bluuebunny/crossref_metadata_2025_split huggingface dataset:
Widespread Occurrence of Tomato Geminiviruses in Brazil, Associated with the New Biotype of the Whitefly Vector
Authors: Ribeiro S. G. , de Ávila A. C. , Bezerra I. C. , Fernandes J. J. , Faria J. C. , Lima M. F. , Gilbertson R. L. , Maciel-Zambolim E. , Zerbini F. M. 
Published: May 2007

Although tomato golden mosaic virus (TGMV) was reported in Brazil more than 20 years ago (3), tomato-infecting geminiviruses have not been of economic significance in the country until recently. However, a sharp increase in the incidence of geminivirus-like symptoms in tomatoes has been reported in several areas of Brazil since 1994. This has coincided with the appearance of the B biotype of Bemisia tabaci, which, as opposed to the A biotype, readily colonizes solanaceous plants (2). We have isolated geminiviruses from symptomatic tomato plants in the Federal District, in two different areas of the state of Minas Gerais, and in the state of Pernambuco. Tomato plants in these areas showed a variety of symptoms, including yellow mosaic, severe leaf distortion, down-cupping, and epinasty. Whitefly infestation was high in all fields sampled, and in some fields, particularly in Pernambuco, incidence of virus-like symptoms was close to 100%, and no tomatoes of commercial value were harvested (1). Using primer pairs PAL1v1978/PAR1c496 and PCRc1/PBL1v2040 (4), DNA-A and -B fragments were polymerase chain reaction (PCR)-amplified from total DNA extracted from diseased plants, cloned, and sequenced. Sequence comparisons of the PCR fragments indicated the existence of at least six different geminiviruses. The nucleotide sequence homologies for DNA-A fragments ranged from 67 to 80% for the 5′ end of the cp gene, and from 44 to 80% for the 5′ end of the rep gene. Data base comparisons indicated the viruses are most closely related to TGMV, bean golden mosaic virus from Brazil (BGMV-Br), and tomato yellow vein streak virus (ToYVSV), although homologies were less than 80% for the fragments compared. A similar lack of a close relationship with each other and other geminiviruses was obtained with two DNA-B component PCR products compared, corresponding to the 5′ end of the BC1 open reading frame. Infectious, full-length genomic clones from the tomato viruses are being generated for biological and molecular characterization. References: (1) I. C. Bezerra et al. Fitopatol. Bras. 22:331, 1997. (2) F. H. França et al., Ann. Soc. Entomol. Bras. 25:369, 1996. (3) J. C. Matyis et al. Summa Phytopathol. 1:267, 1975. (4) M. R. Rojas et al. Plant Dis. 77:340, 1993.
First Report of Colletotrichum coccodes on Soybean in the United States
Authors: Riccioni L. , Conca G. , Hartman G. L. 
Published: May 2007

Anthracnose symptoms were observed on soybean (Glycine max (L.) Merr.) cv. Yale in Illinois in September 1996. Lower stems were girdled by lesions that contained black fungal stroma. Colletotrichum coccodes (Wallr.) S. J. Hughes was isolated from surface-sterilized portions of diseased stems incubated on potato dextrose agar (PDA). Cultures produced abundant black sclerotia and acervuli with setae. Acervuli produced straight and fusiform conidia (15 to 23 × 3 to 4 μm) in honey-colored masses. Ovate or long clavate appressoria were formed on slide microcultures. Pathogenicity tests were carried out in the greenhouse on soybean plants, cvs. Panda and Pony at the V4 growth stage, by (i) spraying a conidial suspension (2 ×106 conidia per ml) on seedlings and (ii) placing a mycelial PDA plug above the first two nodes of the stem, previously wounded with a sterile needle. Plain sterile water and plugs without mycelia were used as controls. Six plants per cultivar and per treatment were used. Plants were covered with polyethylene bags for 3 days. Anthracnose symptoms gradually appeared near maturity and plants senesced prematurely with both inoculation methods. Averaged over both cultivars, 100 and 50% of the plants showed symptoms when inoculated with a conidial suspension and mycelial plugs, respectively. Control plants did not have any symptoms. C. coccodes was consistently reisolated from stems, leaves, petioles, and pod peduncles with symptoms, and was not reisolated from noninoculated plants. Seeds collected from plants inoculated with either method showed infection rates up to 14 and 8% on cvs. Panda and Pony, respectively, while seeds collected from control plants showed 0% infection rate. The most common pathogen associated with soybean anthracnose is C. truncatum (Schwein.) Andrus and W. D. Moore, but other species have been reported to cause anthracnose. C. coccodes was reported on soybean in Italy (1). This pathogen has a wide host range and causes serious damage, mostly on solanaceous crops. This is the first report of the presence of the pathogen on soybean in the United States. Reference: (1) G. Conca et al. Petria 4:193, 1994.
Root Rot by Rhizoctonia solani on Ambrosia grayi in Texas
Authors: Wheeler T. A. , Dotray P. , Winchester J. 
Published: May 2007

Ambrosia grayi (A. Nelson) Shinners is a pernicious perennial weed that infests over 200,000 ha of cotton in Texas and New Mexico. It reproduces primarily by rhizomes, which are found up to 3 m deep in the soil. With the exception of Roundup Ultra on Roundup-ready cotton, no herbicides can be applied in-season to control this weed without injuring cotton. A search was conducted for soilborne pathogens as potential biocontrol agents by surveying cotton fields and small lakes for A. grayi plants with root lesions. Roots were washed with running water for 2 min and segments of root lesions were placed on water agar (1.5%) with hyphae of emerging fungi transferred to potato dextrose agar (PDA). Eighty isolates of fungi were collected; most were Fusarium spp. or Rhizoctonia solani. Replicated experiments with isolates were conducted. Each isolate was grown on PDA and then 1/4 of the media in a petri plate (12.6 cm2) was mixed with 450 cm3 autoclaved soil and placed in a styrofoam cup. A piece of rhizome (3 to 5 cm in length) was placed 5 cm below the soil surface in the infested cup. Roots with necrosis were plated on PDA to recover fungi, which were grown in pure culture and used to reinfest soil. Significant disease (in repeated tests) was caused by two isolates of R. solani, compared with the noninfested check, as indicated by a reduction in number of emerging plants per pot, increase in root necrosis, and decrease in fresh and dried leaf weight. Roots growing from the infected rhizomes were discolored and rotted without distinct lesions. Both of these isolates were identified as AG4 by anastomosis with tester ATCC #46134 by the cellophane technique (1). Reference: (1) D. E. Carling et al. Phytopathology 77:1609, 1987.
Thlaspi arvense, a New Host for Alternaria brassicicola
Authors: Cobb A. C. , Dillard H. R. 
Published: May 2007

A leaf spot was observed on cruciferous weeds growing in a cabbage field located in Geneva, NY, on 1 August 1996. The leaf spots on the weeds were dark gray to black in color and varied in size from pinpoints to 1 mm in diameter. The cabbage (Brassica oleracea L. var. capitata L.) was infected with Alternaria brassicicola (Schwein.) Wiltshire, the cause of Alternaria leaf spot. The weeds were identified as Thlaspi arvense L., a winter annual commonly referred to as field pennycress, stinkweed, or fanweed depending on geographic location. Isolations from the diseased weed tissue yielded A. brassicicola (2). The numerous conidia occurred in chains of 10 or more, ranged in size from 14 to 53 μm in length, were 5 to 18 μm wide, contained from 1 to 6 transverse septa with rare longitudinal septa, and were olivaceous in color. An apical beak was absent. On potato dextrose agar (PDA) the colony was dark olive-green to black in color and velvety. Seed was collected from the T. arvense plannts in the spring of 1997. One hundred seeds were placed in petri plates containing PDA amended with 0.01% of chloramphenicol and streptomycin sulfate. A. brassicicola was not isolated from the seeds. A different area of the field was planted to cabbage in 1997 and the cruciferous weeds were allowed to grow. The 1997 population of T. arvense consisted of plants from the previous season that flowered early and plants from seeds that germinated late in the season but did not flower. A. brassicicola was isolated from nonflowering weeds in September and from flowering weeds in October. Nonflowering plants were removed from the field in November, planted in pots, and placed in the greenhouse to induce flowering. Identity of both plant populations was confirmed as T. arvense (Warren Lamboy, Cornell University, Geneva, NY). Pathogencity of A. brassicicola isolates from T. arvense was demonstrated on cabbage and T. arvense by following Koch's postulates. Conidia (105) from a 5-day-old culture isolated from T. arvense grown on PDA were atomized onto field pennycress and cabbage plants with a Preval sprayer. The plants were enclosed in plastic bags and put under lathe shading in the greenhouse. The pathogen was reisolated from symptomatic tissue of both plants after 5 days. This weed could serve as a potential source of A. brassicicola inoculum because it is not controlled by herbicides used in crucifer production systems. Alternaria raphani has been reported on T. arvense in Canada (1). This is believed to be the first report of A. brassicicola on T. arvense. References: (1) K. Mortensen et al. Can. Plant Dis. Surv. 73:129, 1993. (2) P. Neergaard. 1945. Danish Species of Alternaria and Stemphylium. Oxford University Press, London. pp. 137–138.
Leafroll Virus Is Common in Cultivated American Grapevines in Western New York
Authors: Wilcox W. F. , Jiang Z.-Y. , Gonsalves D. 
Published: May 2007

American grapevines (Vitis labrusca L. ‘Niagara’; Vitis × labruscana L. H. Bailey ‘Concord’ and ‘Catawba’; V. labrusca × V. riparia Michx. ‘Elvira’) from 24 vineyards in the New York portion of the Lake Erie production region (>13,000 ha cultivated) were tested to explore a possible relationship between virus infection and an unexplained fruit set malady in the district. One-year-old cane segments were collected 4 to 6 weeks before budbreak from 65 individual vines, which previously had been identified as malady positive or negative. Preparations from bark scrapings were tested for the presence of double-stranded (ds) RNA and for fan leaf degeneration virus, tobacco streak virus, and grapevine leafroll associated closterovirus-3 (GLRaV-3) by enzyme-linked immunosorbent assay (ELISA). Mechanical transmission of other potential viruses to Chenopodium quinoa was attempted with sap extracted from young shoots forced from intact segments of sampled canes. GLRaV-3 was detected in 17 (26%) of the sampled vines from eight (33%) of the vineyards, but there was no apparent relationship between infected vines and the fruit set malady. Vines of all four cultivars were infected. dsRNA was detected in all 17 samples positive for GLRaV-3 plus four additional samples. No other viruses were detected. Near harvest, nine vines (from two vineyards) previously testing positive for GLRaV-3 were examined and retested; all nine tested positive again, although none showed any overt symptoms of viral infection. This is believed to be the first report of GLRaV-3 from American grape vineyards in New York. The source of these infections is unknown: all vines were self rooted, the individual vineyards had been planted independently at different times, and V. vinifera and its hybrids are rare in the district. Wild grapevines (primarily V. riparia) are abundant in the region, although it has been reported that leafroll disease does not occur naturally in wild North American grapes (1). Nevertheless, our results indicate that cultivated American grapevines can be common reservoirs of GLRaV-3, and furthermore suggest the need to reassess the possibility that wild grapes also may serve as reservoirs of the virus. Trials are currently underway to determine possible effects of GLRaV-3 on cv. Concord, the most widely planted variety in the region. Reference: (1) A. C. Goheen. 1988. Leafroll. Page 52 in: Compendium of Grape Diseases. R. C. Pearson and A. C. Goheen, eds. American Phytopathological Society, St. Paul, MN.
Downy Mildew of Arugula, Caused by Peronospora parasitica, in California
Authors: Koike S. T. 
Published: May 2007

Over the past 5 years, commercial acreage of the leafy crucifer arugula (Eruca sativa) has increased greatly in the Salinas Valley (Monterey County), California, and the crop is an important component in packaged salad products. A foliar disease has affected this crop and at times reduced its quality to the extent that it could not be harvested. Symptoms consisted of small (1 to 4 mm in diameter), irregular, dark brown to black speckling on adaxial leaf surfaces. Speckling sometimes expanded into tan spots 3 to 8 mm in diameter. Corresponding abaxial surfaces usually supported white fungal growth typical of a downy mildew. Conidiophores had main trunks with dichotomous branches ending in slender curved tips. Conidia were ovoid in shape, measuring 22 to 25 μm long and 19 μm wide. The fungus was identified as Peronospora parasitica. Pathogenicity was established by gently pressing diseased leaves onto arugula test plants and incubating plants in a humidity chamber for 48 h. Downy mildew developed after 6 days and the same fungus was observed. Although this disease has occurred on this crop for several years, this is the first documentation of P. parasitica on arugula in California. A previously described foliar bacterial disease caused by Pseudomonas syringae (1) has similar symptoms, making field diagnoses difficult if fungal signs of the downy mildew are not present on the leaf. Reference: (1) S. T. Koike et al. Plant Dis. 80:464. 1996.
Corn Stunt Complex Mollicutes in Belize
Authors: Henríquez N. P. , Kenyon L. , Quiroz L. 
Published: May 2007

Successive plantings of sweet corn in Orange Walk District, Belize (<200 m ASL) were observed to be performing poorly. Plants were stunted with shortened upper internodes, over-production (proliferation) of ears, and chlorosis of ears and leaf bases. Plants of hybrid white corn in Cayo District (<200 m ASL) had leaf-base chlorosis, mid-vein reddening, chlorotic bands on the leaves, and die-back of leaf tips: symptoms attributed to infection by the corn stunt complex (CSC) pathogens. Spiroplasma kunkelii was detected in symptom-bearing leaf-base samples of white corn but not sweet corn, using a specific F(ab')2 protein-A enzyme-linked immunosorbent assay (ELISA; D. Gordon, Ohio). Polymerase chain reactions with maize bushy stunt (MBS) phytoplasma-specific primers (1) resulted in amplification products of the expected size (740 bp) when DNA extracts from either sample type were used as template. DNAs from apparently healthy sweet or white corn from the field, or from glasshouse-grown sweet corn, did not yield this product. MBS and S. kunkelii are transmitted by leafhoppers of the genus Dalbulus, often simultaneously with maize rayado fino virus, the other CSC component (not tested for in this study). All the sweet corn varieties examined had a high incidence of the symptoms, suggesting that they are highly susceptible to one or both of the CSC mollicutes. With the increase in area dedicated to maize production and successive year-round plantings, the potential for spread and increased incidence of MBS or CSC in Belize is considerable. Reference: (1) N. A. Harrison et al. Plant Dis. 80:263, 1996.
Claviceps africana Discovered in India
Authors: Bogo A. , Mantle P. G. 
Published: May 2007

The African ergot pathogen (Claviceps africana Frederickson, Mantle, & de Milliano) of sorghum (Sorghum bicolor (L.) Moench) was recently discovered in the Americas (4) and Australia, having previously only been recognized outside Africa in Thailand and Japan (3). The fungus provides a striking example of intercontinental epiphytotics of uncertain origins. Another fungus (C. sorghi Kulkarni, Seshadri & Hegde), the anamorph of which (Sphacelia sorghi McRae) is morphologically similar to that of C. africana and also causes ergot disease of sorghum, is considered to be the pathogen endemic to the Indian subcontinent (1,2). Five isolates of endemic ergot pathogen of sorghum from different locations in Southern India were provided as C. sorghi by ICRISAT, Hyderabad. The isolates were morphologically indistinguishable when cultivated on an asparagine-sucrose-salts agar, producing a white mycelium but no spores. Suspensions of hyphal fragments of each isolate were inoculated into gaping florets of a male-sterile sorghum grown at the Chelsea Physic Garden, London, in 1998. Infection of a few florets occurred with difficulty (<0.1% efficiency) by two of the isolates (from Andhra Pradesh and Madhya Pradesh states) to give a pathology typical of C. africana (2), especially with respect to the prominent young sphacelium forcing the glumes apart before first exudation of honeydew, the low concentration of honeydew oligosaccharides, and the white cascade of secondary sporulation on honeydew. This sphacelial fructification functioned as highly infective inoculum in other inflorescences, readily producing similar pathology leading to the formation of persistently small, roughly spherical “sclerotia” that were typical of C. africana in the recent American epiphytotics, but bearing none of the sclerotial characteristics of C. sorghi. Analysis of ergot tissue from near-mature inflorescences revealed dihydroergosine, an alkaloid that differentiates C. africana from C. sorghi, together with festuclavine, the identity of which was shown by GCMS (gas chromatography-mass spectrometry) (2). This evidence from pathogen isolates was complemented by analysis of a sample of small, spherical “sclerotia” from ICRISAT that also had a similar alkaloid composition. It is therefore clear that C. africana is now in India and this influences not only the interpretation of data on sorghum ergot disease published in recent years from that region, where the identity of the pathogen may not have been rigorously monitored, but also future phytopathological strategies for sorghum more widely in Asia. References: (1) R. Bandyopadhyay et al. Plant Dis. 82:356, 1998. (2) D. E. Frederickson et al. Mycol. Res. 95:1101, 1991. (3) P. G. Mantle and H. A.-G. Hassan. Int. Sorghum Millets Newsl. 35:97, 1994. (4) E. M. Reis et al. Plant Dis. 80:463, 1996.
Outbreak of Erwinia carotovora on Zantedischia spp. in South Africa
Authors: Mansvelt E. L. , Carstens E. 
Published: May 2007

In South Africa, summer-flowering Arum lilies are grown for the tuber, potted plant, and cut flower markets. In 1998, an outbreak of soft rot was detected on Zantedischia oculata cv. Black Magic and Z. elliottiana plants from several nurseries. Crop losses of up to 25% were incurred. The initial symptom was wilting of leaves. When plants were lifted from the soil, soft rot of the tuber was found. Tuber rot usually developed on one side, and plants developing from affected tubers wilted and died. No discoloration of leaf or tuber tissues was found. Isolations from diseased tissues consistently yielded bacterial colonies that were translucent, white, and glistening and that had entire margins on nutrient agar. Ten representative isolates were chosen for further characterization. Erwinia carotovora subsp. carotovora strain B56 was included as a reference strain. All isolates were gram-negative rods, oxidase and arginine dihydrolase negative, catalase positive, and facultatively anaerobic. They degraded pectate and rotted potato slices but did not hydrolyze starch. All isolates fermented glucose, reduced nitrates to nitrites, and grew at a maximum temperature of 37°C. Isolates produced acids from D(+)-glucose, D(+)-cellobiose, melibiose, amygdalin, L(+)-arabinose, D-mannitol, L(+)-rhamnose, sucrose, ribose, D(-)xylose, and D(-)glucose but not from D-arabinose, D-sorbitol, or maltose. Isolates liquefied gelatin and used citrate, arbutine, esculin, salicin, and cellobiose as the sole carbon source. Pathogenicity to Zantedischia spp. was tested by injection of tubers with an inoculum suspension containing 108 CFU/ml. Control plants were inoculated with sterile distilled water. Inoculated plants were kept in a greenhouse at 24°C. Symptoms developed 2 days after inoculation with the pathogen and appeared to be identical to those observed on diseased material in nurseries. Control plants did not rot. The bacterium was readily reisolated from diseased plants, confirmed to be the inoculated pathogen, and identified as E. carotovora, based on morphological, biochemical, and physiological characteristics and pathogenicity. E. aroideae has been reported to cause soft rot of rhizomes of winter-flowering Arum lilies (Z. aethiopica) in South Africa (1). However, this is the first report of soft rot caused by E. carotovora subsp. carotovora on tubers of Z. oculata and Z. elliottiana plants in South Africa. Reference: (1) V. Wager. 1970. Flower Garden Diseases and Pests. Purnell, Cape Town, South Africa.
First Report of Leaf Blight on Sweet Persimmon Tree by Pestalotiopsis theae in Spain
Authors: Tuset J. J. , Hinarejos C. , Mira J. L. 
Published: May 2007

During July 1998, a leaf blight caused by Pestalotiopsis theae (Saw.) Stey. was observed at an incidence of 18 to 20% in sweet persimmon (Diospyros kaki L.fil.) orchards in Huelva Province (southwestern Spain). Symptoms appeared on leaves as large grayish brown circular ringspots. Usually, they were solitary, but occasionally, two to three spots occurred on an affected leaf. In severe cases, lesions developed on more than one-third of the leaf, resulting in defoliation. Small black acervular conidiomata were visible in the surface of spots. These conidiomata produced fusiform conidia that were straight or rarely curved, four five-celled euseptate, including three olivaceous or dark brown median cells, and hyaline apical and basal cells with appendages that were slightly constricted at septa. Conidiomata were up to 240 μm in diameter; conidiogenous cells were 6 to 13 × 1.2 to 2.8 μm; conidia were 24.7 × 7.8 μm; three median cells were 16.7 μm long; two to three apical appendages (rarely four) were 28.3 μm long; and straight basal appendage was 5.7 μm. P. theae was consistently isolated on potato dextrose agar from diseased leaves and conidiomata. To confirm pathogenicity, both mycelial plugs and a conidial suspension (1.5 × 106 conidia per ml) of the fungus were used as inocula. Young completely developed leaves from persimmon tree cvs. Sharon and Hanafuyu were inoculated in the laboratory and maintained in a moist chamber for 5 days. Lesions resembling symptoms that occurred in the field were observed on leaves after 5 days. Symptoms were not observed on control leaves inoculated with agar media or sprayed with water. The fungus reisolated from diseased leaves was identical to the original isolates. Based on the morphological characteristics of conidiomata and conidia as well as pathogenicity, the fungus was identified as P. theae (1). This is the first report of this fungus as a pathogen of D. kaki in Europe. Possibly the introduction of P. theae to Spain has been through young imported persimmon plants. Unusual climatic conditions (heavy rainfalls during 1997 in southwestern Spain) have been favorable for disease development. The hot and dry conditions that usually occur during flowering, growing, and maturation of persimmon fruits normally prevent dissemination of inoculum and infection of leaves. For these reasons, the wet areas of southwestern Spain could be more favorable for “grey blight” of persimmon trees. Reference: (1) T.-H. Chang et al. Korean J. Plant Pathol. 12:377, 1996.