europe. The disease was previously observed in the United States (1). Reference: (1) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN.
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Cating, R. A., J. C. Hong, A. J. Palmateer, C. M. Stiles, and E. R. Dickstein. "First Report of Bacterial Soft Rot on Vanda Orchids Caused by Dickeya chrysanthemi (Erwinia chrysanthemi) in the United States." Plant Disease 92, no. 6 (June 2008): 977. http://dx.doi.org/10.1094/pdis-92-6-0977a.
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Vanda orchids are epiphytes grown for their attractive flowers by commercial producers and hobbyists throughout Florida. In August 2007, five Vanda hybrids, with an economic value of $150 each, were found at a nursery in central Florida with leaves that were macerated, brown, and water soaked. According to the growers, the plants were normal the previous day but symptoms developed rapidly. The plants were immediately removed from the greenhouse to prevent potential disease spread. Bacteria were isolated according to the method of Schaad et al. (1). Isolated bacteria grew at 37°C, were gram negative, degraded pectate, and produced phosphatase. MIDI (Sherlock version TSBA 4.10; Microbial Identification 16 System, Newark, DE) (SIM 0.906) identified the bacteria as Erwinia chrysanthemi (Dickeya chrysanthemi Burkholder et al. 1953) Samson et al. 2005. PCR was performed on the 16S rRNA gene (GenBank Accession No. EU526397) with primers 27f (5′-GAGAGTTTGATCCTG GCTCAG-3′) and 1495r (5′-TACGGCTACCTTGTTACGA-3′) (2). Subsequent DNA sequencing and GenBank search showed the isolated strain is 99% identical to that of Dickeya chrysanthemi. Four leaves each of six Vanda hybrids were inoculated by injecting approximately 150 μl of a bacteria suspension at 1 × 108 CFU/ml into each leaf. One plant was inoculated with water in each of four leaves. Plants were enclosed in plastic bags and returned to the greenhouse under 50% shade at 29°C day and 17°C night temperatures. Within 24 h, soft rot symptoms appeared on inoculated leaves. The water control appeared normal. D. chrysanthemi was reisolated and identified with the above method, thus Koch's postulates were fulfilled. To our knowledge, this is the first report of a soft rot caused by D. chrysanthemi on Vanda hybrids. Because of the popularity and high value of Vanda orchids, proper identification of this rapidly progressing bacterial disease is of great importance for the commercial producer and homeowner alike. References: (1) N. W. Schaad et al. Erwinia soft rot group. Page 56 in: Laboratory Guide for Identification of Plant Pathogenic Bacteria. 3rd ed. N. W. Schaad et al., eds. American Phytopathological Society. St. Paul, MN, 2001. (2) W. G. Weisburg. J. Bacteriol. 173:697, 1991.
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Koenning, S. R., T. C. Creswell, E. J. Dunphy, E. J. Sikora, and J. D. Mueller. "Increased Occurrence of Target Spot of Soybean Caused by Corynespora cassiicola in the Southeastern United States." Plant Disease 90, no. 7 (July 2006): 974. http://dx.doi.org/10.1094/pd-90-0974c.
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Target spot of soybean (Glycine max (L.) Merr.) caused by Corynespora cassiicola (Berk. & Curt.), although found in most soybean-growing countries, is considered to be a disease of limited importance (1) and has never been reported to cause soybean yield loss in the southeastern United States (2,3). Soybean plants submitted to the North Carolina Plant Disease and Insect Clinic (NCPDIC) in August 2004 from Beaufort, Robeson, Wilson, and Johnston counties, NC had symptoms consistent with target spot. Symptoms consisted of roughly circular, necrotic leaf lesions from minute to 11 mm in diameter, though typically approximately 4 to 5 mm in diameter, and with a yellow margin. Large lesions occasionally exhibited a zonate pattern often associated with this disease. Microscopic examination of the lesions revealed the presence of spores (conidia) typical of C. cassiicola (1). Conidia were mostly three to five septate with a central hilum at the base and ranged in size from 7 to 22 wide × 39 to 520 μm long. Three commercial soybean fields near Blackville, SC (Barnwell County) were severely affected by this disease and it caused premature defoliation. Nineteen of twenty-seven maturity group VII and VIII genotypes in the 2004 Clemson University soybean variety trial near Blackville, SC had visible symptoms of target spot. Heavy rainfall associated with hurricanes during September 2004 probably enhanced the incidence of this disease, and yield suppression due to target spot was estimated at 20 to 40% in some fields. In 2005, 20 of 161 soybean samples submitted to the NCPDIC or collected in surveys from 16 counties were positive for target spot on the basis of microscopic examination. Target spot also was diagnosed in six counties (Baldwin, DeKalb, Elmore, Fayette, Macon, and Pickens) in Alabama and in four additional counties (Bamberg, Hampton, Orange-burg, and Calhoun) in South Carolina in 2005. Records from the NCPDIC indicate that target spot had not been diagnosed on soybean in North Carolina since 1981. The large increase in incidence of target spot in the southeast may be related to changes in weather patterns, changes in pathogen virulence, and/or the introduction of more susceptible host genotypes. References: (1) J. B. Sinclair. Target spot. Page 27 in: Compendium of Soybean Diseases. G. L. Hartman et al. eds. The American Phytopathological Society, St. Paul, MN, 1999. (2) J. A. Wrather et al. Plant Dis. 79:1076. 1995. (3) J. A. Wrather et al. On-line publication. doi:10.1094/PHP-2003-0325-01-RV. Plant Health Progress, 2003.
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Paz Lima, M. L., A. C. Café-Filho, N. L. Nogueira, M. L. Rossi, and L. R. Schuta. "First Report of Clubroot of Eruca sativa Caused by Plasmodiophora brassicae in Brazil." Plant Disease 88, no. 5 (May 2004): 573. http://dx.doi.org/10.1094/pdis.2004.88.5.573b.
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Eruca sativa Mill. (family Brassicaceae), with its origin in western Asia, is a culinary and pharmacological species cultivated in Europe, Brazil, and other countries. In the United States, it is a minor crop known as arugula or roquette. Clubroot on E. sativa has not been reported in Brazil and has been reported once in the United States in 1914 (1,2,3). On several occasions since 2000, stunted and wilted plants (cv. Rúcula Cultivada) were collected from growers' fields and greenhouses that had been direct-seeded in Vargem Bonita, DF (two fields and one greenhouse) and Quatro Barras, PR (two fields). The infected arugula crops were found in areas where other plants from the genus Brassica were traditionally cultivated. Disease incidence in individual fields varied from 20 to 80%. Diseased plants were severely affected with hypertrophic, malformed roots, and root galls resembling Woronin's description (4). Plasmodia and resting spores in thin sections prepared from root galls were observed with compound and electron microscopes. Pathogenicity tests were conducted on arugula and Brassica pekinensis (Lour.) Rupr. (universal host) with inoculum from naturally infected arugula. The soil of potted test plants at the four-to-five-leaf stage was drenched with a suspension of resting spores. Symptoms identical to those observed on the original plants were produced on all inoculated plants 2 to 3 weeks after inoculation. Control plants remained symptomless. The pathogen was positively identified as Plasmodiophora brassicae Wor. with the combination of macroscopic and microscopic symptoms and signs of the disease and pathogen. P. brassicae was first reported in Brazil in 1965 in the state of São Paulo and in the 1980s in Distrito Federal on several members of the Brassicae. To our knowledge, this is the first report of P. brassicae infecting E. sativa in Brazil. Arugula is a susceptible host and should not be planted on P. brassicae-infested land. References: (1) D. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN. 1989. (2) D. F. Farr et al. Fungal Databases. Systematic Botany and Mycology Laboratory, On-line publication. ARS, USDA, 2003. (3) J. S. Karling. The Plasmodiophorales. Published by J. S. karling, NY. 1942. (4) M. S. Woronin. Plasmodiophora brassicae the Cause of Cabbage Hernia. Phytopathological Classics 4. The American Phytopathological Society, Ithaca, NY, 1934.
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Conner, K. N., J. Olive, L. Zhang, J. Jacobi, and M. L. Putnam. "First Report of Bacterial Gall on Loropetalum chinense Caused by Pseudomonas savastanoi in the United States." Plant Disease 97, no. 6 (June 2013): 835. http://dx.doi.org/10.1094/pdis-11-12-1011-pdn.
Full textAbstract:
Bacterial gall symptoms were observed on Loropetalum chinense (R. Br.) Oliv. in two separate commercial nurseries in South Alabama during the spring of 2012. Limb dieback and plant death was first reported by the growers. Plants with dieback symptoms had galling and irregular dark callus formation on the lower stem and lower branches. Galls were small, 0.2 to 1 cm, inconspicuous, and in some cases girdled the stem causing breakage of the main stem. In both locations, 30 to 40% of the crop was affected. Similar symptoms have been observed on L. chinense in nursery and landscape plantings in central Alabama, North Carolina, and Georgia in previous years. Bacterial colonies were isolated from four plants representing two different locations. Isolates were recovered from surface sterilized symptomatic tissue on nutrient agar and King's medium B (KMB). All isolates were gram-negative and fluoresced blue-green under UV light after 48 h of growth at 28°C on KMB. One representative isolate from each site was identified as Pseudomonas savastanoi based on their fatty acid profiles (similarity index of 0.776; MIS-TSBA, version 4.0, MIDI Inc., Newark, DE) and LOPAT tests (2). The identity was confirmed by sequencing a 900-bp portion of the 16S rDNA gene, which revealed 98% similarity to the P. savastanoi type strain in NCBI (Accession No. AB021402). In greenhouse pathogenicity tests, eight Loropetalum liners were inoculated with a bacterial suspension (107 CFU/ml) of each of the two isolates. Plants were inoculated by injecting the suspension into the lower stem after wounding by puncturing with needles or slicing sections of the bark. Controls were inoculated with water. All plants inoculated with the bacteria developed gall symptoms in 8 weeks under 90% relative humidity at 30°C. The bacteria were reisolated from five inoculated plants. DNA was extracted from each isolate, amplified using primer pair 27F/1492R targeting the 16S rDNA gene (1), and sequenced. Sequences (900 bp) from all isolates shared 98 to 99% similarity to P. savastanoi type strain in GenBank (Accession No. AB021402). Nucleotide sequence data reported are available in GenBank under accessions JX915832 to 37. To our knowledge, this is the first report of bacterial gall of L. chinense caused by P. savastanoi in the United States. Given the increasing prevalence of this disease in South Alabama, its confirmation is a significant step toward management recommendations for growers. References: (1) D. J. Lane. 16S/23S rRNA sequencing. Page 115-175 in: Nucleic Acid Techniques in Bacterial Systematics. E. Stackebrandt and M. Goodfellow, eds. John Wiley and Sons, New York, 1991. (2) N. W. Schaad et al. Laboratory Guide for Identification of Plant Pathogenic Bacteria. 3rd ed. The American Phytopathological Society, St. Paul, MN, 2001.
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Mangandi, J. A., T. E. Seijo, and N. A. Peres. "First Report of Myrothecium roridum Causing Myrothecium Leaf Spot on Salvia spp. in the United States." Plant Disease 91, no. 6 (June 2007): 772. http://dx.doi.org/10.1094/pdis-91-6-0772b.
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The genus Salvia includes at least 900 species distributed worldwide. Wild species are found in South America, southern Europe, northern Africa, and North America. Salvia, commonly referred to as sage, is grown commercially as a landscape plant. In August 2006, pale-to-dark brown, circular leaf spots 5 to 20 mm in diameter with concentric rings were observed on Salvia farinacea ‘Victoria Blue’. Approximately 5% of the plants in a central Florida nursery were affected. Lesions were visible on both leaf surfaces, and black sporodochia with white, marginal hyphal tuffs were present mostly on the lower surface in older lesions. Symptoms were consistent with those of Myrothecium leaf spot described on other ornamentals such as gardenia, begonia, and New Guinea impatiens (4). Isolations from lesions on potato dextrose agar produced white, floccose colonies with sporodochia in dark green-to-black concentric rings. Conidia were hyaline and cylindrical with rounded ends and averaged 7.4 × 2.0 μm. All characteristics were consistent with the description of Myrothecium roridum Tode ex Fr. (2,3). The internal transcribed spacer regions ITS1, ITS2, and the 5.8s rRNA genomic region of one isolate were sequenced (Accession No. EF151002) and compared with sequences in the National Center for Biotechnology Information (NCBI) database. Deposited sequences from M. roridum were 96.3 to 98.8% homologous to the isolate from salvia. To confirm pathogenicity, three salvia plants were inoculated by spraying with a conidial suspension of M. roridum (1 × 105 conidia per ml). Plants were covered with plastic bags and incubated in a growth chamber at 28°C for 7 days. Three plants were sprayed with sterile, distilled water as a control and incubated similarly. The symptoms described above were observed in all inoculated plants after 7 days, while control plants remained symptomless. M. roridum was reisolated consistently from symptomatic tissue. There are more than 150 hosts of M. roridum, including one report on Salvia spp. in Brunei (1). To our knowledge, this is the first report of Myrothecium leaf spot caused by M. roridum on Salvia spp. in the United States. Even the moderate level disease present caused damage to the foliage and reduced the marketability of salvia plants. Therefore, control measures may need to be implemented for production of this species in ornamental nurseries. References: (1) D. F. Farr et al. Fungal Databases. Systematic Botany and Mycology Laboratory. Online publication. ARS, USDA, 2006, (2) M. B. Ellis. Page 449 in: Microfungi on Land Plants: An Identification Handbook. Macmillan Publishing, NY, 1985. (3) M. Fitton and P. Holliday. No. 253 in: CMI Descriptions of Pathogenic Fungi and Bacteria. The Eastern Press Ltd. Great Britain, 1970. (4) M. G. Daughtrey et al. Page 19 in: Compendium of Flowering Potted Plant Diseases. The American Phytopathological Society. St. Paul, MN, 1995.
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Jeffers, S. N., G. Schnabel, and J. P. Smith. "First Report of Resistance to Mefenoxam in Phytophthora cactorum in the United States and Elsewhere." Plant Disease 88, no. 5 (May 2004): 576. http://dx.doi.org/10.1094/pdis.2004.88.5.576a.
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Phytophthora cactorum causes crown rot of strawberry (Fragaria × ananassa) (2), a disease that has been particularly severe during the last 5 years in the southeastern United States. In the fall of 2001, strawberry plants (cv. Camarosa) in a field in Lexington County, South Carolina exhibited typical crown rot symptoms (2) 1 to 2 weeks after transplanting, even though plants had been drenched with mefenoxam (Ridomil Gold; Syngenta Crop Protection, Greensboro, NC) immediately after transplanting. Initially, we observed leaves that had marginal necrosis, were smaller than normal, and were discolored. Soon after, diseased plants appeared stunted and unthrifty compared with other plants in the field, and some of these plants eventually wilted and died. Severely affected plants had necrotic roots and decayed crowns. Ten symptomatic plants were collected for isolation. In the laboratory, root and crown tissues were rinsed in running tap water and blotted dry, small pieces of necrotic tissue were placed aseptically on PAR-V8 selective medium (1), and isolation plates were placed at 20°C in the dark for up to 7 days. P. cactorum was recovered from six plants. Isolates produced characteristic asexual and sexual structures directly on the isolation plates (i.e., papillate sporangia on sympodial sporangiophores and oospores with paragynous antheridia) (2). A single hypha of an isolate from each plant was transferred to fresh PAR-V8, and pure cultures were stored on cornmeal agar in glass vials at 15°C in the dark. All six isolates from the Lexington County field and nine other isolates of P. cactorum from strawberry (three from South Carolina, three from North Carolina, and three from Florida) were tested for sensitivity to mefenoxam on fungicide-amended medium. Mefenoxam was added to 10% clarified V8 juice agar (cV8A) after autoclaving so the concentration in the medium was 100 ppm. Agar plugs from active colonies were transferred to mefenoxam-amended and nonamended cV8A (three replicates per treatment), plates were placed at 25°C in the dark for 3 days, and linear mycelium growth was measured. All six isolates from Lexington County were highly resistant to mefenoxam with mycelium growth relatively unrestricted on mefenoxam-amended medium (73 to 89% of that on nonamended medium). In comparison, the other nine isolates were sensitive to mefenoxam with mycelium growth severely restricted by 100 ppm of mefenoxam (0 to 7% of that on nonamended medium). To our knowledge, this is the first report of mefenoxam resistance in P. cactorum on strawberry or any other crop in the United States and elsewhere. Because mefenoxam is the primary fungicide used to manage Phytophthora crown rot in the southeastern United States, resistance may limit use of this fungicide in strawberry production. References: (1) A. J. Ferguson and S. N. Jeffers. Plant Dis. 83:1129, 1999. (2) E. Seemüller. Crown rot. Pages 50–51 in: Compendium of Strawberry Diseases, 2nd ed. J. L. Maas, ed. The American Phytopathological Society, St. Paul, MN, 1998.
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Madia, M., and S. Gaetán. "Outbreak of Powdery Mildew on Common Sage in Argentina." Plant Disease 89, no. 8 (August 2005): 911. http://dx.doi.org/10.1094/pd-89-0911c.
Full textAbstract:
Common sage, Salvia officinalis L., is produced primarily in greenhouses for the culinary herb market in Argentina. Since 2003 during autumn and winter, powdery mildew symptoms have been repeatedly observed on potted common sage plants in commercial greenhouses located on the outskirts of Buenos Aires. The average disease incidence during this period was 85 to 90%. Circular, white, powdery patches developed on leaf surfaces and stems. Heavily infected leaves turned brown and died. Hyaline mycelium and nonlobed appressoria were observed. Conidiophores were simple with straight foot cells measuring 53.0 to 80.0 × 10.0 to 12.3 μm. Conidia were aseptate, hyaline, cylindrical to ovoid, measured 33.0 to 40.5 × 15.0 to 18.5 μm, did not contain fibrosine bodies, and were produced in chains. Cleistothecia were not observed. The pathogen was identified as Erysiphe cichoracearum DC (1). Pathogenicity was confirmed by gently pressing leaves displaying abundant sporulation onto the adaxial surface of healthy leaves. After 10 to 12 days, typical signs and symptoms of powdery mildew appeared on all inoculated plants. Pathogenicity tests were conducted in a greenhouse at 20 to 23°C and included 10 sage plants (five inoculated and five noninoculated). The experiment was performed twice, each time with the same result. Control plants did not show any signs or symptoms. E. cichoracearum DC was previously reported in the United States on Salvia sp. (2).To our knowledge, this is the first report of an outbreak of powdery mildew caused by E. cichoracearun on potted common sage plants produced in greenhouses in Argentina. References: (1) H. J. Boesewinkel. Rev. Mycol. Tome 41:493, 1977. (2) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989.
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Holcomb, G. E., and D. E. Carling. "First Report of Leaf Blight of Dianthus chinensis Caused by Rhizoctonia solani." Plant Disease 84, no. 12 (December 2000): 1344. http://dx.doi.org/10.1094/pdis.2000.84.12.1344d.
Full textAbstract:
Dianthus chinensis (rainbow pink) is a popular seasonal bedding plant for the Gulf Coast of the United States and is primarily grown during the fall, winter, and early spring months. In August 1999, diseased plants were observed in a Baton Rouge, LA, propagation nursery with irregularly oval, tan leaf spots 3 to 10 mm in diameter. Heavily infected leaves became blighted and were killed, but plants survived and roots, crowns, and flowers were not affected. Infected leaf samples were surface-disinfected for 1 to 3 min in 70% ethyl alcohol, blotted dry, and sections were placed on 2% acidified water agar. A fungus that was identified as Rhizoctonia solani, and belonging to anastomosis group (AG)-1 IB, was consistently isolated from infected leaves. Inoculum was prepared by blending one 7-day-old plate culture, grown on acidified potato-dextrose agar, in 100 ml distilled deionized water. Pathogenicity tests were performed by dripping inoculum from a 10-ml pipette on leaf surfaces of healthy rainbow pink plants. Inoculated and noninoculated plants were held in a dew chamber at 26°C for 2 to 3 days and then removed to a greenhouse where temperatures ranged from 25 to 32°C. Inoculated plants developed water-soaked spots after 2 to 3 days that turned tan and became necrotic 5 to 10 days later. These symptoms were like those observed on the original diseased plants. R. solani was reisolated from inoculated plants, and noninoculated plants remained healthy. Although R. solani has been reported previously as a root and stem pathogen of D. chinensis (1), this is the first report of leaf blight disease caused by this fungus. Reference: (1) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN.
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Garibaldi, A., A. Minuto, D. Bertetti, R. Nicoletti, and M. L. Gullino. "First Report of Web Blight on Yellow-Sage (Lantana camara) Caused by Rhizoctonia solani in Europe." Plant Disease 87, no. 7 (July 2003): 875. http://dx.doi.org/10.1094/pdis.2003.87.7.875a.
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Lantana camara is increasingly grown in northern Italy as a potted plant and contributes to the diversification of offerings in the ornamental market. During the spring of 2001, selections of L. camara cuttings growing at a commercial farm located at Albenga (Riviera coast) exhibited tan leaf spots of irregular size and shape. Spots were at first isolated, 4 to 8 mm in diameter, and later coalesced and affected the entire plant. Heavily infected leaves, stems, and branches became blighted and were killed. Infected rooted cuttings also eventually died. Diseased cuttings showed a progressive reduction (to less than 20%) in rooting ability. Isolations from infected leaves and stems on potato dextrose agar (PDA), supplemented with 100 mg/liter of streptomycin sulphate, consistently yielded a fungus with mycelial and cultural characteristics resembling Rhizoctonia solani. The fungal isolates were further characterized as R. solani Kühn AG-4 based on hyphal anastomoses with several AG-4 tester isolates. Pathogenicity tests were performed by placing 5-day-old-fungal mycelial plugs, grown on PDA, at the base of five healthy yellow-sage stems and holding plants in a dew chamber at 18 to 22°C. After 2 days, foliage blight appeared on leaves of inoculated plants, and after 3 days, stems also became infected and entire plants wilted. Five noninoculated plants remained healthy. The fungal pathogen was reisolated from all inoculated plants. R. solani has been observed on L. camara in the United States (1) and the Philippines (2). To our knowledge, this is the first report of R. solani on L. camara in Europe. References: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (2) F. T. Orillo and R. B. Valdez. Philipp. Agric. A. 42:292, 1958.
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Bienapfl, J. C., C. M. Floyd, J. A. Percich, and D. K. Malvick. "First Report of Clonostachys rosea Causing Root Rot of Soybean in the United States." Plant Disease 96, no. 11 (November 2012): 1700. http://dx.doi.org/10.1094/pdis-06-12-0550-pdn.
Full textAbstract:
Multiple fungal species have been associated with root rot of soybean (Glycine max) in the United States, but root rot in Minnesota (MN) also occurs in plants not known to be infected with previously reported pathogens (1). Soybean plants that lacked foliar symptoms, but exhibited taproot and lateral root necrosis were observed in 15 fields from nine counties in MN during 2007 and 2008. Plants were arbitrarily dug up at the R3 growth stage in July as part of a root rot study. Roots were washed, surface disinfested in 0.5% NaOCl for 3 min, rinsed in deionized water, dried, and embedded in potato dextrose agar (PDA). Thirty isolates with morphological characteristics consistent with those of Clonostachys rosea were recovered in total from necrotic lesions on different plants from all fields (3). For further morphological characterization, cultures were grown on PDA for 1 week at 24°C in the dark. Colonies were 39 to 46 mm in diameter, yellowish-white, and the surface was felty to tomentose with thick aerial hyphae. Primary conidiophores were Verticillium-like with two to three levels. The stipe length measured 65 to 105 μm and the base width was 5 μm. Primary conidia were smooth, hyaline, slightly curved, with an average length and width of 7 to 9 × 2.6 to 3 μm. Secondary conidiophores were penicillate with two or three whorls of phialides. The stipe length measured 50 to 75 μm, base width was 5 μm, and penicillus height was 25 to 35 μm. Secondary conidia were 5 to 6 × 2.5 μm. Perithecia were not produced. The identity of isolates was confirmed by sequencing the internal transcribed spacer (ITS) locus using the primers ITS1F/ITS4. BLAST analysis of the sequences in the NCBI database resulted in a 99.8 to 100% match for both C. rosea and its teleomorph Bionectria ochroleuca (e.g., HM751081, GU256766). Each isolate was tested for pathogenicity on soybean by initially growing it on sterile sorghum grain for 2 weeks at 23°C. Sterile sorghum was used for control plants. Seeds of soybean ‘AG2107’ were planted in 11.4-cm square pots containing pasteurized potting mix and a 25-cm3 layer of infested or sterile sorghum placed ~1 cm below the seeds. Two replicate pots containing four plants each were used per treatment and the experiment was repeated once. Root rot was assessed 28 days after planting in a greenhouse at 23°C day and 18°C night with a 14-h photoperiod. Twenty-eight of 30 C. rosea isolates caused taproot necrosis on inoculated plants in both experiments, whereas control roots did not exhibit necrosis. Approximately 6% of inoculated plants also developed interveinal chlorosis and marginal necrosis on trifoliates. Isolations were attempted from roots of all plants, and the isolates recovered from inoculated plants were identified as C. rosea based on morphology and ITS sequences. This fungus was not isolated from control plants. C. rosea was also isolated from petioles of symptomatic trifoliates, indicating systemic colonization of the plants. To our knowledge, this is the first report of C. rosea causing root rot of soybean and systemically colonizing soybean. This fungus may have been previously isolated from asymptomatic soybean plants and identified as Gliocladium roseum (2). The impact of this fungus on soybean production is unknown. References: (1) G. Hartman et al. Compendium of Soybean Diseases. 4th ed. The American Phytopathological Society, St. Paul, MN, 1999. (2) J. D. Mueller and J. B. Sinclair. Trans. Brit. Mycol. Soc. 86:677, 1986. (3) H.-J. Schroers et al. Mycologia 91:365, 1999.
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Trigiano, R. N., T. A. Rinehart, M. M. Dee, P. A. Wadl, L. Poplawski, and B. H. Ownley. "First Report of Aerial Blight of Ruth's Golden Aster (Pityopsis ruthii) Caused by Rhizoctonia solani in the United States." Plant Disease 98, no. 6 (June 2014): 855. http://dx.doi.org/10.1094/pdis-11-13-1181-pdn.
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Ruth's golden aster (Pityopsis ruthii (Small) Small: Asteraceae) is an endangered, herbaceous perennial that occurs only at a few sites along the Hiwassee and Ocoee rivers in Polk County, Tennessee. This species is drought, heat, and submergence tolerant and has ornamental potential as a fall flowering landscape plant. In 2012, we vegetatively propagated various genotypes and established plantings in a landscape at Poplarville, Mississippi. In June and July of 2013, during periods of hot and humid weather, several well-established plants exhibited black or brown necrotic aerial blight symptoms including desiccation of stems and leaves. Blighted leaf samples were surface sterilized (10% commercial bleach, active ingredient 8.25% sodium hypochlorite, 1 min), rinsed in sterile water, air-dried, and plated on 2% water agar amended with 3.45 mg fenpropathrin/liter (Danitol 2.4 EC, Valent Chemical, Walnut Creek, CA) and 10 mg/liter rifampicin (Sigma-Aldrich, St. Louis, MO). Rhizoctonia sp. was identified based on hyphal morphology and cultures were maintained on potato dextrose agar. Colonies were fast growing, consisting of light tan to brown mycelia and tufts of crystalline aerial hyphae. Within 10 days, brown exudates were present in cultures and there was no pigmented reverse to the agar. Hyphae were a mean of 5.2 μm wide (4.6 to 6.1 μm; n = 10) and each compartment contained three or more nuclei. Hyphae were constricted at septa with right angle branching and no clamp connections, which is typical for Rhizoctonia solani (1). Light- to medium-brown, oblong to irregularly shaped sclerotia measuring 1.2 mm long (0.7 to 2.1 mm) × 0.9 mm wide (0.5 to 1.2 mm; n = 20) were formed in cultures after 3 weeks of growth. Total genomic DNA was extracted from two different colonies grown in potato dextrose broth for 7 days, amplified with PCR using ITS1 and ITS4 primers for amplification of the 18S rDNA subunit (2), the products purified, and sequenced. A consensus sequence of 657 bp was deposited in GenBank (Accession Nos. KF843729 and KF843730) and was 96% identical to two R. solani Kühn ITS sequences in GenBank (HF678125 and HF678122). R. solani was grown on twice autoclaved oats for 2 weeks at 21°C and incorporated into Pro-Mix BX, low fertility soilless medium (Premier Horticulture, Rivière-du-Loup, Quebec, Canada) at 4% (w/w) to inoculate seven P. ruthii plants grown in 10 cm-diameter pots; seven additional plants were grown in the same medium amended with 4% (w/w) sterile oats. Plants were grown in a greenhouse and covered with a plastic dome to maintain high humidity. After 2 weeks, six of the seven inoculated plants exhibited the same aerial blight symptoms as did the original infected plants from the field; none of the control plants developed disease symptoms. Colony morphology and hyphal characteristics as well as the sequence for the ITS region of rDNA from the re-isolated fungus were identical to the original isolate. To our knowledge, this is the first report of R. solani infecting Ruth's golden aster. We are not aware of the disease occurring in wild populations of the plant, but may impact plants grown in the landscape or greenhouse. References: (1) B. Sneh et al. Identification of Rhizoctonia Species. The American Phytopathological Society, St Paul, MN, 1991. (2) T. J. White et al. Page 315 in: PCR Protocols: A Guide to Methods and Applications. M. A. Innis et al., eds. Academic Press, San Diego, CA, 1990.
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Garibaldi, A., D. Bertetti, and M. L. Gullino. "First Report of Collar and Root Rot Caused by Phytophthora nicotianae on Daphne odora in Italy." Plant Disease 93, no. 8 (August 2009): 848. http://dx.doi.org/10.1094/pdis-93-8-0848a.
Full textAbstract:
Daphne odora is becoming popular in gardens because of its variegated foliage and fragrant flowers in late winter and early spring. During October of 2008 in a commercial nursery near Maggiore Lake (Verbano-Cusio-Ossola Province) in northwestern Italy, plants of D. odora showed extensive chlorosis and root rot. Diseased plants eventually wilted and died, dropping leaves in some cases. Most frequently, wilted leaves persisted on stems. At the soil level, dark brown-to-black water-soaked lesions that coalesced often girdled the stem. All of the crown and root system was affected. Disease was widespread and severe with 70% of 2,500 potted plants being affected. A Phytophthora-like organism was isolated consistently on a medium selective for oomycetes (4) after disinfestation of lower stem and root pieces of D. odora for 1 min in a solution containing 1% NaOCl. Tissue fragments of 1 mm2 were excised from the margins of the lesions and plated. The pathogen was identified based on morphological and physiological features as Phytophthora nicotianae (= P. parasitica) (2). Sporangia were produced for identification by growing a pure culture in sterilized soil extract solution at neutral pH (obtained by shaking and then centrifuging 300 g of soil in 1 liter of distilled water). They were spherical to ovoid, papillate, and measured 39.2 to 54.5 × 31.7 to 41.7 μm (average 44.8 × 34.5 μm). Papillae measured 2.4 to 4.9 μm (average 3.7 μm). Chlamydospores were spherical with a diameter ranging from 15.8 to 36.1 μm (average 25.4 μm). The internal transcribed spacer (ITS) region of rDNA of a single isolate was amplified using primers ITS4/ITS6 and sequenced. BLAST analysis (1) of the 804-bp segment showed a 100% homology with the sequence of P. nicotianae EF140988. The nucleotide sequence has been assigned GenBank No. FJ843100. Pathogenicity of two isolates obtained from infected plants was confirmed by inoculating 12-month-old plants of D. odora. Both isolates were grown for 15 days on a mixture of 70:30 wheat/hemp kernels and then 80 g/liter of the inoculum was mixed into a substrate containing sphagnum peat moss/pumice/pine bark/clay (50:20:20:10 vol/vol). One plant per 3-liter pot was transplanted into the substrate and constituted the experimental unit. Three replicates were used for each isolate and noninoculated control treatment; the trial was repeated once. All plants were kept in a greenhouse at temperatures from 20 to 25°C. Plants inoculated with isolate no. 1 developed symptoms of chlorosis and root rot within 14 days and then a wilt rapidly followed. Isolate no. 2 was less aggressive causing the same symptoms within 20 days. Control plants remained symptomless. P. nicotianae consistently was reisolated from inoculated plants. Previously, P. nicotianae (= P. parasitica) has been reported in several states of the United States on D. odora (3). To our knowledge, this is the first report of P. nicotianae on D. odora in Italy. The economic importance of the disease is low because of the limited number of farms that grow this crop in Italy, although spread could increase as the popularity of plantings expand. References: (1) S. F. Altschul et al. Nucleic Acids Res. 25:3389, 1997 (2) D. C. Erwin and O. K. Ribeiro. Phytophthora Diseases Worldwide. The American Phytopathological Society, St Paul, MN, 1996. (3) D. F. Farr et al. Fungi on Plants and Products in the United States. The American Phytopathological Society, St Paul, MN, 1989. (4) H. Masago et al. Phytopathology, 67:425, 1977.
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Hollingsworth, C. R., and F. A. Gray. "First Report of Brown Root Rot on Alfalfa Caused by Phoma sclerotioides in the Continental United States." Plant Disease 83, no. 11 (November 1999): 1071. http://dx.doi.org/10.1094/pdis.1999.83.11.1071a.
Full textAbstract:
Phoma sclerotioides G. Preuss ex Sacc. (previously named Plenodomus meliloti Dearn. & G.B. Sanford) is associated with root rot and extensive winterkill of leguminous forage crops, such as clover (Trifolium and Melilotus spp.), sainfoin (Onobrychis viciifolia), and alfalfa (Medicago sativa). Winterkill and root rot of irrigated alfalfa were observed for the first time in a field of cv. Multiplier in western Wyoming during the spring of 1996. Dark brown to black, sunken, rotting lesions were noted on upper secondary roots and taproots of dead and living diseased plants. Superficial and embedded beaked pycnidia and pycnosclerotia were observed near root lesions. A Phoma sp. isolated from a diseased plant in Farson, WY, was maintained on potato dextrose and half-strength V8-juice agars. Beaked pycnidia, typical of P. sclerotioides, were observed in culture when grown at 10°C for 2 months. A pathogenicity test was performed on cv. Multiplier. Two barley seeds colonized by a Phoma sp. derived from a Wyoming isolate were positioned on taproots of healthy, greenhouse-grown, 5-month-old plants ≈2.5 cm below the crown and were covered with a small piece of sterile cotton. Three replicate samples (24 plants inoculated and 24 plants uninoculated per replicate) were winter-hardened for 4 weeks (15.6°C/10°C, day/night, for 2 weeks, followed by 10°C/7.2°C, day/night, for 2 weeks) and placed outside during January 1998 in Laramie, WY, for a 4-month winter exposure period. Plants were rated for disease during June 1998. A disease severity rating of 1 to 5 was assigned to each experimental unit, where 1 = no disease and 5 = dead plant. The percentage of diseased plants at each severity rating for all inoculated plants was 1 = 19%, 2 = 33%, 3 = 31%, 4 = 13%, and 5 = 4%. Mycelium typical of P. sclerotioides was found on 99% of inoculated plant roots whether or not they had pycnidia. Pycnidia were found on the lower stems and petioles of some inoculated plants. Three percent of control plants also developed brown root rot (BRR) symptoms (taproot lesions or discoloration) by June 1998. The percentage of diseased plants at each severity rating for all uninoculated plants was 1 = 96%, 2 = 4%, and 3 through 5 = 0%. Aboveground propagule placement likely contributed to the spread of BRR by raindrop splash and wind-driven plant debris to adjacent alfalfa. Most inoculated plants had immature pycnidia or protopycnidia (94%), whereas 6.9% of the plants also had fully mature, beaked pycnidia. Pure fungal cultures were obtained from several diseased roots and compared with the original Wyoming Phoma sp. culture and a Canada isolate of P. sclerotioides (ATCC no. 56515) (2): colony, pycnidial, and conidial morphologies were identical, completing Koch's postulates. This is the first report of BRR on alfalfa in the continental United States. References: (1) J. G. N. Davidson. 1990. Brown root rot. Pages 29–31 in: Compendium of Alfalfa Disease. 2nd ed. The American Phytopathological Society, St. Paul, MN. (2) C. R. Hollingsworth et al. Phytopathology 88(suppl.):S39, 1999.
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Dawson, J. H. "Witchweed Research and Control in the United States – Edited by Paul F. Sand, Robert E. Eplee, and Randy G. Westbrooks. Published in 1990 by Weed Science Society of America, 309 W. Clark St., Champaign, IL 61820." Weed Technology 5, no. 1 (March 1991): 251–52. http://dx.doi.org/10.1017/s0890037x00033662.
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Inglis, D. A., M. L. Derie, and K. C. Volker. "Evidence that Cercospora carotae Causes Leaf Spot on Carrot in Western Washington." Plant Disease 85, no. 5 (May 2001): 559. http://dx.doi.org/10.1094/pdis.2001.85.5.559a.
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During 1999, a leaf spot on carrot (Daucus carota L. subsp. sativus [Hoffm.] Arcang.) was observed on nearly every plant in a 20-ha field of carrots (cv. Red Chantenay) grown for processing in western Washington. Circular to elongate, light brown lesions surrounded by chlorosis were present on leaflet margins and petioles of affected plants. Conidia of Cercospora carotae (Pass.) Solheim were present in the lesions. Small pieces of surface-sterilized leaf tissue were placed onto potato dextrose agar plates and incubated at room temperature to obtain fungal isolates. Koch's postulates were completed by atomizing the upper and lower leaves of carrot seedlings at the three to four leaf stage with sterile water or C. carotae at 1.0 × 104 conidia/ml in sterile 0.01% Tween 80. Treatments were replicated five times using single plants. The plants were bagged in clear plastic and placed in a greenhouse at 25°C for 72 h. Disease symptoms developed within 10 days as light brown lesions on leaflet margins and petioles, and were similar to those found in the field. The fungus was reisolated as described above. Symptoms did not develop in control plants sprayed with water. Farr et al. (1) report that C. carotae occurs in several states but not Washington, and Shaw (2) lists C. carotae only from British Columbia and Oregon. To our knowledge, this is the first report of Cercospora leaf spot on carrot in Washington. References: (1) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN. (2) C. G. Shaw. W.S.U. Agric. Exp. Sta. Bull. 765, 1969.
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Garibaldi, A., D. Bertetti, and M. L. Gullino. "First Report of Powdery Mildew Caused by Podosphaera aphanis var. aphanis on Potentilla fruticosa in Italy." Plant Disease 89, no. 12 (December 2005): 1362. http://dx.doi.org/10.1094/pd-89-1362c.
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Potentilla fruticosa L. (bush cinquefoil), belonging to the family Rosaceae, is an ornamental plant used in parks and gardens. During the spring and summer of 2005, severe outbreaks of a previously unknown powdery mildew were observed in several private gardens located near Biella (northern Italy). The adaxial and abaxial surfaces of leaves as well as the stems were covered with white mycelium. Buds and flowers also were affected. As disease progressed, infected leaves turned yellow and dehisced. Conidia formed in chains and were hyaline, ovoid, and measured 24.0 to 36.0 × 15.8 to 24.0 μm (average 30.1 × 20.0 μm). Fibrosin bodies were present. Chasmothecia were numerous, sphaerical, amber colored, and diameters ranged from 84.0 to 98.4 μm (average 90.4 μm). Each chasmothecium contained one ascus with eight ascospores. Ascospores measured 26.5 to 27.2 × 13.2 to 15.6 μm (average 26.8 × 14.0 μm). On the basis of its morphology, the causal agent was determined to be Podosphaera aphanis (Wallr.) U. Braun & S. Takamatsu var. aphanis U. Braun (1). Pathogenicity was confirmed through inoculations by gently pressing diseased leaves onto leaves of healthy P. fruticosa plants. Three plants were inoculated. Three noninoculated plants served as a control. Plants were maintained at temperatures ranging from 12 to 23°C. Ten days after inoculation, typical symptoms of powdery mildew developed on inoculated plants. Noninoculated plants did not show symptoms. The pathogenicity test was carried out twice. To our knowledge, this is the first report of powdery mildew on P. fruticosa in Italy. Erysiphe polygoni D.C. and Sphaerotheca macularis (Wallr.:Fr.) Lind were observed in the United States on P. fruticosa (2), while in Japan, the presence of S. aphanis var aphanis was reported (3). Voucher specimens are available at the AGROINNOVA Collection, University of Torino. References: (1) U. Braun and S. Takamatsu. Schlechtendalia 4:1, 2000 (2) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St Paul, MN, 1989. (3) S. Tanda et al. J. Agric. Sci. 39:258, 1995.
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Koike, S. T., O. Daugovish, and J. A. Downer. "Sclerotinia Petiole and Crown Rot of Celery Caused by Sclerotinia minor in California." Plant Disease 90, no. 6 (June 2006): 829. http://dx.doi.org/10.1094/pd-90-0829a.
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Celery (Apium graveolens) is grown extensively in the coastal counties (Ventura, Santa Barbara, San Luis Obispo, Monterey, and Santa Cruz) of California. In 2004 and 2005, field plantings of celery in Ventura and Monterey counties showed symptoms of a petiole and crown rot. Initial symptoms consisted of a light tan discoloration at the crowns and on outer petioles that were in contact with soil. These discolored areas developed a soft, brown, watery rot. Affected petioles wilted and later collapsed. White mycelium and small (0.5 to 3.0 mm in diameter), irregularly shaped, black sclerotia formed on diseased tissues. Isolations from symptomatic petioles, crowns, mycelium, and sclerotia produced colonies of Sclerotinia minor. Eight-week-old celery transplants (cv. Conquistador) grown in a peat-moss based rooting medium in 10-cm2 pots were used to test pathogenicity. Colonized agar plugs (one plug per plant) from eight celery isolates were inserted into slots made in the potting mix adjacent to the crowns and lower petioles of the transplants. Noncolonized plugs were placed in slots for control celery plants. Twenty plants were used for each isolate and control, and all test plants were incubated in a greenhouse at 21 to 23°C. Disease development was rapid, and after 4 days, inoculated celery plants exhibited brown necrosis at inoculation points. After 9 days, celery crowns were decayed and petioles collapsed. S. minor was reisolated from necrotic crown and petiole tissues. Noninoculated plants were asymptomatic. The experiment was repeated and results were similar. To our knowledge, this is the first report of celery as a host of S. minor in California (2). In the United States, S. minor has been reported on celery in Florida (1). Celery in California is only occasionally infected by S. minor and is more often infected by S. sclerotiorum. Reference: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society. St. Paul, MN, 1989. (2) M. S. Melzer et al. Can. J. Plant Pathol. 19:272, 1997.
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Swart, W. J., C. Mathews, and K. B. Saxena. "First Report of Leaf Rust Caused by Uredo cajani on Pigeonpea in South Africa." Plant Disease 84, no. 12 (December 2000): 1344. http://dx.doi.org/10.1094/pdis.2000.84.12.1344b.
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Pigeonpea (Cajanus cajan [L.] Mills.) is an important legume with potential as a dryland crop with multiple uses in the semi-arid areas of South Africa. Approximately 150 tons of dry, split seeds are imported monthly to meet the needs of South Africa. In May 2000, field trials and farmer's plots with plant ages varying from 1 to 3 years old were visited in Mpumalanga and Kwazulu-Natal to assess problems associated with pigeonpea cultivation. Rust was prevalent on more than 80% of plants on young and old leaves at all sites but was most severe at sites in Mpumalanga, where severe rust was observed on all 17 ICRISAT varieties evaluated. Leaf lesions began as chlorotic flecks that expanded and developed into necrotic spots with several orange red to brown uredinia present mostly on the abaxial sides of leaves. Urediospores were 1-celled and initially hyaline, turning dark orange, minutely echinulate, spherical with 2 to 4 circular germpores and measured 20–27 × 17 to 21μ. No telia were found and all morphological characteristics therefore correspond with the CMI description of Uredo cajani Syd. (1). In Africa, pigeonpea rust has been reported from Kenya, Nigeria, Sierra Leone, Tanzania, and Uganda. In South Africa, rust, described as Uromyces dolicholi Arthur (2), has only once been reported on pigeonpea. In the United States, U. dolicholi has also once been reported on pigeonpea (3). However, since U. dolicholi, unlike U. cajani, produces telia and occurs only on Rhyncosia spp. (4), these reports can be considered incorrect. This is therefore the first report of U. cajani on pigeonpea in South Africa. References: (1) K. H. Anahosur and J. M. Waller. 1978. No. 590: Descriptions of Plant Pathogenic Fungi and Bacteria. Commonw. Mycol. Inst., Kew, England. (2) E. M. Doidge. Bothalia 5:1-1094, 1950. (3) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN, 1989. (4) A. Sivanesan. 1970. No. 269: Descriptions of Plant Pathogenic Fungi and Bacteria. Commonw. Mycol. Inst., Kew, England.
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Garibaldi, A., A. Minuto, and M. L. Gullino. "First Report of Sclerotinia sclerotiorum on Campanula carpatica and Schizanthus × wisetonensis in Italy." Plant Disease 86, no. 1 (January 2002): 71. http://dx.doi.org/10.1094/pdis.2002.86.1.71a.
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The production of potted ornamental plants is very important in the Albenga Region of northern Italy, where plants are grown for export to central and northern Europe. During fall 2000 and spring 2001, sudden wilt of tussock bellflower (Campanula carpatica Jacq.) and butterfly flower (Schizanthus × wisetonensis Hort.) was observed on potted plants in a commercial greenhouse. Initial symptoms included stem necrosis at the soil line and yellowing and tan discoloration of the lower leaves. As stem necrosis progressed, infected plants growing in a peat, bark compost, and clay mixture (70-20-10) wilted and died. Necrotic tissues were covered with whitish mycelia that produced dark, spherical (2 to 6 mm diameter) sclerotia. Sclerotinia sclerotiorum was consistently recovered from symptomatic stem pieces of both plants disinfested for 1 min in 1% NaOCl and plated on potato dextrose agar amended with streptomycin sulphate at 100 ppm. Pathogenicity of three isolates obtained from each crop was confirmed by inoculating 45- to 60-day-old C. carpatica and Schizanthus × wisetonensis plants grown in containers (14 cm diameter). Inoculum that consisted of wheat kernels infested with mycelia and sclerotia of each isolate was placed on the soil surface around the base of previously artificially wounded or nonwounded plants. Noninoculated plants served as controls. All plants were maintained outdoors where temperatures ranged between 8 and 15°C. Inoculated plants developed symptoms of leaf yellowing, followed by wilt, within 7 to 10 days, while control plants remained symptomless. White mycelia and sclerotia developed on infected tissues and S. sclerotiorum was reisolated from inoculated plants. To our knowledge, this is the first report of stem blight of C. carpatica and Schizanthus × wisetonensis caused by S. sclerotiorum in Italy. The disease was previously observed on C. carpatica in Great Britain (2) and on Schizanthus sp. in the United States (1). References: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (2) J. Rees. Welsh J. Agric. 1:188, 1925.
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Garibaldi, A., A. Minuto, D. Bertetti, and M. L. Gullino. "First Report of the Presence of Albugo tragopogonis on Cineraria maritima in Italy." Plant Disease 87, no. 4 (April 2003): 450. http://dx.doi.org/10.1094/pdis.2003.87.4.450b.
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Cineraria maritima L. (synonym Senecio cineraria DC.), commonly known as dusty-miller, is grown in Italy for landscape use in parks and gardens. In the spring of 2001, severe outbreaks of a previously unknown disease were observed in commercial farms located in northern Italy. Leaves of infected plants showed several sori on the abaxial surface, progressing to the adaxial surface, and often in the interveinal areas. On the adaxial surface of leaves, chlorotic areas developed and eventually turned brown. Severely infected leaves wilted, but remained attached to the stem. Signs of the fungus were present as whitish and catenulate sporangia emerging from the sori. Sporangia, organized in chains, had an average diameter of 20.5 × 26.5 μm. On the basis of the microscopic observations, the causal agent of the disease was identified as Albugo tragopogonis. Pathogenicity was confirmed by inoculating leaves of healthy C. maritima plants with a sporangial suspension (5 × 102 sporangia per ml) obtained from infected plants. Noninoculated plants served as a control. Plants were kept covered with plastic bags for 72 h and maintained at 15°C. After 10 days, typical symptoms of white rust developed on inoculated plants starting from the basal leaves. Within 30 days, affected leaves were completely wilted. Microscopic examination of sporangia within sori verified the pathogen to be A. tragopogonis. No symptoms developed on the control plants. A. tragopogonis has been reported as the causal agent of white rust on several species belonging to the genus Senecio in the United States (1). In New Zealand, the presence of A. tragopogonis was reported on the genus Cineraria in 1959 (2). To our knowledge, this is the first report of the presence of white rust on Cineraria maritima in Italy. References: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St Paul, MN, 1989. (2) J. M. Dingley. N. Z. J. Agric. Res. 2:380, 1959.
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Garibaldi, A., A. Minuto, and M. L. Gullino. "First Report of White Mold Caused by Sclerotinia sclerotiorum on Persian Buttercup (Ranunculus asiaticus) in Italy." Plant Disease 87, no. 9 (September 2003): 1151. http://dx.doi.org/10.1094/pdis.2003.87.9.1151a.
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Persian buttercup (Ranunculus asiaticus L.) is grown in the Albenga Region of northern Italy for cut flower production and exportation to central and northern Europe. During the winter of 2003, sudden wilt was observed in commercial plantings of R. asiaticus. Initial symptoms included stem necrosis at the soil level and yellowing and tan discoloration of leaves. As stem necrosis progressed, infected plants wilted and died. Wilt occurred within a few days on young plants and was characterized by the presence of soft and watery tissues. Necrotic tissues became covered with whitish mycelium that produced dark, spherical sclerotia (1 to 4 mm in diameter). Sclerotinia sclerotiorum (Lib.) de Bary (1) was consistently recovered from infected stem pieces of R. asiaticus that were disinfested for 1 min in 1% NaOCl and plated on potato dextrose agar (PDA) amended with 100 ppm of streptomycin sulfate. Pathogenicity of three isolates obtained from infected plants of persian buttercup was confirmed by inoculating 30-day-old plants grown in containers. Inoculum that consisted of wheat kernels infested with mycelium and sclerotia of each isolate was placed on the soil surface around the base of each of five plants. Noninoculated plants served as controls. The inoculation trial was repeated once. All plants were kept at temperatures ranging between 8 and 22°C and watered as needed. Inoculated plants developed symptoms of leaf yellowing followed by wilt within 15 days, while control plants remained symptomless. White mycelium and sclerotia developed on infected tissues, and S. sclerotiorum was reisolated from inoculated plants. S. sclerotiorum has been previously reported on R. asiaticus in the United States (2) and Japan (3). To our knowledge, this is the first report of wilt of R. asiaticus caused by S. sclerotiorum in Italy and Europe. References: (1) N. F. Buchwald. Den. Kgl. Veterin.er-og Landbohojskoles Aarsskrift, 1949. (2) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (3) T. Urushibara et al. Annu. Rep. Kanto-Tosan Plant Prot. Serv. 46:61, 1999.
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Oliver, C. L., R. Cai, B. A. Vinatzer, E. A. Bush, and M. A. Hansen. "First Report of Bacterial Spot of Peony Caused by a Xanthomonas sp. in the United States." Plant Disease 96, no. 4 (April 2012): 581. http://dx.doi.org/10.1094/pdis-11-11-0919.
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In early May 2008 and 2009, peony samples (Paeonia spp.) with symptoms of leaf spot and blight were submitted to the Virginia Tech Plant Disease Clinic. The 2008 peony was an unknown cultivar from a northern Virginia landscape. The three cultivars (Dr. Alexander Fleming, Felix Crousse, and Karl Rosenfield) submitted in 2009 were from a commercial nursery in southwestern Virginia that was reporting leaf spot progressing to severe blight, which rendered plants unsalable, on 75% of a 1,219 m2 block during a 10-day period of heavy rainfall. Bacterial streaming from spots was observed. On the basis of phenotypic and biochemical tests, the isolates were determined to be xanthomonads. Two isolates (one recovered from the 2008 sample and one from the 2009 sample) were used in the following work. Isolates were characterized by multilocus sequencing (MLST) (4). PCR reactions were prepared and cycled using 2X ImmoMix (Bioline, Tauton, MA) according to manufacturer's recommendations with an annealing temperature of 58°C. Template DNA was added by touching a single colony with a 20-μl pipette tip and placing the tip into the reaction mix for 1 min. Four bands of the expected size were visualized on an electrophoresis gel and cleaned products were sequenced in forward and reverse directions at the University of Chicago, Cancer Research Center DNA Sequencing Facility. Corresponding gene fragments of each isolate were identical. A consensus sequence (PAMDB Isolate ID No. 936) for each of the four gene fragments was constructed and compared with sequences in NCBI ( http://www.ncbi.nlm.nih.gov/nuccore/ ) and PAMDB ( http://genome.ppws.vt.edu/cgi-bin/MLST/home.pl ) (1) databases using Blastn (2). No perfect match was found. Genetic distances between the peony isolates and all strains in PAMDB were determined by MegAlign (Lasergene; DNAStar, Madison, WI). The Xanthomonas strain most similar to the isolates recovered from the peony samples was Xanthomonas hortorum pv. hederae ICMP 1661 with a genetic distance of 0.023; this strongly suggests that the peony isolates belong to X. hortorum. For Koch's postulates, six surface-disinfested young leaflets from Paeonia lactiflora ‘Karl Rosenfield’ were inoculated by forcefully spraying a phosphate-buffered saline suspension of each bacterial isolate (~4.3 × 109 CFU/ml) into the underside of the leaf until leaf tissue appeared water soaked. Controls were inoculated similarly with phosphate-buffered saline solution. Moist chambers with inoculated leaves were incubated at ambient temperature under two 48W fluorescent grow lights with 12 h of light and dark. Circular spots were observed on leaves inoculated with the 2009 and 2008 isolates in 18 and 20 days, respectively. No symptoms were observed on controls. Bacterial streaming from leaf spots was observed by phase-contrast microscopy; bacteria were isolated and confirmed to be identical to the original isolates by the methods described above. To our knowledge, this is the first report of a Xanthomonas sp. causing leaf spot and blight on peony. Although bacterial blight of peony has been attributed to a xanthomonad in recent years, the pathogen had not been further characterized (3). References: (1) N. F. Almeida et al. Phytopathology 100:208, 2010. (2) D. J. Altschul et al. J. Mol. Biol. 215:403, 1990. (3) M. L. Gleason et al. Diseases of Herbaceous Perennials. The American Phytopathological Society, St. Paul, MN. 2009. (4) J. M. Young et al. Syst. Appl. Microbiol. 31:366, 2008.
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Kropf, S. M., M. L. Putnam, M. Serdani, M. C. Twomey, J. L. Woods, and D. H. Gent. "Sclerotinia Wilt of Hop (Humulus lupulus) Caused by Sclerotinia sclerotiorum in the Pacific Northwest United States." Plant Disease 96, no. 4 (April 2012): 583. http://dx.doi.org/10.1094/pdis-12-11-1039.
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In June 2009, wilted hop bines were observed in a yard in Marion County, OR. The wilt was associated with a stem rot that occurred ~1 m from the ground near the point where bines are tied together for horticultural purposes. Samples of affected stems were submitted to the Oregon State University Plant Clinic. White hyphae and large, black sclerotia were present on the stems, with a clear delineation between healthy and diseased tissue. The pathogen was identified as Sclerotinia sclerotiorum based on morphological characters. In June 2011, bine wilting was observed on the same farm but in a different hop yard (cv. Nugget) ~10 km from the 2009 occurrence. Affected plants had upward curled leaves with necrotic margins or wilted bines that were severed at the soil line. Wilted bines tended to have smaller diameters than bines with foliar symptoms only. Of 100 plants examined, 75% displayed some foliar symptoms and 66% had at least one bine that was wilted. Yield loss was estimated at 10 to 20% due to bine wilting before cone development. Unlike the 2009 occurrence, wilted bines did not display aerial signs of S. sclerotiorum. Rather, water-soaked lesions covered in white, cottony mycelium were apparent on affected stems 2.5 to 5 cm below the soil surface, some bearing large, irregularly shaped sclerotia. Isolations made onto potato dextrose agar yielded isolates with rapid growth rates and morphological characters consistent with S. sclerotiorum (1). DNA was extracted (2) and pathogen identity was confirmed by PCR amplification and sequencing of the internal transcribed spacer regions from isolates SS001 and SS002 as described before (4). The amplicons were sequenced bidirectionally and consensus sequences were 100% similar to S. sclerotiorum (GenBank No. AAGT01000678.1). Two nucleotide polymorphisms were present that differentiated the sequences from those of 12 S. trifoliorum accessions in GenBank that could be aligned (2). Greenhouse assays utilizing a toothpick inoculation procedure (3) were conducted to fulfill Koch's postulates. Stems of five 4-week-old hop plants of cv. Agate were pierced with a toothpick colonized with S. sclerotiorum. Five control plants were similarly inoculated with toothpicks without the fungus. Inoculated plants developed symptoms similar to those observed in the field within 11 days; four of five plants inoculated with isolate SS001 and two of five plants inoculated with isolate SS002 completely wilted. S. sclerotiorum was reisolated from all inoculated plants but not the control plants. To our knowledge, this is the first report of Sclerotinia wilt on hop in Oregon or the Pacific Northwest (1), where nearly all commercial hop production occurs in the United States. The disease appears to be localized to a limited number of yards, although given the widespread distribution and host range of S. sclerotiorum, it is plausible that the disease may occur in other yards. Recurrent outbreaks and spread of the disease among yards on the affected farm suggests that Sclerotinia wilt has the potential to become a perennial problem on hop and efforts to limit the introduction of S. sclerotiorum into other yards are warranted. References: (1) D. H. Gent. Page 32 in: Compendium of Hop Diseases and Pests. The American Phytopathological Society, St. Paul, MN, 2009. (2) E. N. Njambere et al. Plant Dis. 92:917, 2008. (3) M. L. Putnam. Plant Pathol. 53:252, 2004. (4) T. J. White et al. PCR Protocols: A Guide to Methods and Applications. Academic Press, San Diego, 1990.
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Díaz Arias, M. M., G. P. Munkvold, and L. F. Leandro. "First Report of Fusarium proliferatum Causing Root Rot on Soybean (Glycine max) in the United States." Plant Disease 95, no. 10 (October 2011): 1316. http://dx.doi.org/10.1094/pdis-04-11-0346.
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Fusarium spp. are widespread soilborne pathogens that cause important soybean diseases such as damping-off, root rot, Fusarium wilt, and sudden death syndrome. At least 12 species of Fusarium, including F. proliferatum, have been associated with soybean roots, but their relative aggressiveness as root rot pathogens is not known and pathogenicity has not been established for all reported species (2). In collaboration with 12 Iowa State University extension specialists, soybean roots were arbitrarily sampled from three fields in each of 98 Iowa counties from 2007 to 2009. Ten plants were collected from each field at V2-V3 and R3-R4 growth stages (2). Typical symptoms of Fusarium root rot (2) were observed. Symptomatic and asymptomatic root pieces were superficially sterilized in 0.5% NaOCl for 2 min, rinsed three times in sterile distilled water, and placed onto a Fusarium selective medium. Fusarium colonies were transferred to carnation leaf agar (CLA) and potato dextrose agar and later identified to species based on cultural and morphological characteristics. Of 1,230 Fusarium isolates identified, 50 were recognized as F. proliferatum based on morphological characteristics (3). F. proliferatum isolates produced abundant, aerial, white mycelium and a violet-to-dark purple pigmentation characteristic of Fusarium section Liseola. On CLA, microconidia were abundant, single celled, oval, and in chains on monophialides and polyphialides (3). Species identity was confirmed for two isolates by sequencing of the elongation factor (EF1-α) gene using the ef1 and ef2 primers (1). Identities of the resulting sequences (~680 bp) were confirmed by BLAST analysis and the FUSARIUM-ID database. Analysis resulted in a 99% match for five accessions of F. proliferatum (e.g., FD01389 and FD01858). To complete Koch's postulates, four F. proliferatum isolates were tested for pathogenicity on soybean in a greenhouse. Soybean seeds of cv. AG2306 were planted in cones (150 ml) in autoclaved soil infested with each isolate; Fusarium inoculum was applied by mixing an infested cornmeal/sand mix with soil prior to planting (4). Noninoculated control plants were grown in autoclaved soil amended with a sterile cornmeal/sand mix. Soil temperature was maintained at 18 ± 1°C by placing cones in water baths. The experiment was a completely randomized design with five replicates (single plant in a cone) per isolate and was repeated three times. Root rot severity (visually scored on a percentage scale), shoot dry weight, and root dry weight were assessed at the V3 soybean growth stage. All F. proliferatum isolates tested were pathogenic. Plants inoculated with these isolates were significantly different from the control plants in root rot severity (P = 0.001) and shoot (P = 0.023) and root (P = 0.013) dry weight. Infected plants showed dark brown lesions in the root system as well as decay of the entire taproot. F. proliferatum was reisolated from symptomatic root tissue of infected plants but not from similar tissues of control plants. To our knowledge, this is the first report of F. proliferatum causing root rot on soybean in the United States. References: (1) D. M. Geiser et al. Eur. J. Plant Pathol. 110:473, 2004. (2) G. L. Hartman et al. Compendium of Soybean Diseases. 4th ed. The American Phytopathologic Society, St. Paul, MN, 1999. (3) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual. Blackwell Publishing, Oxford, UK, 2006. (4) G. P. Munkvold and J. K. O'Mara. Plant Dis. 86:143, 2002.
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Neumann Brebaum, S., and G. J. Boland. "First Report of Phoma herbarum and Phoma exigua as Pathogens of Dandelion in Southern Ontario." Plant Disease 83, no. 2 (February 1999): 200. http://dx.doi.org/10.1094/pdis.1999.83.2.200c.
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Diseases of dandelion (Taraxacum officinale) were surveyed in southern Ontario from 1993 to 1997 to identify promising pathogens for biological weed control. Two new pathogens of dandelion, Phoma herbarum Westend. and Phoma exigua Desm., were recovered and characterized from small necrotic lesions on dandelion foliage. Both Phoma spp. were frequently isolated from multiple locations and during various years of the survey, indicating that they were endemic and widespread on T. officinale in southern Ontario. Pathogenicity was assessed by inoculating detached leaves or seedlings with colonized agar disks (6 mm in diameter) or spore suspensions (1 × 106 conidia per ml). Inoculated leaves and seedlings were incubated at 22°C and 48 h of continuous leaf wetness. Lesion diameters were measured 3 days post-inoculation. Isolates that gave rise to necrotic lesions were reisolated from leaves and grown in pure culture. Their growth characteristics were compared with those of the initial isolate. Spores were ellipsoid, hyaline, and 5 × 2 μm for both species. Identification of representative isolates of both species was confirmed by the Centraalbureau voor Schimmelcultures, Oosterstraat 1, 3742 SK Baarn, The Netherlands. This is the first report of these two species as pathogens of dandelion in North America (1,2). References: (1) I. L. Conners 1967. An Annotated Index of Plant Diseases in Canada. Research Branch, Canada Dept. Agric. Pub.1251. (2) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN.
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Koike, S. T., and G. S. Saenz. "First Report of Powdery Mildew, Caused by an Oidium sp., on Poinsettia in California." Plant Disease 82, no. 1 (January 1998): 128. http://dx.doi.org/10.1094/pdis.1998.82.1.128a.
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In December 1996 and January 1997, powdery mildew was observed on potted poinsettia (Euphorbia pulcherrima Willd. ex Klotzsch) plants in Monterey County, CA. Mycelia were observed on stems, petioles, mature and immature leaves, and bracts. Severely diseased leaves became twisted and bent and senesced prematurely. The white mycelia were conspicuous, epiphytic, and amphigenous; hyphae measured 4.6 to 6.9 μm in diameter. Growth initially was in patches but eventually became effused. Appressoria were slightly lobed to lobed and sometimes opposite. Conidiophore foot cells were cylindrical, sometimes bent at the base, and slightly flexuous to flexuous. Foot cells measured 30.0 to 46.2 μm × 5.8 to 6.9 μm and were followed by one to two shorter cells. Conidia were cylindrical to slightly doliform and measured 25.4 to 32.3 μm × 11.6 to 18.5 μm. The length-to-width ratios of conidia generally were greater than 2.0. Conidia were produced singly, placing the fungus in the Pseudoidium-type powdery mildew group. Conidia germinated at the ends, and no fibrosin bodies were observed. Cleistothecia were not found. The fungus was identified as an Oidium species. Pathogenicity was demonstrated by gently pressing infected leaves having abundant sporulation onto leaves of potted poinsettia plants (cvs. Freedom Red, Peter Star Marble, and Nutcracker White), incubating the plants in a moist chamber for 48 h, and then maintaining plants in a greenhouse. After 12 to 14 days, powdery mildew colonies developed on the inoculated plants, and the pathogen was morphologically identical to the original isolates. Uninoculated control plants did not develop powdery mildew. This is the first report of powdery mildew on poinsettia in California. This fungus appears similar to Microsphaera euphorbiae but has longer, slightly flexuous foot cells that do not match the description for M. euphorbiae (1,2). An alternative identification would be Erysiphe euphorbiae; however, there are no available mitosporic descriptions for morphological comparisons (1,2). In the United States, powdery mildew of poinsettia previously has been reported in various states in the Pacific Northwest, Midwest, and Northeast. References: (1) U. Braun. Beih. Nova Hedwigia 89:1, 1987. (2) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN.
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Garibaldi, A., D. Bertetti, and M. L. Gullino. "First Report of Leaf Blight on Hosta fortunei Caused by Rhizoctonia solani AG 4 in Italy." Plant Disease 93, no. 4 (April 2009): 432. http://dx.doi.org/10.1094/pdis-93-4-0432c.
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Hosta fortunei (Liliaceae) is used in semishaded areas of gardens for its lavender-colored flowers produced in midsummer. In April of 2008, in a greenhouse at the University of Torino, located in Grugliasco (northern Italy), a leaf blight was observed on 15% of potted 60-day-old plants growing at temperatures ranging between 20 and 25°C and relative humidity of 60 to 90%. Semicircular, water-soaked lesions developed on leaves just above the soil line at the leaf-petiole junction and later along leaf margins. Lesions expanded for several days along the midvein until the entire leaf was destroyed. Blighted leaves turned brown, withered, and clung to the shoots. Severely infected plants died. Diseased tissue was disinfested for 10 s in 1% NaOCl, rinsed with sterile water, and plated on potato dextrose agar (PDA) amended with 25 mg/liter streptomycin sulfate. A fungus with the morphological characters of Rhizoctonia solani (4) was consistently recovered, then transferred and maintained in pure culture. Ten-day-old mycelium grown on PDA at 22 ± 1°C appeared light brown, rather compact, and had radial growth. Sclerotia were not present. Isolates of R. solani obtained from affected plants were successfully anastomosed with tester isolate AG 4 (AG 4 RT 31 obtained from tobacco plants). Results were consistent with other reports on anastomosis reactions (2). Pairings were also made with tester isolates of AG 1, 2.1, 2.2, 3, 6, 7, 11, and BI, but no anastomosis was observed. The internal transcribed spacer (ITS) region of rDNA was amplified using primers ITS4/ITS6 and sequenced. BLASTn analysis (1) of the 646-bp fragment showed a 100% homology with the sequence of R. solani AG-4 AB000018. The nucleotide sequence has been assigned GenBank Accession No. FJ 534556. For pathogenicity tests, the inoculum of R. solani was prepared by growing the pathogen on PDA for 10 days. Six-month-old plants of H. fortunei were grown in 1-liter pots. Inoculum, which consisted of an aqueous suspension of PDA and mycelium disks (10 g of mycelium per pot), was placed at the collar of plants. Plants inoculated with water and PDA fragments alone served as control treatments. Five plants per treatment were used. Plants were maintained in a growth chamber at 20 ± 1°C. The first symptoms, similar to those observed in the nursery, developed 15 days after inoculation. R. solani was consistently reisolated from infected leaves and stems. Control plants remained healthy. The pathogenicity test was carried out twice with similar results. R. solani was reported on plants belonging to the genus Hosta in the United States (3). This is, to our knowledge, the first report of leaf blight of H. fortunei caused by R. solani in Italy as well as in Europe. References: (1) S. F. Altschul et al. Nucleic Acids Res. 25:3389, 1997. (2) D. E. Carling. Grouping in Rhizoctonia solani by hyphal anastomosis reactions. In: Rhizoctonia Species: Taxonomy, Molecular Biology, Ecology, Pathology and Disease Control. Kluwer Academic Publishers, The Netherlands, 1996. (3) D. F. Farr et al. Fungi on Plants and Products in the United States. The American Phytopathology Society, St Paul, MN, 1989. (4) B. Sneh et al. Identification of Rhizoctonia species. The American Phytopathological Society, St Paul, MN, 1991.
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Cating, R. A., A. J. Palmateer, R. T. McMillan, and E. R. Dickstein. "First Report of a Bacterial Soft Rot on Tolumnia Orchids Caused by a Dickeya sp. in the United States." Plant Disease 93, no. 12 (December 2009): 1354. http://dx.doi.org/10.1094/pdis-93-12-1354b.
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Tolumnia orchids are small epiphytic orchids grown for their attractive flowers. In the fall of 2008, approximately 100 Tolumnia orchids with soft, brown, macerated leaves were brought to the University of Florida Extension Plant Diagnostic Clinic in Homestead. Ten plants were randomly selected and bacteria were isolated from the margins of symptomatic tissues of each of the 10 plants on nutrient agar according to the method described by Schaad et al. (2). Four reference strains were used in all tests, including the molecular tests: Erwinia carotovora subsp. carotovora (obtained from J. Bartz, Department of Plant Pathology, University of Florida, Gainesville), E. chrysanthemi (ATCC No. 11662), Pectobacterium cypripedii (ATCC No. 29267), and Acidovorax avenae subsp. cattleyae (ATCC No. 10200). All 10 of the isolated bacteria were gram negative, grew at 37°C, degraded pectate in CVP (crystal violet pectate) medium, grew anaerobically, produced brown pigment on NGM (nutrient agar-glycerol-manganese chloride) medium (1), were sensitive to erythromycin, and produced phosphatase. Three of the strains were submitted for MIDI analysis (Sherlock version TSBA 4.10; Microbial Identification, Newark DE) (SIM 0.732 to 0.963), which identified them as E. chrysanthemi. A PCR assay was performed on the 16S rRNA gene with primers 27f and 1495r described by Weisburg et al. (3) from two of the isolates and a subsequent GenBank search showed 99% identity of the 1,508-bp sequence to that of Dickeya chrysanthemi (Accession No. FM946179) (formerly E. chrysanthemi). The sequences were deposited in GenBank (Accession Nos. GQ293897 and GQ293898). Pathogenicity was confirmed by injecting approximately 100 μl of a bacterial suspension at 1 × 108 CFU/ml into leaves of 10 Tolumnia orchid mericlones. Ten plants were also inoculated with water as controls. Plants were placed in a greenhouse at 29°C with 60 to 80% relative humidity. Within 24 h, soft rot symptoms appeared on all inoculated leaves. The water controls appeared normal. A Dickeya sp. was reisolated and identified using the above methods (biochemical tests and MIDI), fulfilling Koch's postulates. To our knowledge, this is the first report of a soft rot caused by a Dickeya sp. on Tolumnia orchids. Although 16S similarity and MIDI results suggest the isolated bacteria are D. chrysanthemi because of its close similarity with other Dickeya spp., these results are not conclusive. Further work should be conducted to confirm the identity of these isolates. Through correspondence with South Florida Tolumnia growers, it appears this disease has been a recurring problem, sometimes affecting international orchid shipments where plant losses have been in excess of 70%. References: (1) Y. A. Lee and C. P. Yu. J. Microbiol. Methods 64:200, 2006. (2) N. W. Schaad et al. Erwinia soft rot group. Page 56 in: Laboratory Guide for Identification of Plant Pathogenic Bacteria. 3rd ed. N. W. Schaad et al., eds. American Phytopathological Society. St. Paul, MN, 2001. (3) W. G. Weisburg et al. J. Bacteriol. 173:697, 1991.
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Schwingle, B. W., J. A. Smith, R. A. Blanchette, S. Gould, B. L. Blanchette, J. Pokorny, and S. D. Cohen. "First Report of Dieback and Leaf Lesions on Rhododendron sp. Caused by Phytophthora hedraiandra in the United States." Plant Disease 90, no. 1 (January 2006): 109. http://dx.doi.org/10.1094/pd-90-0109a.
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Surveys for Phytophthora ramorum in Minnesota nurseries revealed the presence of P. hedraiandra de Cock & Man in't Veld and several other Phytophthora species but not P. ramorum. Symptomatic leaf and stem tissues from diseased Rhododendron and Quercus species were cultured on PARP, a selective growth medium for Phytophthora (3). The Phytophthora isolates obtained were later identified by sequencing the internal transcribed spacer (ITS) region of the rDNA and comparing the sequences with those in GenBank using BLAST searches (1). The ITS sequences of six cultures (GenBank Accession Nos. DQ139804-DQ139809), isolated during 2003 from various Rhododendron cultivars exhibiting leaf lesions and shoot dieback, showed 100% identity with the ITS sequence of P. hedraiandra (GenBank Accession No. AY707987) (2). This is a recently described pathogenic species from the Netherlands responsible for causing leaf spots on Viburnum spp. Since the ITS sequence of P. hedraiandra differs little from that of P. cactorum (2), we verified one isolate to be P. hedraiandra by sequencing the mitochondrial cytochrome c oxidase subunit I gene (cox1) (GenBank Accession No. DQ139810). Comparison of this sequence with the P. hedraiandra voucher specimen in GenBank (Accession No. AY769115) showed 99% identity, which was the closest match. Reproductive structures were measured on V8 juice agar. The average oogonium diameter for three isolates was 29 μm with a range of 26 to 32 μm, while the average antheridium length was 13 μm (11 to 15 μm). Sporangium length and width averages on crushed hemp seeds were 32 μm (28 to 36 μm) and 26 μm (21 to 30 μm), respectively, with the average length to width ratio of 1.25 (1.23 to 1.29). Pathogenicity tests on Rhododendron cv. Mikkeli were carried out using three of our P. hedraiandra isolates. Spore suspensions of 2 × 104 zoospores per ml were used to mist-spray shoots of five, 3-year-old plants for each isolate. Five controls were mist sprayed with water. After inoculation, plants were placed in plastic bags in a dark growth chamber (22°C) for 7 days and then moved to a greenhouse. Leaf blotches and shoot dieback were apparent 5 days after inoculation, and P. hedraiandra was reisolated from those symptomatic tissues and identified by an exact match of the ITS sequence. Necrotic areas lengthened from the shoot tips to the main stems of the plants while expanding into petioles and leaves. No symptoms were observed on control plants. To our knowledge, this is the first report of P. hedraiandra in the United States as well as the first report of Koch's postulates performed with P. hedraiandra on Rhododendron cv. Mikkeli. The significance of this disease to other woody plants in nurseries or the landscape is unknown, and further study is needed to determine the host range and extent of the disease that may occur from this introduction. References: (1) S. F. Altschul et al. J. Mol. Biol. 215:403, 1990. (2) A. W. A.M de Cock and C. A. Lévesque. Stud Mycol 50:481, 2004. (3) D. C. Erwin and O. K. Ribeiro. Phytophthora Diseases Worldwide. The American Phytopathological Society, St. Paul, MN, 1996.
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Park, J. H., and J. Juzwik. "Fusarium Canker of Bitternut Hickory Caused by Fusarium solani in the North-Central and Northeastern United States." Plant Disease 96, no. 3 (March 2012): 455. http://dx.doi.org/10.1094/pdis-09-11-0766.
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Multiple annual cankers were observed on the upper main stems of bitternut hickory (Carya cordiformis) exhibiting top dieback in Indiana, Iowa, Minnesota, New York, Ohio, and Wisconsin during a 2006 to 2008 survey of declining hickory. The top-killed trees had normal-sized, green leaves below and the cankers were oval, sunken, and bounded by heavy callus that seemed to arrest further canker expansion. Fusarium solani was consistently isolated from the margins of inner bark lesions or discolored sapwood of the cankers. When cultured on potato dextrose agar, the isolates grew rapidly with abundant aerial mycelium. On carnation leaf agar, thick-walled macroconidia with 4 to 5 septa were produced in cream, blue-green, or blue sporodochia. Macroconidia were generally cylindrical with a blunt or rounded apical cell and a rounded or foot-shaped basal cell. Microconidia were oval to kidney shaped with 0 to 1 septa and were produced in false heads on elongate monophialides. Chlamydospores were formed singly or in pairs. These morphological characteristics are consistent with descriptions of F. solani (2). The identities of 42 representative isolates were confirmed by sequencing the translation elongation factor (tef) 1-α gene. BLAST analysis of the sequences from each isolate against the GenBank and FUSARIUM-ID database found 98 to 100% similarities to F. solani isolates (GenBank Accession Nos. DQ246841, DQ247025, DQ247282, and DQ247436 and FUSARIUM-ID isolate FD01041). Two haplotypes (BB and BC) were distinguished based on the tef 1-α gene sequences that differed by 10 bp. Pathogenicity tests were conducted with two isolates of each haplotype on asymptomatic C. cordiformis (12 to 21 cm in diameter) in forest stands. In May 2009 in Wabasha County, MN, 0.1-ml spore suspensions (1 × 104 macroconidia/ml) or sterile water was placed in one of three holes (0.6 cm in diameter) drilled to the cambium of 12 trees. The holes were sealed with moist cotton and moldable putty. A duplicate trial, but with BB and BC isolates from Wisconsin, was initiated in Chippewa County, WI in June 2009. The extent of inner bark necrosis was assessed 13 months after inoculation in both sites. Inoculations with F. solani in Minnesota resulted in inner bark lesions with average lengths of 20 and 30 mm for the BB and BC haplotypes, respectively. In Wisconsin, BB and BC haplotypes caused inner bark lesions with average lengths of 34 and 38 mm, respectively. While sunken or open cankers were found for all the BC isolate inoculations, relatively small and callus-bounded cankers were found for BB isolate inoculations. All control wounds were callus-closed with average wound lengths of 12 and 23 mm in Minnesota and Wisconsin, respectively. The same haplotype of F. solani used for inoculation was recovered from each canker as confirmed by analysis of tef 1-α gene sequences. F. solani was not obtained from control wounds. To our knowledge, this is the first report of a canker caused by F. solani on bitternut hickory (1). The same fungus has been previously reported to cause cankers on stems of other hardwood tree genera in the eastern United States and Canada. We hypothesize that numerous main-stem cankers caused by F. solani lead to top dieback of bitternut hickory. References: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (2) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual. Blackwell Publishing, Ames, IA, 2006.
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Jossey, S., and M. Babadoost. "First Report of Tobacco ringspot virus in Pumpkin (Cucurbita pepo) in Illinois." Plant Disease 90, no. 10 (October 2006): 1361. http://dx.doi.org/10.1094/pd-90-1361b.
Full textAbstract:
During a survey of commercial pumpkin and squash fields for viruses, conducted in Illinois in 2005, Tobacco ringspot virus (TRSV) was identified for the first time in symptomatic pumpkin samples collected during August and September from Douglas, Kankakee, Piatt, and Tazewell counties in one of three, one of three, one of one, and one of seven samples tested, respectively. In an earlier study from southern Illinois, the only viruses detected in pumpkins were Cucumber mosaic virus, Papaya ringspot virus, Squash mosaic virus, Watermelon mosaic virus, and Zucchini yellow mosaic virus (2). TRSV has been reported in cucurbits from some states in the United States (1). We detected TRSV in symptomatic leaves exhibiting mild mosaic with leaf yellowing using a double-antibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA) kit (Agdia, Inc., Elkhart, IN). Samples were considered positive if the absorbance readings at 405 nm exceeded 3× the absorbance of the negative control. The presence of TRSV was confirmed by reverse transcription-polymerase chain reactions (RT-PCR). Total RNA was extracted from the symptomatic plants using TRIzol Reagent and reverse transcribed by M-MLV Reverse Transcriptase (Invitrogen, Carlsbad, CA). PCR was conducted using forward primer 5′-CTTGCGGCCCAAATCT ATAA-3′ and reverse primer 5′-ACTTGTGCCCAGGAGAGCTA-3′, which anneal to the conserved region in the coat protein gene. The reaction produced an amplification product of the expected size (348 bp). Hence, utilizing ELISA and RT-PCR tests, the presence of TRSV in pumpkin was determined, to our knowledge, for the first time in Illinois. References: (1) R. Provvidenti. Tobacco ringspot. Page 42 in: Compendium of Cucurbit Diseases. T. A. Zitter et al., eds. The American Phytopathological Society, St. Paul, MN. 1996. (2) S. A. Walters et al. HortScience 38:65, 2003.
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Rodriguez-Salamanca, L. M., T. B. Enzenbacher, M. L. Derie, L. J. du Toit, C. Feng, J. C. Correll, and M. K. Hausbeck. "First Report of Colletotrichum coccodes Causing Leaf and Neck Anthracnose on Onions (Allium cepa) in Michigan and the United States." Plant Disease 96, no. 5 (May 2012): 769. http://dx.doi.org/10.1094/pdis-01-12-0022-pdn.
Full textAbstract:
In July of 2010, dry, oval lesions, each with a salmon-colored center and bleached overall appearance, were observed on the leaves and neck of onions plants growing in production fields of Newaygo, Ottawa, Kent, and Ionia counties, Michigan. Acervuli and setae that are characteristic of Colletotrichum spp. were observed with a dissecting microscope, and elliptical conidia (8 to 23 × 3 to 12 μm) with attenuated ends were observed with a compound microscope. Symptomatic tissues were excised and cultured onto potato dextrose agar amended with 30 and 100 ppm of rifampicin and ampicillin, respectively. The cultures produced pale salmon-colored sporulation after growing for 5 days at 22 ± 2°C and black microsclerotia after 2 weeks. Six isolates were confirmed as C. coccodes based on sequence analysis of the internal transcribed (ITS) region of the ribosomal DNA and a 1-kb intron of the glutamine synthase gene (GS) (2). Sequences were submitted to GenBank (Accession Nos. JQ682644 and JQ682645 for ITS and GS, respectively). Pathogenicity tests were conducted on two- to three-leaved ‘Stanley’ and ‘Cortland’ onion seedlings. Prior to inoculation, seedlings were enclosed in clear plastic bags overnight to provide high relative humidity. The bags were removed, and seedlings were sprayed inoculated with a C. coccodes conidial suspension (5 × 105 conidia/ml and 25 ml/plant) in sterile double-distilled water. Control seedlings were sprayed with sterile double-distilled water. Tween (0.01%) was added to the conidial suspension and the water. Plants were enclosed in bags for 72 h postinoculation and incubated in growth chambers at 28°C day/23°C night with a 12-h photoperiod. Sunken, oval lesions were observed on the foliage of the onion seedlings inoculated with C. coccodes 4 days postinoculation. Lesions coalesced and foliage collapsed 7 days postinoculation. Control plants remained asymptomatic. When five leaf samples per replication were detached and incubated in a moist chamber for 3 days at 21 ± 2°C, abundant acervuli and setae were observed on the symptomatic tissue but not on control tissue. C. coccodes was consistently recovered from the onion seedling lesions. Six different Colletotrichum spp. have been reported to cause diseases on onions worldwide (1,4). C. circinans, which causes smudge, is an occasional onion pathogen in Michigan, while C. gloeosporioides has only been reported to be infecting onions in Georgia (3). To our knowledge, this is the first report of C. coccodes infecting and causing disease in onions plants. References: (1) D. F. Farr and A. Y. Rossman. Fungal Databases. Systematic Mycology and Microbiology Laboratory, ARS, USDA. Retrieved from http://nt.ars-grin.gov/fungaldatabases/ , August 6, 2010. (2) J. C. Guerber et al. Mycologia 95:872. 2003. (3) C. Nischwitz et al. Plant Dis. 92:974. 2008. (4) H. F. Schwartz, and K. S. Mohan. Compendium of Onion and Garlic Diseases and Pests, 2nd ed. The American Phytopathological Society, St. Paul, MN. 1995.
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Swift, C. E., A. Blessinger, N. Brandt, and N. Tisserat. "First Report of Summer Patch of Kentucky Bluegrass Caused by Magnaporthe poae in Colorado." Plant Disease 91, no. 11 (November 2007): 1519. http://dx.doi.org/10.1094/pdis-91-11-1519a.
Full textAbstract:
The ectotrophic, root-infecting fungus Magnaporthe poae is the cause of summer patch of Kentucky bluegrass (Poa pratensis). The disease is widely distributed in the mid-Atlantic Region of the United States and west to central Nebraska and Kansas (2). It also has been found in certain locations of Washington and California (2) but has not been confirmed in the Rocky Mountain Region. In August 2005 and 2006, tan patches and rings of dead turf ranging from 10 to 30 cm in diameter were observed in Kentucky bluegrass swards in Grand Junction and Greeley, CO, respectively. The sites, separated by approximately 360 km, are located west and east of the Continental Divide. A network of ectotrophic hyphae were observed on diseased root segments collected from both sites. A fungus morphologically similar to M. poae (2) was consistently isolated from these segments. DNA was extracted from mycelium of one isolate from each location and amplified by PCR with the M. poae species-specific primers MP1 and MP2 (1). A 453-bp DNA fragment was consistently amplified from DNA of both isolates, diagnostic of M. poae. To our knowledge, this is the first report of summer patch in Colorado and indicates that M. poae may be widely distributed in the central Rocky Mountain Region. References: (1) T. E. Bunting et al. Phytopathology 86:398, 1996. (2) B. B. Clarke and A. B. Gould, eds. Turfgrass Patch Diseases Caused by Ectotrophic Root-Infecting Fungi. The American Phytopathological Society, St. Paul, MN, 1993.
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Intini, M., M. Gurer, and S. Ozturk. "First Report of Bleeding Canker Caused by Phytophthora cactorum on Horse Chestnut in Turkey." Plant Disease 86, no. 6 (June 2002): 697. http://dx.doi.org/10.1094/pdis.2002.86.6.697c.
Full textAbstract:
Bleeding canker on horse chestnut (Aesculus sp.), caused by Phytophthora cactorum (Lebert and Cohn) Schröeter previously has been reported from the United States and Europe (1). In August 2000, it was found for the first time in a park in Ankara Province, Turkey. Symptoms included sparse yellowish brown foliage with abnormally small leaves, and dark-stained spots or dark brown necrosis of the bark on the trunk and main branches, with or without a reddish black gummy exudate. P. cactorum was isolated from tissues taken from the margins of necrotic bark. Pure cultures were slightly radiate, fluffy but not dense, and had short aerial hyphae when grown on carrot agar, potato dextrose agar, or V8 agar. Sporangia were ovoid, strongly papillate, and averaged 35.6 μm in length and 26.8 μm in width (range: 24 to 55 μm × 19 to 40 μm). The isolates were homothallic with smooth-walled paragynous oogonia ranging from 23.5 to 34.5 μm in diameter. To satisfy Koch's postulates, mycelium of P. cactorum was placed under the bark of six branches of healthy horse chestnut. Noninoculated wounds served as controls. Four months later a reddish black gummy exudate was observed oozing from the inoculated wounds, and the bark tissue was necrotic for 3 to 4 cm around each infection. P. cactorum was successfully reisolated from the necrotic bark tissue. Control wounds remained healthy. To our knowledge, this is the first report of this disease on horse chestnut in Asia Minor. Reference: (1) D. C. Erwin and O. K. Ribeiro. Phytophthora Diseases Worldwide. The American Phytopathological Society, St. Paul, MN, 1996.
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Garibaldi, A., D. Bertetti, M. Scortichini, and M. L. Gullino. "First Report of Bacterial Leaf Spot Caused by Pseudomonas syringae pv. viburnii on Viburnum sargentii in Italy." Plant Disease 89, no. 7 (July 2005): 777. http://dx.doi.org/10.1094/pd-89-0777a.
Full textAbstract:
During the spring of 2003, plants of Viburnum sargentii, a species mostly used in gardens as low-maintenance hedges, showing symptoms unlike those of known diseases were observed in some private gardens in the Biella area (northern Italy). Lesions on leaves were the only symptoms seen. Lesions started as water-soaked, circular areas that in 4 days developed into irregular, shrunken, brown spots from 2 to 4 mm in diameter. The core of older lesions appeared somewhat transparent. Leaves dried up completely 3 weeks after symptoms were first seen. No fungal structures were observed in lesions. Microscopic examination of affected leaf tissues revealed abundant bacterial ooze from the cut margin of lesions. Small fragments of tissue from affected leaves were macerated in nutrient yeast dextrose broth (NYDA) and dilutions of the resulting suspension were streaked onto NYDA and potato dextrose agar (PDA). Isolations were made from at least 25 leaves. Plates were maintained at 22 ± 1°C for 48 h. Slightly yellow colonies typical of Pseudomonas species were consistently isolated on NYDA. No fungi were isolated from the spots on NYDA or PDA. Levan production, oxidase production, pectinolytic activity, arginin dihydrase production, and tobacco hypersensitivity (LOPAT) were tested. Strains were positive for levan and negative for oxidase, arginine dihydrolase, and nitrate reductase. Strains did not rot potato slices but induced a hypersensitive reaction on tobacco leaves. Protein analysis (1) indicated that the bacterium isolated was similar to Pseudomonas syringae pv. viburnii NCPPB 1921. The pathogen was identified as Pseudomonas syringae pv. viburnii (2,3). Pathogenicity of 10 colonies was tested by growing inoculum in nutrient broth shake cultures for 48 h, suspending bacterial cultures in water, diluting to 106 CFU/ml, and spraying five 1-year-old healthy plants of Viburnum sargentii. Five control plants were sprayed with sterile nutrient broth. Inoculated and control plants were kept covered with plastic bags for 72 h. After 7 days in a growth chamber at 20 ± 1°C, leaf spots identical to those observed in the field developed on leaves of inoculated plants. Control plants remained symptomless. The pathogenicity test was repeated once. Strains were isolated from the spots and identified as P. syringae pv. viburnii. To our knowledge, this is the first record of bacterial leaf spot of Viburnum sargentii in Europe. A bacterial spot on Viburnum opulus, V. tomentosum, and V. dentatum was reported in the United States (4). References: (1) D. H. Bergey et al. Bergey's Manual of Determinative Bacteriology. Williams and Wilkins, Baltimore, MD, 1994. (2) J. W. Pscheidt et al. Diseases of Woody Ornamentals and Trees in Nurseries. The American Phytopathological Society, St. Paul, MN, 2001. (3) N. W. Schaad. Laboratory Guide for Identification of Plant Pathogenic Bacteria. The American Phytopathological Society, St Paul, MN, 1998 (4) H. H. Thornberry and H. W. Anderson. Phytopathology 21:907, 1931.