bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Phytoplasma Associated with Ramu Stunt Disease of Sugarcane Is Closely Related to the White Leaf Phytoplasma Group
Authors: Cronjé C. P. R. , Bailey R. A. , Jones P. , Suma S. 
Published: May 2007

Ramu stunt disease of sugarcane (ScRS) was responsible for large yield losses in commercial sugarcane varieties (interspecific hybrids of Saccharum spp.) in the Ramu Valley in northeast Papua New Guinea during the late 1980s. Losses were total in the cultivar Ragnar; Q90 and Yasawa were also affected but Cadmus and Q107 were resistant. Since that time, replanting with resistant cultivars has kept the disease under control. The disease spreads rapidly in susceptible cultivars, where it results in severe stunting of the cane and a yellow mottled striping of the leaves. Although several attempts have been made to detect a viral pathogen, no evidence for viral etiology exists and the causal agent remains unknown. With a nested polymerase chain reaction (PCR) of general phytoplasma primers from the 16S rDNA (1), phytoplasma-specific products were consistently amplified from the leaves of field-grown sugarcane, from sugarcane with ScRS symptoms grown in the glasshouse at IACR-Rothamsted, UK, and from samples of the putative vector collected at Ramu, the delphacid plant hopper Eumetopina flavipes Muir, which had been found to transmit symptoms of Ramu stunt in pot trials (2). Digestion of the amplimers with restriction enzymes RsaI and HaeIII gave profiles that matched those of members of the sugarcane white leaf (SCWL) phytoplasma group. The DNA sequence of the intergenic spacer region of the phytoplasma associated with ScRS showed a 95.98% homology with that of SCWL, suggesting that this newly discovered phytoplasma can provisionally be placed in this group. The 16S-23S intergenic spacer sequence has been submitted to GenBank (accession no. AF 106061). References: (1) C. P. R. Cronjé et al. Ann. Appl. Biol. 133:177, 1998; (2) L. S. Kuniata et al. J. Aust. Entomol. Soc. 33:185, 1994.
First Report of Powdery Mildew, Caused by Erysiphe cichoracearum, on Coneflowers
Authors: Sholberg P. L. , Ginns J. H. , Li T. S. C. 
Published: May 2007

Purple coneflowers (Echinacea purpurea) are grown in North America and Europe for their medicinal properties and as ornamental plants. In September 1997 and again in 1998, a previously undescribed disease was noticed on fully grown coneflower plants in Summerland and Oliver, British Columbia. Mycelia were observed on stems, foliage, and flowers, and distinct dark red to black, round (approximately 5 mm in diameter) lesions were observed on the flower petals. The disease appeared similar to powdery mildews that have been reported on numerous genera of the Asteraceae. Samples of the diseased tissue were examined and the salient features of the fungus on two specimens were determined: cleistothecia infrequent, subglobose or flattened on the side next to the leaf surface, 121 to 209 μm in diameter; epidermal (surface) cells 20 μm in diameter; appendages hyphoid, 5 μm in diameter, up to 200 μm long; asci, 10 to 19 in each cleistothecium, broadly ellipsoid, 47 to 85 × 28 to 37 μm with a short stalk, about 8 to 13 μm long and 8 μm in diameter; ascospores, immature, two per ascus, ellipsoid to broadly ellipsoid, 17 to 25 × 11 to 13 μm, thin walled, hyaline, and smooth; conidia oblong with sides slightly convex and apices truncate, 27 to 40 × 14 to 20 μm, walls hyaline, thin, smooth. Based on the occurrence of asci that contained two ascospores and the hyphoid appendages on the cleistothecia we concluded that the fungus was Erysiphe cichoracearum DC. Damage due to this disease was minimal in 1997 and 1998 because it developed very late in the growing season and occurred sporadically within the plantings. In order to complete Koch's postulates, Echinacea purpurea plants grown in the greenhouse were inoculated with a conidial suspension (105 to 106 conidia per ml) from field-infected plants. Powdery mildew first appeared 3 months later, eventually infecting leaves and stems of 12 of 49 inoculated plants. It was distinctly white and in discrete patches on leaves, compared with coalescing dark brown areas on the stems. Microscopic examination of the conidia confirmed that they were E. cichoracearum. Although powdery mildew caused by E. cichoracearum has been widely reported on lettuce, safflower, and other cultivated and wild Compositae, we found no reference to it on Echinacea spp. in Canada (1,2), the U.S. (3), or elsewhere in the world (4). The specimens have been deposited in the National Mycological Herbarium of Canada (DAOM) with accession numbers 225933 and 225934 for Oliver and Summerland, B.C., respectively. References: (1) U. Braun. Beih. Nova Hedwigia 89:1, 1987. (2) I. L. Conners. 1967. An annotated index of plant diseases in Canada and fungi recorded on plants in Alaska, Canada, and Greenland. Canada Dept. of Agric. Pub. 1251. (3) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN. (4) J. Ginns. 1986. Compendium of plant disease and decay fungi in Canada, 1960-1980. Agriculture Canada Pub. 1813.
First Report of Fusarium oxysporum Causing a Leaf Twisting Disease on Allium cepa var. ascalonicum in Sri Lanka
Authors: Kuruppu P. U. 
Published: May 2007

A disease of shallot onions, Allium cepa var. ascalonicum, that caused yield losses of up to 20 to 30% in some fields was reported from Kalpitiya Peninsula in the North Western Province of Sri Lanka in the late 1980s. Disease symptoms consisting of chlorosis followed by curling and twisting of leaves and abnormal elongation of the neck region appeared after germination of the onion bulbs, subsequently causing plant collapse. Symptomatic plants occurred randomly in most fields and the disease was prevalent throughout the year. Tissue pieces from leaves and the neck region of symptomatic plants plated on potato dextrose agar containing 1% streptomycin (PDAS) produced purplish pink fungal colonies identified as Fusarium oxysporum. Pathogenicity tests were performed with single-spore fungal isolates grown at 25°C for 14 days on PDAS. Shallot onion cv. Vathalan was inoculated by soaking bulbs, pierced with a sterilized needle, in a spore suspension containing 2 × 106 spores per ml for 10 min. Control bulbs were wounded, and soaked for 10 min in sterilized water. Bulbs were then planted in sterile sand and maintained in a green house at 25 to 28°C. After 2 to 3 weeks, typical symptoms, as observed in the field, developed in plants produced from bulbs inoculated with the F. oxysporum isolate. Symptoms were not observed on plants from the control bulbs. Koch's postulates were confirmed by reisolating the same fungus from the neck region of diseased plants. Onion twister disease described by Ebenebe (1) also had been observed in this region in Sri Lanka during 1992-1993. There were differences between these two diseases in disease symptoms and disease development in the field. Acer-vuli of Colletotrichum spp. were always detected in lesions of the neck region, as well as on leaf blades, of plants severely affected by onion twister disease. This disease developed from foci in fields that spread over time. Moreover, onion twister disease occurred only from October until January, coinciding with the rainy season. Reference: (1) A. C. Ebenebe. Plant Dis. 64:1030, 1980.
Damping-off of Swiss Chard, Caused by Rhizoctonia solani, in California
Authors: Koike S. T. , Subbarao K. V. 
Published: May 2007

In California, various leafy vegetables are planted at extremely high seeding rates (up to three million seed per acre), grown to the four- to eight-leaf stage, then mechanically clipped and bagged for market as “spring mix” or “baby leaf” salad products. The crops are planted in separate strips, usually four to 16 beds of each, and include Japanese mustard (Brassica campestris subsp. nipposinica), red mustard (Brassica juncea subsp. rugosa), tah tsai (Brassica campestris subsp. narinosa), multiple lettuce (Lactuca sativa) cultivars, spinach (Spinacia oleracea), arugula (Eruca sativa), and Swiss chard (Beta vulgaris subsp. cicla). In 1997 and 1998, severe damping-off disease of Swiss chard was observed in the Salinas Valley (Monterey County). Symptoms on emergent plants consisted of wilting, brown necrosis of crown tissue, and eventual death of seedlings. Because of the high plant density, disease incidence increased rapidly, affecting large numbers of plants. Rhizoctonia solani was isolated consistently from symptomatic plants. Pathogenicity was tested by placing agar plugs of representative isolates adjacent to crowns of potted Swiss chard at the two- to four-leaf stage. Brown stem necrosis and plant collapse occurred within 5 days after inoculation, and R. solani was reisolated. Control plants, inoculated with sterile agar plugs, did not develop disease. Tests were repeated and results were similar. Anastomosis group testing revealed that all five isolates belonged to AG3 (1). For California, this appears to be the first documentation of damping-off of Swiss chard caused by R. solani. Reference: (1) B. Sneh et al. Identification of Rhizoctonia Species. American Phytopathological Society, St. Paul, MN, 1991.
First Report of Root Rot of Soybeans Caused by Corynespora cassiicola in Wisconsin
Authors: Raffel S. J. , Kazmar E. R. , Winberg R. , Oplinger E. S. , Handelsman J. , Goodman R. M. , Grau C. R. 
Published: May 2007

Corynespora cassiicola (Berk. & M. A. Curtis) C. T. Wei was isolated from diseased soybean plants (Glycine max) collected in two fields near Racine and Arlington, WI. Plants sampled at seedling emergence (VC), late vegetative (V5), and mid-reproductive (R5) stages exhibited reddish to dark brown longitudinal lesions on the exterior of the tap root extending vertically on the hypocotyl to the soil line, and extensive necrosis of lateral roots. Sample size at each growth stage was 144 plants per site. Roots were surface sterilized in 0.5% sodium hypochlorite for 2 min and sections of symptomatic tissue placed on water agar (12 g/liter) containing 100 μg of streptomycin per ml. Sporulation occurred on lesions and on mycelium that had grown out from the plant tissue onto the water agar following a 2-week incubation at 24°C under fluorescent light (280 μmol s-1 m-2). Incidence of isolation of C. cassiicola at both sites was 40% of plants sampled at growth stage VC, 67% at V5, and 78% at R5. Conidia characteristic of C. cassiicola were particularly abundant on the surface of necrotic lateral root tissue. Elongated conidia produced on water agar were 151 ± 5 μm × 15 ± 0.5 μm with an average of 13 ± 0.4 cells separated by hyaline pseudosepta (1). To confirm pathogenicity, a 1-cm lateral slice into each of four 5-day-old soybean seedling roots was made and a plug of agar taken from the margin of a colony of C. cassiicola grown on potato dextrose agar was placed in each wound and incubated for 14 days at 24°C in a growth chamber. Symptoms similar to those of diseased field plants were observed and C. cassiicola was reisolated from all plants inoculated with C. cassiicola; all controls treated with agar alone had no symptoms and C. cassiicola was recovered from none of the noninoculated controls. This is the first report of root rot caused by C. cassiicola on soybean in Wisconsin. Reference: (1) W. L. Seaman and R. A. Shoemaker. Can. J. Bot. 43:1461, 1965.
First Report of Powdery Mildew of Greenhouse Pepper Caused by Leveillula taurica in Canada
Authors: Cerkauskas R. F. , Brown J. , Ferguson G. , Khosla S. 
Published: May 2007

In 1999, powdery mildew on cvs. Oberon and Triple 4 of greenhouse pepper (Capsicum annum L.) and cv. FireFlame of chili pepper was reported simultaneously in two commercial greenhouses at two separate locations, Leamington and Vineland, geographically separated by 290 km, in southern Ontario. Losses of 10 to 15% each in the 2 and 3.1 ha greenhouse pepper operations were noted. The greenhouse pepper industry in Canada consists of 89.4 ha with sales of $43.6 million (Canadian). Lesions appeared as a white, powdery coating on the abaxial leaf surface only, generally on the lower foliage of pepper plants, while diffuse chlorotic spots were present at corresponding locations on the adaxial surface. In chili pepper, this chlorosis was restricted to interveinal tissue, causing the leaves to have a somewhat netted appearance. In some cases, pale yellow spots appeared on the adaxial portion of the affected foliage during later stages of disease development. No cleistothecia were observed. Pyriform and cylindrical, hyaline, single-celled conidia were present in equal numbers. Both conidia had a network of crests and granules containing tiny, thornlike projections on the surface. These projections were also evident on the lower half of conidiophores. Pyriform conidia ranged in length from 61.6 to 84.0 μm (mean = 70.8, SE = 0.7) and in width from 14.0 to 25.8 μm (mean = 21.1, SE = 0.4, n = 50), with a mean length to width ratio of 3.4. Cylindrical conidia ranged in length from 54.9 to 80.1 μm (mean = 66.3, SE = 0.9) and in width from 15.7 to 24.1 μm (mean = 18.6, SE = 0.3, n = 50), with a mean length to width ratio of 3.1. Short conidial chains borne on conidiophores consisted of a pyriform conidium first followed by cylindrical conidium. Stomatal penetration and extensive endophytic mycelial growth in the mesophyll layer were evident in foliar tissue cleared with glacial acetic acid:EtOH (1:2) and stained with lactophenol cotton blue. To confirm pathogenicity, conidia from infected pepper leaves were dusted onto the water-misted abaxial leaf surface of 41-day-old greenhouse pepper cvs. Cubico and Edison, and onto the similarly treated adaxial leaf surface of 58-day-old field pepper cv. Renegade. Plants were enclosed in plastic bags for 24 h on a bench. Control plants were treated identically but not inoculated. Inoculated plants developed foliar powdery mildew symptoms, including sporulation similar to that of naturally infected plants. Occurrence of the fungus on the abaxial surface of pepper foliage, presence of endophytic mycelium, and the morphological characteristics of the imperfect state confirm the identity of the fungus. This is the first report of Leveillula taurica (Lév.) G. Arnaud on pepper in Canada. Reference: J. Palti. Bot. Rev. 54:423, 1988.
Symptomatology of Barley Yellow Dwarf Virus-RMV Infection in Sweet Corn
Authors: Itnyre R. L. C. , D'Arcy Cleora J. , Pataky J. K. , Pedersen W. L. 
Published: May 2007

Infection of sweet corn (Zea mays L.) by barley yellow dwarf viruses (BYDVs) caused different symptoms on hybrids with shrunken-2 (sh-2) when compared with hybrids with sugary-1 (su-1) endosperm mutations. Sweet corn hybrids inoculated with BYDV-RMV in Urbana, IL, developed either yellow or red-purple leaf symptoms similar to those caused by phosphorus and/or potash deficiency (1). In a field trial near Rochelle, IL, 329 of 339 sweet corn hybrids naturally infected by BYDV exhibited one or the other of these symptoms. Eighteen of the hybrids with severe symptoms were tested for two strains of BYDVs in enzyme-linked immunosorbent assays (1). All of the hybrids tested were positive for BYDV-RMV; none were positive for BYDV-PAV. Symptoms on su-1 hybrids were typically characterized by dark red to purple coloration of leaf margins from the tip down to the mid-leaf. Leaves of sh-2 hybrids exhibited chlorosis in a similar pattern. A single sh-2 hybrid exhibited red-purple leaf symptoms, probably as a result of a crossover between the anthocyanin production (a1) and sh-2 genes, which are linked about 0.25 map units apart on chromosome 3 (2). Infection of sh-2 sweet corn hybrids by BYDV-RMV is most likely to induce chlorosis, whereas infection of su-1 sweet corn hybrids can result in either chlorosis or red-purple discoloration of leaves. Sweet corn hybrids with these symptoms should be tested for BYDVs, particularly the RMV strain. References: (1) R. L. C. Itnyre et al. Plant Dis. 83:566, 1999. (2) E. B. Mains. J. Hered. 40:21, 1948.
First Report of Verticillium dahliae Causing Artichoke Wilt in California
Authors: Bhat R. G. , Subbarao K. V. , Bari M. A. 
Published: May 2007

In mid-August 1998, artichoke (Cynara scolymus L.) plants of cultivar Imperial Star in a field in the Salinas area of the central coast of California developed wilt symptoms. The plants were stunted with chlorotic, drooping, and dried leaves near the bottom and middle of the plants as previously described in Italy (1). Diseased plants produced smaller edible buds and, in severe cases, buds were discolored with dried outer bracts. Roots exhibited the characteristic vascular discoloration of Verticillium infection. In one part of the infested field, artichoke was near harvest with 85% of plants showing wilt symptoms with vascular discoloration whereas the other part had a 60-day-old crop with 98% of plants infected. Yield in the field was reduced by as much as 50%. Verticillium dahliae was isolated from infected plant samples on NP-10 medium (2), and isolates were single spored before storing on potato dextrose agar at 4°C. Identity of the pathogen was confirmed based on colony morphology and formation of microsclerotia. In root-dip inoculation tests in the greenhouse, two V. dahliae isolates from artichoke infected 1-month-old artichoke seedlings that wilted within 6 weeks of inoculation. V. dahliae was reisolated from plants showing vascular discoloration. Cross-inoculation studies revealed that artichoke isolates caused a moderate level of disease in lettuce, but only a trace of vascular discoloration in cauliflower. Lettuce isolates caused a severe wilt in artichoke. Cauliflower isolates did not cause wilt in lettuce and caused only slight vascular discoloration in artichoke. This is the first report of a Verticillium wilt of artichoke in California. References: (1) M. Cirulli et al. Plant Dis. 78:680, 1994. (2) L. H. Sorensen et al. Phytopathology 81:1347, 1991.
Association of Phialophora gregata with Fusarium solani f. sp. pisi in Garbanzo Beans in California
Authors: Smith S. N. 
Published: May 2007

In 1992, a vascular disease was found in two fields of cultivar UC-15 garbanzo beans (Cicer arietinum). The fields were located on the central coast of California and Phialophora gregata was consistently isolated from the aboveground tissue in the host UC-15 plants. Diseased patches in the fields mimicked the more common Fusarium wilt with its discolored vascular tissue in the stems, but in these instances P. gregata was the sole fungus that grew out of the tissue after 5 to 8 days of incubation on isolation agar. Greenhouse pathogenicity tests yielded only minor symptoms whether a dip technique or stem puncture inoculations were used. In subsequent years it was noted that this disease was observed only in garbanzo fields where a pea crop (Pisum sativum) had been previously grown. Further isolation from small foot and root lesions of diseased field plants revealed that they were infected with Fusarium solani f. sp. pisi (Fsp) in addition to P. gregata. In greenhouse experiments with a combination of soilborne Fsp and/or stem inoculations with P. gregata, both pathogens infected the host. The symptoms from both pathogens, the strongest including occasional plant death, were similar to those observed in the fields. The effect was more than additive. Neither pathogen alone caused severe damage. In these tests Fsp was reisolated from root and foot cortical tissue along with P. gregata from stem vascular tissue near the top of the plants. Peas were an important crop along the central coast long before garbanzo beans were grown there. Fsp, a pathogen of both pea and garbanzo bean (1), has been known to attack garbanzos there since 1973 (2). The presence of yet another vascular disease of significance in this coastal area, besides those caused by Fusarium oxysporum f. sp. ciceri and Verticillium dahliae, has not been previously noted. Help in identification of P. gregata came from Diane Fogle, California Department of Food and Agriculture, Sacramento. References: (1) J. M. Kraft. Plant Dis. Rep. 53:110, 1969. (2) F. V. Westerlund Jr., et al. Phytopathology 64:432, 1974.
First Report of Sudden Death Syndrome Caused by Fusarium solani f. sp. glycines on Soybean in Pennsylvania
Authors: Pennypacker B. W. 
Published: May 2007

A small, circular patch of soybean (Glycine max) showing symptoms consistent with sudden death syndrome (SDS) (2) was noted on July 25, 1998, in a producer's field in Jersey Shore, PA. Foliar symptoms included interveinal chlorosis and necrosis, leaf cupping, and leaf abscission. The vascular cylinder of roots and stems had areas of reddish-brown discoloration. A slow-growing Fusarium sp., which produced a bluish-purple color on potato dextrose agar, was isolated from the roots of several symptomatic plants. The fungus was identified as Fusarium solani by The Fusarium Research Center, The Pennsylvania State University. Koch's postulates were tested on soybean cultivars A2506, Stine 3171, Pioneer 9305 and 9306, and Jack. Five plants per cultivar were inoculated at growth stage V1 by pouring 35 ml of a 4 × 107 spores per ml suspension on the growth mix in each pot. Five plants per cultivar were treated similarly with sterile water. Foliar symptoms of SDS began to appear 3 weeks after inoculation. Seven weeks after inoculation, symptoms of interveinal chlorosis and/or necrosis, leaf cupping, and occasional leaf abscission were apparent on the inoculated plants and on several noninoculated plants. The percentage of the plant showing symptoms was recorded and converted to the 0 to 5 scale (in which 0 = 0%, 1 = 1–10%, 2 = 11–30%, 3 = 31–40%, 4 = 41–90%, and 5= 91–100% of the leaf area affected) used by Rupe (3). Regardless of the rating method, there was a significant difference (P = 0.0001) between inoculated and noninoculated plants. There were no significant differences among cultivars. Roots of the inoculated plants were frequently discolored, in contrast to those of the noninoculated plants. F. solani was isolated from the roots of 97% of the inoculated plants and 23% of the noninoculated plants. Fungus gnats were suspected of spreading the pathogen to the noninoculated plants (1). F. solani f. sp. glycines causes SDS in soybean and its identity is confirmed by the symptoms produced on soybean (2). The symptoms produced when soybean plants were inoculated in the greenhouse were consistent with those of SDS (2) and indicate that the F. solani isolate recovered from symptomatic plants in the field was F. solani f. sp. glycines. This is the first documented occurrence of SDS on soybean in Pennsylvania. References: (1) D. W. Kalb and R. L. Millar. Plant Dis. 70:752, 1986. (2) K. W. Roy et al. Plant Dis. 81:1100, 1997. (3) J. C. Rupe. Plant Dis. 73:581, 1989.