bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Report of Gummy Stem Blight, Caused by Didymella bryoniae, on Watermelon Transplants in California
Authors: Koike S. T. 
Published: May 2007

In 1997, greenhouse-produced transplants of watermelon (Citrullus lanatus) developed water-soaked lesions on leaf petioles and main stems. As disease progressed, petioles and stems became necrotic and shriveled, and exuded a sticky, translucent tan liquid. Symptoms spread to leaves, which wilted and collapsed. Affected transplants eventually died. Although fruiting bodies were not observed on diseased plants, a fungal agent was consistently isolated from symptomatic tissues. When incubated under lights (12 h light/12 h dark cycle), isolates on potato dextrose agar produced numerous pycnidia with hyaline, cylindrical, one-septate conidia with mean dimensions of 5.6 × 2.8 μm. Under the same incubation conditions, isolates on V8 juice agar produced sparse ostiolate pseudothecia with bitunicate asci and hyaline, oval, one-septate ascospores with mean dimensions of 12.0 × 4.0 μm. Based on these characters, the isolates were identified as Didymella bryoniae (anamorph Phoma cucurbitacearum) (1,2). Pathogenicity was tested by producing conidial inocula of representative isolates and inoculating wounded cotyledons, true leaves, and petioles of watermelon (cv. Sangria), and wounded true leaves and petioles of cucumber (Cucumis sativus cv. Premier Hybrid) (3). Sterile, distilled water was applied to corresponding wounded tissues of control plants. All plants were kept in a humid chamber for 4 days. After 6 (watermelon) to 10 (cucumber) days, inoculated plants exhibited water-soaked lesions followed by necrosis, petiole and leaf wilting, and shriveling of tissues. Pycnidia were observed on cucumber plants after 18 days. The pathogen was reisolated from all inoculated plants and identified as D. bryoniae. Control plants developed no disease symptoms. In addition, agar plugs colonized with the watermelon isolates were placed onto cucumber fruit that were wounded slightly with a sterile scalpel. Fruit were incubated at 22 to 24°C in humid chambers and after 2 days sunken, circular lesions developed. The same pathogen was reisolated from the margins of fruit lesions. Wounded control fruit received sterile agar plugs and did not develop any symptoms. This is the first documentation of gummy stem blight on watermelon transplants in California. References: (1) W. F. Chiu and J. C. Walker. J. Agric. Res. 78:81, 1949. (2) A. P. Keinath et al. Phytopathology 85:364, 1995. (3) A. J. Wyszogrodzka et al. Euphytica 35:603, 1986.
First Report of Tomato Gray Leaf Spot Caused by Stemphylium solani in the Andes Region of Venezuela
Authors: Cedeño L. , Carrero C. 
Published: May 2007

Since 1994, tomato (Lycopersicon esculentum Mill.) grown in Mérida State, located in the Venezuelan Andes, have been consistently affected by a gray leaf spot disease with symptoms on leaves, petioles, and stems. Yield is reduced, and in some cases entire crops have been destroyed over short time. Because of its prevalence, distribution, and severity, the disease has become the major factor limiting tomato production in this region. Disease symptoms were commonly observed on seedlings and plants. On leaves the disease first appeared as circular to elongated dark specks. As the spots enlarged, they became gray and bright. Old lesions dried and usually cracked. Severely infected leaves turned yellow and then died and dropped. Lesions on petioles and stems were elongate. Disease severity was generally higher following the beginning of fruiting. The fungus was isolated from leaves, petioles, and stems of tomato cv. Rio Grande on 2% water agar acidified with lactic acid. On potato-carrot agar, conidiophores and conidia were produced with the characteristics of Stemphylium. Two species of Stemphylium, S. solani G. F. Weber and S. lycopersici (Enjoji) W. Yamamoto, cause gray leaf spot symptoms on tomato. Based on morphology, size, and the length/width ratio of the conidia, the fungus was identified as S. solani (1). Inoculations done by spraying a conidial suspension on plants of tomato cv. Rio Grande produced symptoms similar to those observed in the field. S. solani was consistently isolated from experimentally infected tissues, thus confirming Koch's postulates. This is the first report of S. solani causing gray leaf spot on tomato grown in the Andes of Venezuela. Reference: (1) G. F. Weber. Phytopathology 20:513, 1930.
First Report of Papaya Leaf Curl Disease in Pakistan
Authors: Nadeem A. , Mehmood T. , Tahir M. , Khalid S. , Xiong Z. 
Published: May 2007

Papaya plants with virus-disease-like symptoms were observed in back yards and commercial groves in Multan, Pakistan. Leaves of the diseased plants displayed downward curling and thickened, dark green veins. Leaf-like enations grew from the base of the diseased leaves. These symptoms are similar to those of cotton leaf curl disease. In addition, diseased papayas were stunted and distorted. Leaf extracts from 3 diseased and 2 healthy papayas were tested in enzyme-linked immunosorbent assay against antibodies to geminiviruses. SCRI-52 and SCRI-60, two monoclonal antibodies to Indian cassava mosaic virus (2), reacted positively (more than 7× healthy background) with the diseased samples but not with the healthy ones. Total nucleic acids from the papaya samples were used as templates in polymerase chain reaction with primers F500 and R1800 (1), which are capable of amplifying a region of DNA A component of the whitefly-transmitted geminiviruses. A DNA fragment of approximately 1.4 kb was amplified from the nucleic acids of the diseased but not the healthy papayas. Under high stringency conditions (1), cloned DNA A fragments of both cotton leaf curl virus and cotton leaf crumple virus cross-hybridized with the amplified DNA fragment, but the hybridization signals were much weaker than those of the homologous hybridization. This is the first report of the papaya leaf curl disease in Pakistan. These data demonstrated that a geminivirus may be the causative agent of this papaya disease. We are currently determining the relationship between the geminivirus infecting papaya and cotton leaf curl virus. References: (1) A. Nadeem et al. Mol. Plant Pathol. (On-line: /1997/0612nadeem). (2) M. M. Swanson et al. Ann. Appl. Biol. 211:285, 1992.
Sirococcus clavigignenti-juglandacearum on Heartnut (Juglans ailantifolia var. cordiformis)
Authors: Ostry M. E. 
Published: May 2007

Branch dieback was observed throughout the crown of a 25-year-old heartnut, a variety of Japanese walnut, growing in a mixed plantation with black walnut (J. nigra) in central Iowa in the spring of 1997. No cankers were evident. However, hyphal pegs and hyaline, two-celled, fusiform conidia were present on the affected 1996 branch wood. These are characteristic of S. clavigignenti-juglandacearum, the cause of branch and stem cankers on butternut, also called white walnut, (J. cinerea) (1). The fungus was isolated in pure culture from symptomatic twigs. The ability of this isolate to cause canker on butternut was compared with an isolate from butternut in Minnesota by inoculating the stems of potted, 2-year-old butternut seedlings in a greenhouse. Lignified stem portions of the seedlings were wounded by removing a 5-mm2 area of bark with a scalpel, exposing the cambium, and placing a plug cut from the margin of an actively growing culture on potato dextrose agar (PDA) fungus-side-down on the wound. Each of 30 seedlings received both isolates, 15 with the heartnut isolate on top (10 cm from shoot apex), and 15 with it on the bottom (30 cm from shoot apex) position of the stems. Noncolonized PDA control plugs were similarly placed on wounds in the middle position of each stem. Parafilm was used to hold the agar plugs in place and was removed 2 weeks later. After 10 weeks, canker lengths were recorded. Stem segments were surface sterilized, and wood chips from canker margins were placed onto PDA at 20°C. Cankers characteristic of S. clavigignenti-juglandacearum developed on all seedlings at each inoculation site. The means of lengths of cankers for the heartnut and butternut isolates (37.1 and 37.2 mm, respectively) did not differ significantly (P > 0.9). Hyphal pegs and conidia of S. clavigignenti-juglandacearum developed at inoculation sites of stems with both isolates. The fungus was recovered in pure culture from the canker margins. No cankers developed at the control wound sites and all wounds were callused over. This is the first report of S. clavigignenti-juglandacearum on Japanese walnut. This report and an earlier report of this fungus causing dieback on black walnut (2) indicate this fungus may occur on other Juglans spp. than previously reported and could be considered a potential pathogen in walnut plantings. References: (1) V. M. G. Nair et al. Mycologia 71:641, 1979. (2) M. E. Ostry et al. Plant Dis. 81:830, 1997.
Occurrence of Cowpea Stunt Disease Causing Viruses on Wild Bean in Arkansas
Authors: Kline A. S. , Anderson E. J. , Smith E. B. 
Published: May 2007

Cucumber mosaic cucumovirus (CMV) and blackeye cowpea mosaic potyvirus (BlCMV) interact synergistically in dually infected plants to cause cowpea stunt disease (1,2). During a July 1996 survey of cowpea stunt-affected fields in the Arkansas River valley, several wild bean (Strophostyles helvola L. Elliott) plants expressing mosaic symptoms were observed and collected. Sap was extracted from symptomatic leaves and used as inoculum to conduct a host range study. Virus symptoms diagnostic for BlCMV, CMV, or cowpea stunt were observed 6 to 8 days post-inoculation on Vigna unguiculata (L.) Walp. subsp. unguiculata cv. Coronet, while chlorotic lesions and mild systemic mosaic symptoms developed on Nicotiana benthamiana. Enzyme-linked immunosorbent assays (ELISAs) conducted on extracts from symptomatic cowpea and N. benthamiana 14 days after inoculation verified the presence of CMV and BlCMV in single and mixed infections. Additional symptomatic wild bean plants were collected from the same site in October 1996. ELISAs and Ouchterlony gel diffusion assays confirmed the presence of CMV and BlCMV, as well as soybean mosaic potyvirus (SMV), cowpea chlorotic mottle bromovirus, and alfalfa mosaic virus (AlMV) in symptomatic wild bean plants. While some of the collected plants were infected with only one virus, others had combined infections of CMV and BlCMV or these two viruses with AlMV. Interestingly, AlMV isolated from wild bean caused symptoms on greenhouse-grown cowpeas that were as severe or more severe than those caused by the cowpea stunt synergy, often resulting in plant death within 8 to 10 days after inoculation. The SMV from wild bean did not induce symptoms on cowpea and was not detected in extracts from inoculated cowpea plants by Ouchterlony gel diffusion assays, but was able to systemically infect soybean (Glycine max L.) cvs. Bragg and Lee. Another virus known to infect cowpea, southern bean mosaic sobemovirus, was not detected in any of the samples tested. To our knowledge, this is the first report that wild bean can serve as an alternate host for cowpea stunt-causing viruses in single and mixed infections. In addition, these data suggest that AlMV may pose a threat to Arkansas-grown cowpeas. References: (1) E. J. Anderson et al. Ark. Farm Res. 43:14, 1994. (2) G. Pio-Ribeiro et al. Phytopathology 68:1260, 1978.
Bacterial Leaf Spot of Cilantro in Florida
Authors: Pernezny K. , Raid R. N. , Jones J. B. 
Published: May 2007

In the 1995 to 1996 winter vegetable season, a leaf spot disease of cilantro (fresh coriander) (Coriandrum sativum L.) was widespread throughout commercial plantings in the Everglades Agricultural Area south and east of Lake Okeechobee. Symptoms first appeared as water-soaked spots ≤1 mm in diameter. These spots became dark brown to black and enlarged up to 2 mm in diameter. No chlorotic haloes developed around the lesions. The disorder was observed in numerous plantings of the cultivar Longstanding at four separate locations. Symptoms were apparent throughout each planting, with disease severity ranging from a few individual spots to numerous lesions covering nearly entire leaflets. Severe outbreaks were correlated with heavy precipitation events. In several instances, disease levels were great enough to render entire plantings totally unmarketable. A non-fluorescent bacterium was consistently isolated on King's medium B when a cooled inoculation needle was pushed through lesions. Six representative strains were chosen for further characterization. All strains were aerobic, gram-negative rods, and were oxidase and arginine dihydrolase negative. Levan was produced, but potato slices were not rotted. Tests for utilization of l-tartrate, l-lactate, and erythritol were negative. Biolog analysis identified all strains of the bacterium as Pseudomonas syringae. Highest similarity indices (0.52 to 0.81) were with P. syringae pv. pisi for four of the six strains. Suspensions of each strain were swab inoculated onto leaves of 4-week-old Longstanding cilantro seedlings in the greenhouse. Control plants were swabbed with sterile water only. Plants were covered with clear polyethylene bags for 72 h. Watersoaked spots were evident on test plants when bags were removed. Typical brown, greasy-looking leaf spots were seen by 6 days after inoculation. Control plants were symp-tomless. In a host-range study, cilantro and the following plants were mist-inoculated with a 107 CFU/ml suspension of each of the six test strains: carrot (Daucus carota L. ‘Fancy Pack’), celery (Apium graveolens L. var. dulce (Mill.) Pers., ‘June Belle’), garden pea (Pisum sativum L. ‘Melting Sugar’), snap bean (Phaseolus vulgaris L. ‘Pod Squad’), and onion (Allium cepa L. ‘Evergreen Bunching’). Six days after inoculation, characteristic symptoms were evident on the cilantro. Four of the six strains produced a few (less than 10 per plant) bacterial leaf spot symptoms in carrot from which P. syringae was readily recovered. Some necrosis was observed on young, emerging leaves of snap bean. No symptoms were recorded for the other host species or the controls. This disease is similar to one reported on cilantro in California (1) and Germany (2). References: (1) D. A. Cooksey et al. Plant Dis. 75:101, 1991. (2) H. M. Toben and K. Rudolph. J. Phytopathol. 144:169, 1996.
Detection of Virulence to Lr41 in a South African Pathotype of Puccinia recondita f. sp. tritici
Authors: Pretorius Z. A. 
Published: May 2007

The Lr41 gene for resistance to leaf rust, caused by Puccinia recondita f. sp. tritici, was transferred from Triticum tauschii accession TA2460 to bread wheat (T. aestivum) at the Wheat Genetics Resource Center, Kansas State University (1). Due to the high degree of resistance (primary leaf infection types [ITs] 0; to ;1= [0 to 4 scale]) conferred to South African pathotypes of leaf rust, the gene was considered potentially valuable in local programs directed at wheat germ plasm improvement. During routine glasshouse tests for seedling resistance to the South African leaf rust pathotype UVPrt16, several sporulating pustules (IT 4) were observed among flecks on wheat line KS90WGRC10 (TAM107*3/TA2460). Rust cultures multiplied from these pustules were tested on seedlings of 31 wheat lines with different Lr genes in a growth cabinet at 20°C. Their avirulence/virulence characteristics suggested a single-step mutation for virulence to Lr41. According to North American nomenclature (2), the Lr41-virulent isolate is classified as race FDC-14b,20,23,25,33,41. Low ITs were recorded on additional testers with Lr3bg, 14a, 15, 18, 19, 27+31, 28, and 29, and intermediate ITs on lines with Lr2b, 10, 21, 32, and 36. Infection studies on adult plants showed that KS90WGRC10 and its recurrent parent TAM107 produced similar susceptible reactions (Its 3++C) to the mutant. T. tauschii accession TA2460, however, was moderately susceptible (IT 2+) to this culture. Virulence to Lr41 has not been recorded in field populations of the pathogen in South Africa. The occurrence of virulence to Lr41 emphasized the nondurability of monogenic resistance and thus the importance of conserving genetic diversity for leaf rust resistance. To protect Lr41 from becoming obsolete, it should be used only in combination with other effective resistance gene(s). References: (1) T. S. Cox et al. Crop Sci. 32:506, 1992. (2) D. L. Long and J. A. Kol-mer. Phytopathology 79:525, 1989.
Purple Coneflower Is a Host of the Aster Yellows Phytoplasma
Authors: Stanosz G. R. , Heimann M. F. , Lee I.-M. 
Published: May 2007

The perennial plant purple coneflower (Echinacea purpurea (L.) Moench, Asteraceae) is native to open woods and prairies of the eastern U.S. and is gaining popularity as a garden and roadside ornamental. It is propagated both by seed and by division of established plant crowns. During late summer 1996, three of seven purple coneflower plants located in a residential garden in Dane County, WI, exhibited symptoms associated with diseases caused by phytoplasmas. These plants had been established from seed in spring 1995. Stems were thickened and brittle. Leaves were slightly twisted and drooped, and flower parts lacked normal pigmentation. Petals of ligulate flowers were narrow. Clusters of short, thin stems bearing sterile, dwarfed, distorted, green heads had grown from the receptacles of severely affected flower heads. A presumptive fluorescence test with 4′,6-diamidino-2-phenylindole staining was positive for phytoplasmalike bodies in phloem sieve elements in the midveins of leaves from a symptomatic plant. Nested polymerase chain reaction (PCR) amplification of extracted DNA with phytoplasma-specific oligo-nucleotide primer pairs (1,2) confirmed the presence of phytoplasmas in this plant. Based on restriction fragment length polymorphism analysis of the PCR products, the associated phytoplasma was identified as phytoplasma 16S rRNA group I (aster yellows [AY] and related phytoplasmas), subgroup A. This is the first report of a host of the AY phytoplasma in the genus Echinacea. Because no attempt was made to transfer the phytoplasma via leafhoppers, the potential for purple coneflower to be a source of inoculum is unknown. References: (1) D. E. Gunderson and I.-M. Lee. Phytopathol. Mediterr. 35:144, 1996. (2) I.-M. Lee et al. Phytopathology 84:559, 1994.
First Report of Mucor Rot in Commercially Sold Cherries Caused by Mucor piriformis
Authors: Sholberg P. L. , Michailides T. J. 
Published: May 2007

In August 1996, a commercial retailer of high quality cherries from the Okanagan Valley of British Columbia, Canada, reported severe losses in at least 150 boxes (11.3 kg per box) of packed cherries cv. Stella. Upon examination of a representative box of these cherries, it was found that approximately 80% of the fruit was affected by what appeared to be Mucor spp. The decayed cherries were concentrated below the surface layer and small pockets of cherries had prominent salt-and-pepper-colored whiskers emanating from individual cherries. Counting the exact number of rotten cherries was difficult because they disintegrated on handling. Several infected cherries were surface sterilized by immersing in a 0.5% NaClO solution for 1 min and rinsing with sterile, distilled water. Pieces of the surface-sterilized cherries were plated onto dishes containing potato dextrose agar and incubated at 6°C for 10 days. Ten typical isolates derived from single spores from these dishes were all identified as Mucor piriformis A. Fischer (1). Samples of 200 g of cherries cv. Sweetheart (20 ± 1 cherries) were sprayed with a water suspension containing 1 × 106 sporangiospores per ml with one of the isolates identified as M. piriformis and incubated at 1, 6, 10, 15, and 20°C for up to 25 days. This same procedure was repeated for two other isolates of M. piriformis isolated from infected cherries. As a control, cherries were misted with sterile water and incubated at 20°C for 6 days. At 6°C, a temperature at which cherries are often stored, the three isolates decayed, respectively, 100, 60, and 60% of the cherries in 18 days. In general, all three isolates caused greater than 50% decay at 20, 15, 10, and 1°C in 6, 6, 11, and 25 days, respectively. Decay did not occur in cherries misted only with sterile water. Careful visual examination of decayed cherries revealed similar whiskerlike growth of Mucor as seen in the commercial cherries. Microscopic examination of sporangiophores infecting the fruit found them to be the same as the original M. piriformis isolate, successfully completing Koch's postulates. Previous to this report, M. piriformis, M. hiemalis, and M. plumbeus were isolated from Lambert cherries stored for 4 weeks at 4.5°C in Oregon (2); however, it is unclear if all or any of these isolates were pathogenic because pathogenicity tests were not conducted. References: (1) T. J. Michailides and R. A. Spotts. Plant Dis. 74:537, 1990. (2) P. G. Sanderson and R. A. Spotts. Fungic. Nematic. Tests 47:43, 1992.
Wood Decay Associated with Pileated Woodpecker Roosts in Western Redcedar
Authors: Parks C. G. , Raley C. M. , Aubry K. B. , Gilbertson R. L. 
Published: May 2007

The pileated woodpecker (Dryocopus pileatus) is a species of concern to forest managers because it uses cavities in large snags and decadent trees for nesting and roosting. A radio-telemetry study of pileated woodpeckers on the Olympic Peninsula of western Washington (1) found that large western redcedar (Thuja plicata Donn ex D. Don) were frequently used for roosting. These roost trees were partially hollow or softened by internal decay. Western redcedar is thought to be less susceptible to most fungal pathogens than are other conifers. This misconception probably arose because of the high resistance to decay of cedar heartwood under service conditions. Many heartwood fungi do, however, attack living redcedar during their lifespan (often over 1,000 years), and large western redcedar have a high incidence of heartwood decay (2). Two to four wood cores were removed below openings used by radio-tagged woodpeckers at heights of 7.5 to 10.5 m on each of 10 large (200 to 300 cm diameter at 1.4 m above ground), living western redcedars. Wood samples were cultured on malt extract agar. No pure cultures of wood-decay fungi were obtained from two trees, although the samples were visually decayed. Oligoporus sericeomollis (Romell) Bondartzeva (= Poria asiatica (Pilát) Overh.) was the only wood-decay fungus isolated from the remaining eight trees. O. sericeomollis causes a brown, cubical heartrot in living western redcedar. In late stages of decay, the rot column typically forms a piped or tubular shape, can extend 25 or more meters up the bole of the tree, and can spread out into large branches (2). Pileated woodpeckers often roost in large, longitudinal tree cavities having multiple openings that provide a means of escape from potential predators. The decay columns produced by O. sericeomollis may create optimal roosting conditions in western redcedar for pileateds. During the telemetry study, woodpeckers were observed entering redcedars at one opening, but exiting from another opening some distance away. Large western redcedars that contain heartrot before they die may be particularly important to pileated woodpeckers because these trees persist in the landscape and provide potential roost sites far longer than other tree species in western Washington, perhaps even for centuries. Information from this and similar studies may be useful for developing inoculation techniques that use fungi with specific decay characteristics to create habitat for woodpeckers. References: (1) K. B. Aubry and C. M. Raley. Northwest Env. J. 6:432, 1990. (2) D. C. Buckland. Can. J. Res. C. 24:158, 1946.