bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Report of Natural Occurrence of Zucchini Lethal Chlorosis Tospovirus on Cucumber and Chrysanthemum Stem Necrosis Tospovirus on Tomato in Brazil
Authors: Nagata Tatsuya , Resende Renato de O. , Kitajima Elliot W. , Costa Helcio , Inoue-Nagata Alice K. , de Ávila Antonio C. 
Published: May 2007

During a field survey in 1994, five cucumber (Cucumis sativus) cv. Hokushin plants showing symptom of yellowing, mottling, and vein banding on the leaves were collected from a commercial field of the Federal District. By electron microscopy, quasi-spherical particles with double membrane, typical tospovirus-like particles were found in the infected leaf material. All samples strongly reacted with antibody of zucchini lethal chlorosis tospovirus (ZLCV), but not with antibodies of other to-spoviruses reported in Brazil (1): tomato spotted wilt virus (TSWV), tomato chlorotic spot virus (TCSV), groundnut ringspot virus (GRSV), chrysanthemum stem necrosis virus (CSNV), or iris yellow spot virusonion isolate (IYSV-BR). The virus was identified as ZLCV, which was first isolated in 1994 from zucchini (Cucurbita pepo) in São Paulo State, Brazil. Tomato (Lycopersicon esculentum) plants showing stem necrosis and necrotic spots and rings on the leaves were collected in Viçosa, Minas Gerais State. By electron microscopy, molecular studies, and enzyme-linked immunosorbent assay with antibodies of the six tospoviruses occurring in Brazil, the virus was identified as CSNV. This virus was first reported in 1995 on a Chrysanthemum sp. in São Paulo State and recently reported in the Netherlands from Dendranthema indicum. This is the first report of the natural occurrence of ZLCV and CSNV on cucumber and tomato, respectively. Reference: (1) A. C. de Ávila et al. 1998. Pages 32–34 in: Int. Symp. on Tospoviruses and Thrips in Floral and Vegetable Crops, 4th.
Fusarium moniliforme and F. proliferatum Isolated from Crown and Root Rot of Asparagus and Their Association with Asparagus Decline in Argentina
Authors: Lori G. , Wolcan S. , Mónaco C. 
Published: May 2007

During the summer of 1995-1996, an 80-ha field of 6-year-old asparagus plants (cv. UC 72) in Saladillo (Province of Buenos Aires) was affected by a decline syndrome (1). The plants showed a decline in vigor and approximately 60 to 70% of the plants died. The symptomatic plants were chlorotic, stunted, with stem lesions and crown and root rot. Fusarium moniliforme and F. proliferatum were isolated from vascular and epidermal tissues of roots, crowns, and stems. Identification of Fusarium to species was made by examining conidiogenous cells from colonies cultured on KCl medium (2). Microconidia were born in long and short chains and false heads. The isolates were identified based on the the presence of polyphialides in F. proliferatum and their absence in F. moniliforme, which produces monophialides only (2). In two separate trials, asparagus seeds (cv. UC 72) were surface sterilized and placed in steamed soil infested with a conidial suspension of each species. The viable propagules in the soil (CFU per g) were estimated by soil plate dilutions on Nash & Snyder-PCNB (pentachloronitrobenzene) medium. The F. moniliforme and F. proliferatum soil densities were 19.2 × 103 and 23 × 103 CFU per g of soil, respectively. The pots were placed in the greenhouse on different benches to avoid cross-contamination. After 4 months, inoculated plants showed root and crown discoloration. F. moniliforme and F. proliferatum were reisolated (64 and 75%, respectively) from discolored portions of internal and external root and crown tissues. Although the stems did not show symptoms, F. moniliforme and F. proliferatum were also recovered (27 and 38%, respectively) from asymptomatic tissues. Six months after inoculation the plants developed chlorotic symptoms with crown and root rot, and then wilted. F. moniliforme and F. proliferatum were reisolated from root systems, crowns, and stems of all inoculated plants. F. moniliforme and F. proliferatum are involved in corn stalk and ear rot in Argentina. Corn and asparagus are frequently grown in close proximity and often follow one another at a particular site. Airborne and soil debris carrying F. moniliforme and F proliferatum from corn may be an additional source of inoculum for asparagus in Argentina. The results indicate that the presence of F. moniliforme and F. proliferatum is a factor that contributes to asparagus decline in Argentina. References: (1) W. H. Elmer et al. Plant Dis. 80:117, 1996. (2) P. E. Nelson et al. Fusarium Species: An Illustrated Manual for Identification. Pennsylvania State University, University Park, 1983.
Interception of Xanthomonas campestris pv. dieffenbachiae on Anthurium Plants from the Netherlands
Authors: Sathyanarayana N. , Reddy O. R. , Latha S. , Rajak R. L. 
Published: May 2007

Xanthomonas campestris pv. dieffenbachiae, the causal agent of anthurium bacterial blight, is a major concern of the anthurium industry worldwide. This pathogen has many hosts in the family Araceae (e.g., Anthurium, Dieffenbachia, Syngonium, Aglaonema, Philodendron, Xanthosoma, Caladium, and Colocasia). Most anthurium cultivars are susceptible to bacterial blight, making it very difficult to manage the disease once introduced to a production area. Therefore, sanitation and exclusion of the pathogen through pathogen-free propagative stock are vital aspects of anthurium cultivation. The anthurium industry is expanding in India, and as many new cultivars are being imported, the plant material is subject to thorough quarantine inspection at the port of arrival. During routine inspections on three separate occasions, Anthurium andreanum plants imported from The Netherlands had watersoaked spots at leaf margins bordered by chlorotic or necrotic zones. Xanthomonas-like colonies were isolated from four different cultivars with semiselective media (2). Bacteriological tests confirmed that the cultures were X. campestris. Pathogenicity tests, performed by rubbing leaves with a cotton swab dipped into a suspension of the bacteria (approx. 107 CFU/ml), resulted in production of leafspots in 6 days and early blight symptoms in 10 to 12 days. The bacterium was further identified as X. campestris by carbon source utilization (similarity coefficient = 0.582; Biolog, Hayward, CA). Enzyme-linked immunosorbent assay reaction patterns with a panel of monoclonal antibodies for X. campestris pv. dieffenbachiae designated as Xcd1 (clone 72E-E3-B9-C5, isotype IgG2a), Xcd2 (clone 97-2-1-01, isotype IgM), Xcd3 (clone 72B-F9-B6-E9, isotype IgM), Xcd7 (clone72D-E10-C2-D9, isotype IgM), T1 (clone 92-16, isotype IgM), and T2 (clone 92-59-1-1, isotype IgG) showed that the intercepted strain belong to the serogroup 5 of X. campestris pv. dieffenbachiae (1). This pathogen is not known to occur in India, and there is high probability of risk of introduction through large-scale import of anthurium plants with either visible or latent infections. References: (1) R. L. Lipp et al. Phytopathology 82:677, 1992. (2) D. J. Norman and A. Alvarez. Plant Dis. 73:654, 1989.
Occurrence of Petunia Vein-Clearing Virus in the U.S.A.
Authors: Lockhart B. E. L. , Lesemann D.-E. 
Published: May 2007

Petunia vein-clearing virus (PVCV), a tentative member of the caulimovirus group of plant pararetroviruses, was first identified in petunia (Petunia hybrida Vilm.) in Germany in the hybrid cv. Himmelröschen (1). A similar virus was recently identified in Minnesota in the petunia cv. Fantasy Pink grown from seed in commercial greenhouses. This virus has spherical particles 46 to 47 nm in diameter in preparations negatively stained with 1% uranyl acetate or sodium phosphotungstate, pH 7.0, and which contain a double-stranded DNA genome approximately 7.3 kb in size. The virus was shown by immunoelectron microscopy (IEM) to be closely related serologically to PVCV. No serological relationship to any other caulimoviruses was detected. Like PVCV, which is transmitted only by seed and grafting, the Minnesota virus isolate was not transmitted by mechanical inoculation to petunia or any other indicator plant. Symptoms associated with infection by PVCV in cv. Fantasy Pink consisted of mild vein clearing to severe vein yellowing, and reduction in leaf size and internode length. Symptoms were most frequently expressed when plants were under water and nutrient stress. Vigorously growing plants usually showed no symptoms, and no virions were detected by IEM in partially purified extracts from such plants. This suggests that infection of petunia hybrids by seed-borne PVCV may possibly be more widespread, but may go unnoticed because virus-induced symptoms may not be elicited in plants growing under favorable conditions. References: (1) D. Lesemann and R. Casper. Phytopathology 63:1118, 1973.
First Report of Sclerotium Production by Sclerotinia sclerotiorum in Soil on Infected Soybean Seeds
Authors: Yang X. B. , Workneh F. , Lundeen P. 
Published: May 2007

Stem rot of soybean caused by Sclerotinia sclerotiorum (Lib.) de Bary was not recognized as an important problem in the North Central Region of the United States until severe outbreaks occurred in 1992, 1994, and 1996 (2). Although sclerotia mixed with seeds are known to be important to the spread of this disease, the role of internally infested soybean seed in dissemination of the disease is unknown. Tu (1) demonstrated in dry bean, which differs from soybean in seed size and plant architecture, that internally infected seeds are important to the spread of the disease, by producing sclerotia in the soil after the seeds are planted. Experiments were conducted to determine if sclerotia are formed in soils from internally infected soybean seeds. Soybean seed from a field with 70% disease severity were collected and sorted into three classes: (i) normal quality seed, which included moderate or good seed; (ii) poor quality seed (shriveled and/or whitish); and (iii) seed of regular size with visible mycelial mats (S. sclerotiorum or Peronospora manshurica (Naumov) Syd. in Gäum) on the seed coat. Transfer of surface-disinfested seeds to potato dextrose agar and subsequent production of sclerotia showed that 2, 44, and 6% of the seed from each respective class were infested with S. sclerotiorum. One hundred seeds from each of these classes were planted into sterilized and nonsterilized soil at a rate of 5 seeds per pot. Toothpicks were placed to identify the location of each seed, and seeds were covered with 2 cm of soil. Pots were placed in growth chambers with a 14-h photoperiod under two temperature regimes: (i) at 20°C; and (ii) at 10°C for 10 days and then raised to 20°C. Soil was kept saturated by periodically top watering the pots for the first 10 days and bottom watering after that. Two weeks after planting, seeds were examined for formation of sclerotia and the percentages of seeds from which sclerotia were formed were calculated. The experiments were conducted four times. One to two (occasionally three) sclerotia were found in place of each seed that did not germinate. Sclerotia were mainly found from seeds of poor quality, with an average of 12% seeds that produced sclerotia. The frequency of sclerotia found in normal quality seeds was 0.4%, and no sclerotia were found from seeds with mycelial mats. The sclerotia were 2.36 ± 1.07 mm in width, 3.33 ± 1.11 mm in length, and 6.8 ± 3.7 mg in weight, with an averaged germination rate of 88% 8 months after production. Sclerotia production frequencies were 11.4 and 15.4% for temperature regimes (i) and (ii), respectively. Higher percentages of sclerotium production were found in sterilized soil (15.6%) than nonsterilized soil (7.5%). Our results indicate the possibility of internally infected soybean seeds as a means for field-to-field dissemination of S. sclerotiorum. References: (1) J. C. Tu. J. Phytopathol. 121:40, 1988. (2) X. B. Yang. ICM Newsl. 18, 1997.
Report on First Detection of Anthracnose (Colletotrichum gloeosporioides) on Lupins in Poland
Authors: Frencel I. M. 
Published: May 2007

A previously unreported lupin disease—anthracnose (Glomerella cingulata (Stoneman) Spauld. & H. Schrenk; anamorph Colletotrichum gloeosporioides (Penz.) Penz. & Sacc. in Penz.)—was first encountered in Poland in July 1995 on white lupin (Lupinus albus L.), grown in experimental fields of the Plant Breeding Station at Wiatrowo. Initially the disease was observed on a few plants or small clusters of plants distributed randomly within the field. Distinct symptoms of anthracnose, including bending of the plant terminal and pinkish-brown lesions on stems, were first observed at the early flowering stage. Diseased stems collapsed, displaying characteristic necrotic, crook-shaped distortions. Field surveys in 1996 indicated the rapid spread of the pathogen within white lupin inbred lines, apparently from natural infection in 1995. Later in the season, symptoms of anthracnose also appeared on yellow (L. luteus L.) and narrow-leafed (L. angustifolius L.) lupins in close proximity to white lupin plots. A fungal pathogen was consistently isolated by plating surface-disinfected symptomatic stem segments on water agar. After 7 to 10 days, heavy sporulation was observed from which a single-spore subculture was made on potato dextrose agar (PDA). Conidia were one-celled, hyaline, and oblong with obtuse or rounded ends, and were 16 to 20 μm in length, consistent with the conidial descriptions of C. gloeosporioides (1). Acervuli were mostly single and setae inconspicuous. Six fungal isolates were selected to complete Koch's postulates. Conidia from PDA cultures were suspended in sterile water agar and injected into surface wounds on the main stem of white lupin plants. Moist cotton was fastened to the inoculation area for 24 h, then plants were placed in a glasshouse. Within 5 to7 days, typical lesions resembling natural symptoms developed. Symptoms did not appear on control plants. The teleomorph stage of the pathogen was not observed in the field or on inoculated plants. The potential risk of lupin seed infection by C. gloeosporioides is indicated from our preliminary bioassays. Blotter tests were done by plating surface-disinfected seeds of three white lupin seed lot (super-elite) samples, collected from experimental fields in two consecutive years. The seed-borne infection by C. gloeosporioides in samples from 1996 ranged from 9 to 12%, in comparison with no detection of seed-borne infection in 1995 samples examined. In many phytosanitary inspections of seed production fields in 1997, a high level of anthracnose, including total epiphytotics and widespread disease in lupin crops countrywide, was observed. This is the first documented report of C. gloeosporioides causing anthracnose on lupins in Poland. Reference: (1) J. A. von Arx. 1987. Plant Pathogenic Fungi. Beihefte zur Nova Hedvigia. Vol. 87. J. Cramer, ed. Berlin. pp. 218, 220.
Western Dwarf Mistletoe Parasitizing Colorado Blue Spruce and Norway Spruce in California
Authors: Mathiasen R. L. , Allison J. R. , Geils B. W. 
Published: May 2007

Western dwarf mistletoe (Arceuthobium campylopodum Engelm.), a common parasite of ponderosa pine (Pinus ponderosa Dougl. ex Laws.) and Jeffrey pine (Pinus jeffreyi Grev. & Balf.), was found parasitizing planted Colorado blue spruce (Picea pungens Engelm.) and Norway spruce (Picea abies (L.) H. Karsten) in Upper Cuddy Valley, CA (Kern County, T. 9 N., R. 21 W., Sec. 25). One tree greater than 6 m in height of each spruce species was infected and both trees were within 12 m of a Jeffrey pine severely infected with western dwarf mistletoe. Five to 10 branches were infected on each tree and a few of these had abundant mistletoe shoot production, which allowed identification of the parasite. This is the first report of western dwarf mistletoe on Colorado blue spruce. Although this is the first report of natural infection of Norway spruce in California, this mistletoe/host combination has been reported by Weir from artificial inoculation (2) and collected by Russell in central Washington (1). We recommend that these spruce species not be planted within 15 m of pines infected with western dwarf mistletoe. Specimens of western dwarf mistletoe on Colorado blue spruce and Norway spruce were collected and deposited at the Deaver Herbarium, Northern Arizona University, Flagstaff. References: (1) F. G. Hawksworth and D. Wiens. 1996. Dwarf Mistletoes: Biology, Pathology, and Systematics. USDA Agric. Handb. 709. (2) J. R. Weir. Bot. Gaz. 56:1, 1918.
Black Root Rot, Caused by Thielaviopsis basicola, on Tomato Transplants in California
Authors: Koike S. T. , Henderson D. M. 
Published: May 2007

In 1997, greenhouse-produced transplants of tomato (Lycopersicon esculentum) exhibited stunting, yellowing of leaves, and lack of vigorous growth. Roots of affected plants had numerous small (2 to 10 mm long), brown lesions. Isolations from symptomatic roots onto acidified potato dextrose agar and TBM-V8 medium (1) consistently resulted in gray fungal colonies that formed catenulate, cylindrical, hyaline endoconidia and catenulate, subrectangular, thick-walled, dark aleuriospores. The fungus was identified as Thielaviopsis basicola (Berk. & Broome) Ferraris based on colony characteristics and conidial morphology. Pathogenicity was tested by producing endoconidial suspensions of representative isolates and applying them as root drenches to 2-month-old tomato (cv. Early Girl) plants in soil-less, peat-based potting mix. Sterile, distilled water was applied to control plants. After 14 days in a greenhouse, symptoms similar to those originally observed developed and the pathogen was reisolated from lesions on the roots. Control plants developed no disease symptoms. The test was repeated and the results were similar. This is the first documentation of black root rot caused by T. basicola on tomato transplants in California. Disease incidence reached as high as 50 to 60% in certain plantings. Reference: (1) J. N. C. Maduewesi et al. Phytopathology 66:526, 1976.
First Report of Fusarium solani f. sp. glycines Causing Sudden Death Syndrome of Soybean in Canada
Authors: Anderson T. R. , Tenuta A. U. 
Published: May 2007

Sudden death syndrome (SDS), caused by Fusarium solani (Mart.) Sacc. f. sp. glycines, is a disease of soybean (Glycine max (L.) Merr.) in several central and southern states of the United States. In Ontario, Canada, individual soybean plants with typical foliar symptoms of SDS (1) have been observed annually in Kent County since 1993 but the causal organism was not isolated or identified. In 1996, plants with symptoms of SDS were observed in six fields located in Essex, Kent, and Lambton counties. Interveinal chlorosis and necrosis occurred on top leaves of affected plants and a pale brown discoloration occurred in the vascular system in lower stems and upper tap roots. Slow-growing isolates of F. solani f. sp. glycines with typical blue sporodochia were isolated from symptomatic plants on acidified potato dextrose agar (1). Root inoculation of 15 2-week-old seedlings with colonized oat kernals with each of five single-spore isolates caused typical SDS symptoms on 5-week-old soybean plants of cvs. Conrad, A2540, S19-90, and Ripley in the greenhouse. The severity and incidence of symptoms varied with cultivar and isolate. Of 125 plants inoculated, 6% of Conrad, 10% of A2540, 14% of S19-90, and 17% of Ripley plants developed foliar symptoms. Symptoms did not develop on noninoculated controls. F. solani f. sp. glycines was reisolated from roots of symptomatic plants. Although Ripley is known to have resistance to SDS (2), foliar and root symptoms developed following inoculation with each Ontario isolate of F. solani f. sp. glycines. Yield losses in 1996 were difficult to assess because of the scattered distribution of diseased plants in most fields. Diseased plants had few and poorly filled pods. In two fields, soybean growth was severely restricted in large areas covering 2 ha each; however, soybean cyst nematode (SCN) was present in both fields. SCN was present at all locations. Although total yield losses are currently low, it is evident that F. solani f. sp. glycines causing SDS has become widely distributed in southwest Ontario and disease severity is increasing. References: (1) K. W. Roy et al. Phytopathology 79:191, 1989. (2) P. A. Stevens et al. Crop Sci. 33:929, 1993.
First Record of Faba Bean Necrotic Yellows Virus and Beet Western Yellows Luteovirus Affecting Lentil and Chickpea in Pakistan
Authors: Makkouk Khaled M. , Bashir Muhammad , Jones Roger 
Published: May 2007

In an intensive survey of lentil and chickpea fields and Research Station plots in the Punjab province of Pakistan, more than 6,505 samples were collected and tested for presence of 14 different viruses by the tissue-blot immunoassay (TBIA) procedure (2). All antisera used were virus specific, including those for faba bean necrotic yellows virus (FBNYV) (1) and beet western yellows luteovirus (BWYV) (ATCC 647). Counting plants with virus symptoms greatly underestimated virus incidence in lentil crops but was a better guide to virus occurrence in chickpeas. Overall, about 1 in 5 plants of lentil were virus infected with 15% of fields having incidence over 50%. In contrast, levels of infection were mostly low in chickpea. Pea seed-borne mosaic virus (PSbMV) followed by cucumber mosaic virus (CMV), both of which are aphid- and seed-borne, were the most abundant viruses in lentils, but also occurred in chickpea. PSbMV incidence was 17% in lentil and 0.1% in chickpea fields, whereas CMV incidence was 1% in lentil and 0.1% in chickpea fields. The other viruses found on both lentil and chickpea were FBNYV, BWYV, chickpea chlorotic dwarf geminivirus, chickpea luteovirus, and alfalfa mosaic alfamovirus. Because of yield losses associated with PSbMV infection, the high levels of infection in lentils are cause for concern. This is the first record of FBNYV and BWYV affecting lentil and chickpea in Pakistan, but their incidence in the fields where they have been detected was low (less than 1%). FBNYV was detected in three of the 33 lentil and two of the 34 chickpea fields surveyed. BWYV was detected in two of the 33 lentil and three of the 34 chickpea fields surveyed. References: (1) A. Franz et al. Ann. Appl. Biol. 128:255, 1996. (2) K. M. Makkouk and A. Comeau. Eur. J. Plant Pathol. 100:71, 1994.