bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Report of Formosan Michelia Seedling Root Rot Caused by Pythium splendens in Taiwan
Authors: Fu C. H. , Chen C. M. , Hsieh H. J. 
Published: May 2007

Formosan michelia (Michelia compressa (Maxim.) Sargent) is a valuable evergreen tree in Taiwan that is distributed from low to medium (200 to 1,800 m) altitudes. In many nurseries in Taiwan, Formosan michelia seedlings grow poorly or wilt. The etiology of the disease observed in April 2004 in a nursery in Jinshan was investigated. Diseased seedlings with chlorotic leaves and decayed feeder roots lost leaves, died back, and then wilted. The putative pathogen, Pythium splendens Braun, was isolated and identified on a morphological basis (1). P. splendens was isolated from the roots of diseased seedlings on 2% water agar with 100 ppm of ampicillin. Isolates increased daily on potato dextrose agar at 24°C by 27 to 30 mm and on malt extract agar (MEA) by 23 to 25 mm. No zoosporangia and zoospores were produced. The main hyphae were as much as 9 μm wide on MEA. Hyphal swellings were abundant, globose, smooth, terminal, and 33 to 42 μm in diameter, often with dark, densely granulated contents. Attempted matings of four P. splendens isolates in V8 medium failed. To prove pathogenicity, the four isolates were cultured in 300-ml flasks containing 150 ml of 2% malt extract medium at room temperature for 14 days. The mycelia were homogenized in sterile water at 4,500 rpm for 5 min. The suspension was adjusted to 5 × 106 hyphal swellings per ml. Roots of the 2-month-old seedlings were immersed in the suspension for 2 h, whereas the control seedlings were immersed in sterilized water. Five seedlings of each of three replicates were inoculated with one of the four isolates for a total of 60 seedlings. Controls were replicated in the same way. The inoculated plants were transplanted into plastic flowerpots containing sterilized peat and moss and kept in the greenhouse at 20 to 24°C. After 14 days, inoculated seedlings developed symptoms like those of the original plants. The putative pathogen was reisolated from the roots of inoculated plants. Cultures are maintained at the Forest Pathology Lab of the National Taiwan University. To our knowledge, this is the first report of proof of pathogenicity of P. splendens on Formosan michelia seedlings. Reference: (1) A. J. Van der Plaats-Niterink. Stud. Mycol. 21:151, 1981.
First Report of Cherry green ring mottle virus on Sweet Cherry in Poland
Authors: Komorowska B. , Cieślińska M. 
Published: May 2007

Cherry green ring mottle virus (CGRMV), a member of the genus Foveavirus, infects several Prunus species including sweet cherry, sour cherry, ornamental cherry, peach, and apricot throughout North America and Europe. On sour cherry, the virus causes leaf yellowing and dark mottle around secondary veins. Sweet cherry trees are symptomless hosts of CGRMV. During the 2004 growing season, 27 sour and sweet cherry trees were tested for the presence of CGRMV. RNA was isolated from leaves using an RNeasy kit (Qiagen GmbH, Hilden, Germany) and then evaluated by reverse transcription-polymerase chain reaction (RT-PCR) amplification. Two primer sets, GRMV7956/GRMV8316 (1) and NCP5/NCP3 (2), were used for amplification of the CGRMV coat protein gene (807 bp) or its fragment (366 bp), respectively. The cDNA fragments were cloned into bacterial vector pCR 2.1-TOPO, sequenced and analyzed using the Lasergene (DNASTAR, Madison, WI) computer program. Nucleotide sequence of the C328 isolate (GenBank Accession No. AY841279) was compared with corresponding regions of published sequences of CGRMV isolates. The nucleotide sequence of this isolate was 98% identical to the Leb isolate (GenBank Accession No. AF533157) from sour cherry. The lowest similarity (80%) was between the CP sequences of isolate C328 and an isolate from apricot (GenBank Accession No. AY172334.1). Results of biological indexing on Prunus serrulata ‘Shirofugen’ and ‘Kwanzan’ confirmed the infection of ‘Star’ sweet cherry with CGRMV. The indicators showed leaf epinasty and necrosis of fragments of midrib or veins characteristic for CGRMV (2). The CGRMV infection of the indicators was confirmed using RT-PCR. References: (1) M. E. Rott and W. Jelkmann. Eur. J. Plant Pathol. 107:411, 2001. (2) Y. Zhang et al. J. Gen. Virol. 79:2275, 1998.
First Report of Phytophthora cactorum Causing Fruit Rot on Avocado in Spain
Authors: López-Herrera C. J. , Pérez-Jiménez R. M. , Zea-Bonilla T. 
Published: May 2007

The area of avocado (Persea americana Mill.) orchards in southern Spain has increased recently and is currently at 8,063 ha. Avocado production in this part of Spain was 72,581 t during 2003. During February 2004, apical necrosis was observed on avocado fruits (cv. Hass) in one orchard in Vélez-Málaga, Málaga Province, southern Spain. Dark brown lesions and necrotic flecking of the flesh also were observed on fruits. Isolations from the skin of the fruit previously washed with tap water and disinfested with 20% sodium hypochlorite on potato dextrose agar (PDA) consistently resulted in mycelial colonies. Sporangia produced on V8 juice by successive washing of mycelia with saline solution (1) measured 31 to 37.2 (33.3) × 21.7 to 28.8 (24.2) μm in size. The pathogen was identified as Phytophthora cactorum on the basis of morphological structures (mycelia, sporangia, chlamydospores, and oospores) formed when grown on V8 juice and PDA (2). To confirm pathogenicity, a mycelial suspension was obtained by blending mycelia grown for 1 week on PDA in 200 ml of sterile water. Three healthy avocado fruits were inoculated with the suspension by injection; three other fruits were inoculated by placing a drop of suspension on the unbroken skin of the fruit. The same number of fruit was inoculated as controls using sterile water instead of mycelial suspension. The inoculated fruits were incubated for 5 days in a moist chamber at 24°C in darkness. Spots appeared on all fruits for both inoculation methods, and the pathogen was isolated and identified as P. cactorum. No symptoms appeared on the control fruits. To our knowledge, this is the first report of P. cactorum causing fruit rot on avocado in Spain. References: (1) D. Chen and G. A. Zentmeyer. Mycologia 62:397, 1970. (2) G. M. Waterhouse and J. M. Waterston. No. 111 in: Descriptions of Pathogenic Fungi and Bacteria. CMI, Kew, Surrey, UK, 1966.
A Begomovirus Associated with Leaf Curling and Chlorosis of Soybean in Sinaloa, Mexico is Related to Pepper golden mosaic virus
Authors: Méndez-Lozano J. , Quintero-Zamora E. , Barbosa-Jasso M. P. , Leyva-López N. E. , Garzón-Tiznado J. A. , Argüello-Astorga G. R. 
Published: May 2007

Since June 2001, symptoms of yellowing, leaf curling, crumpling, and stunted growth were observed on soybean (Glycine max Merr.) plants in Sinaloa, Mexico. These symptoms and the presence of whiteflies (Bemisia tabaci Gennadius) in the affected fields suggested a viral etiology. Samples from symptomatic plants were collected from commercial fields and analyzed for the presence of begomoviruses using DNA hybridization, and as a probe, the DNA A of Pepper huasteco virus at low stringency (2). Thirty-five positive samples were subsequently used for polymerase chain reaction (PCR) amplification with the degenerate primers RepMot and CPMot (1). These primers direct the amplification of a DNA A segment comprising the entire intergenic region (IR) and the first 210 bp of the coat protein (CP) gene, which is highly variable in size and nucleotide sequence among begomoviruses. PCR products were obtained for 25 of 35 samples and five of these were cloned into the pGEM-T easy vector (Promega, Madison, WI) and sequenced. The 571-bp DNA sequence (GenBank Accession No. AY905553) was compared with sequences of other begomoviruses in GenBank using the Clustal alignment method (MegAlign, DNASTAR software, London). The sequence was 74 and 70% identical to the Pepper golden mosaic virus (PepGMV; GenBank Accession No. U57457) and Cabbage leaf curl virus (CaLCuV; GenBank Accession No. U65529) sequences, respectively. Interestingly, the partial coat protein gene sequence (210 nt) of this soybean-infecting virus was 98% identical to the CP gene of Tobacco apical stunt virus (TbASV; GenBank Accession No. AF076855). Nonetheless, the known sequence of TbASV intergenic region (GenBank Accession No. AF077744) is very different from the homologous region of the soybean virus (34% of nucleotide identity). Analysis of the soybean virus intergenic region revealed that it harbors almost identical iterons (i.e., Rep-binding sites) to PepGMV, suggesting a close relationship between these two viruses. Soybean-infecting geminiviruses have been previously reported only from Asia; however, the partial sequence of a begomovirus isolated from soybean in Brazil was recently deposited in Genbank (Accession No. AY436328). Sequence comparisons between the Brazilian and Mexican isolates showed these viruses are less related with a nucleotide identity of 46%. Taken together, our data indicate that the virus identified in this study might be either a different strain of PepGMV adapted to leguminous plants or a new begomovirus species. To our knowledge, this is the first report of a begomovirus infecting soybean in Mexico. References: (1) J. T. Ascencio-Ibañez et al. Plant Dis. 86:692, 2002. (2) J. Méndez-Lozano et al. Phytopathology 93:270, 2003.
First Report in Sweden of Downy Mildew on Parsley Caused by Plasmopara petroselini
Authors: Amein T. , Olsson C. H. B. , Wikström M. , Findus R , AB D , Wright S. A. I. 
Published: May 2007

During September 2004, downy mildew of parsley caused by a species of Plasmopara was observed in an experimental field of parsley (Petroselinum crispum subsp. crispum L. cv. Gigante d'Italia/Hilmar) in Borgeby in southern Sweden. The summer of 2004 was exceptionally wet and humid. Disease became widespread throughout the field in just a few days. Local growers reported that symptoms consistent with downy mildew had appeared in their parsley fields every year since 2001. Plasmopara, under P. nivea, has been reported on parsley in Europe since the middle of the 19th century (4). In recent years, this disease has caused severe damage to parsley grown in several European countries, e.g., France, Germany, Switzerland, and Belgium (1,3). The first symptoms appeared as faint chlorotic spots on the upper surfaces of the leaves. On the corresponding lower surfaces, mycelium and sporangiophores grew profusely and developed a white mat that in part turned dark gray. Eventually, the leaves and stalks became necrotic and died. The sporangiophores were monopodially branched, 248.4 ± 13.36 μm long (n = 17), each branch ending in 2 to 5 ultimate branchlets tapered toward the tip. The trunk diameter measured 7.0 ± 0.77 μm (n = 9) above the basal part and 6.1 ± 0.81 μm just below the first branch. The sporangia were broadly ellipsoidal to ellipsoidal, hyaline, 22.5 ± 0.73 μm long and 16.6 ± 0.48 μm wide (n μ 40). They were mostly nonpapillate when young, although exit pores 4.8 ± 0.32 μm (n = 10) were visible. Mature sporangia exhibited a dehiscence apparatus and a plug in the exit pore. On the basis of the characteristics above, the pathogen was identified as P. petroselini (= P. nivea pro parte [2]). Independent verification of the identity was done by O. Constantinescu at the Botanical Museum, Uppsala, Sweden. A voucher specimen was deposited at the Herbarium UPS, in Uppsala under the number UPS F-118873. To our knowledge, this is the first report of P. petroselini on parsley in Sweden. References: (1) E. Bèliard and J. Thibault. Phytoma 554:2, 2002. (2) O. Constantinescu. Taxon 54:813, 2005. (3) C. Crepel and S. Inghelbrecht. Plant Dis. 87:1266, 2003. (4) A. de Bary, Ann. Sci. Nat. Bot., Sér. 4, 20:5, 1863.
Beet Root-Rot Inducing Isolates of Fusarium oxysporum from Colorado and Montana
Authors: Hanson L. E. , Jacobsen B. J. 
Published: May 2007

A root-tip rot of sugar beet (Beta vulgaris L.) caused by Fusarium oxysporum Schlecht. emend. Snyd. & Hans. has been reported from Texas (2). This disease is typified by yellowing of the foliage, vascular discoloration, and a rot of the root tip. During 2002 and 2003, sugar beet samples from several fields in Colorado and Montana, some with tip rot symptoms, were received by the authors. Isolations were made from the root vascular tissue and tissue adjacent to the rot in Colorado and from the rot tissue in Montana. Isolates of Fusarium were obtained and identified as Fusarium oxysporum. At the ARS laboratory in Colorado, F. oxysporum isolates were tested for pathogenicity by dipping roots of 5-week-old sugar beet plants (FC716) in a suspension of 104 spores per ml for 8 min, 10 plants per isolate. One known isolate of F. oxysporum f. sp. betae that causes Fusarium yellows, Fob13, was used for comparison. For a negative control, plants were dipped in sterile water. Beets were planted in Cone-Tainers (3.8 cm in diameter × 21 cm) containing pasteurized potting mix. Plants were placed in a greenhouse at 24 to 27°C and fertilized with 15-30-15 fertilizer every 2 weeks to avoid chlorosis from nutrient deficiency. Plants were rated weekly for foliar symptoms for 6 weeks with a Fusarium yellows rating scale of 0 to 4, in which 0 = no disease and 4 = complete plant death (1). After the final rating, plants were removed from the soil and the taproot was examined for rot symptoms. Root segments were surface disinfested with 0.5% sodium hypochlorite and cultured on potato dextrose agar to confirm the presence of the pathogen. The experiment was done twice. Six of ten F. oxysporum isolates tested caused root vascular discoloration and foliar symptoms, including interveinal yellowing and wilting, of inoculated plants. A rot of the root tip was observed on the roots of plants inoculated with three of the six pathogenic isolates. Isolate Fob13 caused only vascular discoloration and foliar symptoms with no rot. Similar experiments were done in Montana with the exception that 3-week-old plants (cv. Monohikari) were used and planted in 10-cm plastic pots with five seedlings per pot. Inoculum levels were 105 spores per ml of F. oxysporum f. sp. betae (isolate 216C) or tip rot isolates (3 isolates), and the experiments were terminated 4 weeks after planting. The root rot isolates caused foliar symptoms, vascular discoloration, and root rot similar to that seen in the field, whereas isolate 216C caused only foliar wilt symptoms and vascular discoloration. Isolations from inoculated plants in Colorado and Montana resulted in F. oxysporum cultures similar to those used in inoculation. To our knowledge, this is the first report of F. oxysporum causing root rot of sugar beet outside of Texas. References: (1) L. E. Hanson and A. L. J. Hill. Sugarbeet Res. 41:163, 2004. (2) R. M. Harveson and C. M. Rush. Plant Dis. 82:1039, 1998.
First Report of Phomopsis Fruit Decay on Apple Caused by Phomopsis mali in Greece
Authors: Karaoglanidis G. S. , Bardas G. 
Published: May 2007

From 2002 to 2005, a previously unreported disease causing significant yield losses was observed on apple fruits (cv. Red Chief) in the region of Imathia in northern Greece. Almost all apple orchards in that area, cultivated with Red Chief, showed disease symptoms on 3 to 10% of the fruits. Diseased fruits showed irregularly shaped, water-soaked areas on the skin and extensive decay internally. In most of the fruits, decay appeared to initiate internally from the calyx tube. Infected fruits remained firm during the early stages of decay. Fungal isolates obtained from small pieces of decayed tissue on potato dextrose agar (PDA) medium were identified as Phomopsis mali Roberts on the basis of morphological characteristics (2). Cultures grew rapidly on PDA at 22°C in the dark. They were initially white, but approximately 30 days after inoculation they turned gray because of the formation of pycnidia that contained α- and β-spores. α -Spores were short and elliptical in shape (8 to 10 × 2 to 3 μm) while β-spores were long (22 to 25 × 1 to 2 μm). Pathogenicity of the isolated cultures was tested by wound inoculating five mature apple fruits (cv. Red Chief) after surface sterilization with 0.5% NaOCl. PDA plugs, 5 mm in diameter with actively growing mycelium, were transferred into the flesh of the fruits. Sterile PDA plugs were used to inoculate five control apple fruits. Inoculated fruits were kept at 23°C for 10 days in the growth chamber. Extensive decay, similar to that observed on diseased fruits in the field, was observed on the inoculated fruits, whereas control fruits showed no decay. P. mali was reisolated from the decayed tissues. Commercial losses due to fruit decay caused by the pathogen have previously been reported in the United States and Northern Ireland (1). To our knowledge, this is the first report of Phomopsis fruit decay on apples in Greece. References: (1) A. C. Jones and H. S. Aldwinckle eds. Compendium of Apple and Pear Diseases. The American Phytopathological Society. St. Paul, MN, 1990. (2) D. A. Rosenberger and T. J. Burr.
First Report of Tomato spotted wilt virus on Tomatoes in Lebanon
Authors: Abou-Jawdah Y. , El Mohtar C. , Sobh H. , Nakhla M. K. 
Published: May 2007

During the spring and summer of 2004, an epidemic of Tomato spotted wilt virus (TSWV) (genus Tospovirus, family Bunyaviridae) was observed in an isolated tomato field at an elevation of 1,000 m in Lebanon. Symptoms were characteristic of TSWV (2). Seedlings came from a nursery in the coastal area of Byblos. In the spring of 2005, TSWV-like symptoms (2) appeared on tomato in the same mountainous area, as well as on tomato, pepper, and lettuce crops in the Byblos coastal area. Initial diagnosis using TSWV ImmunoStrip Tests (Agdia, IN) gave positive results on tomato and lettuce samples. When these samples were analyzed using reverse transcription-polymerase chain reaction, a specific band (619 nt) was observed in symptomatic samples but not in healthy controls (1). Amplicons were cloned into the pGEM-T easy vector (Promega, Madison, WI) and three clones were sequenced in both directions (GenBank Accession No. DQ131804). Sequence analysis revealed more than 99% nucleotide identity (GenBank Accession Nos. AY744476, AJ297611, and AJ418781) and 99% amino acid identity and 100% amino acid similarity (GenBank Accession Nos. AAU95409, CAA85356, and CAD11452) to the nucleocapsid protein of several TSWV isolates. To our knowledge, this is the first report of TSWV in Lebanon. To prevent rapid spread, farmers were informed about the disease, its vector, and appropriate preventive control measures. References: (1) S. Adkins and E. N. Rosskopf. Plant Dis. 86:1310, 2002. (2) G. Marchoux et al. Plant Pathol. 40:347, 1991.
First Report of Onion (Allium cepa) Naturally Infected with Iris yellow spot virus in Peru
Authors: Mullis S. W. , Gitaitis R. D. , Nischwitz C. , Csinos A. S. , Rafael Mallaupoma Z. C. , Inguil Rojas E. H. 
Published: May 2007

Onions have become an important export crop for Peru during the last few years. The onions produced for export are primarily short-day onions and include Grano- or Granex-type sweet onions. The first of two growing seasons for onion in Peru occurs from February/March until September/October and the second occurs from September/October to December/January. Iris yellow spot virus (IYSV [family Bunyaviridae, genus Tospovirus]), primarily transmitted by onion thrips (Thrips tabaci), has been reported in many countries during recent years, including the United States (1,2). In South America, the virus was reported in Brazil during 1999 (3) and most recently in Chile during 2005 (4). During 2003, an investigation of necrotic lesions and dieback in onions grown near the towns of Supe and Ica, Peru led to the discovery of IYSV in this region. Of 25 samples of symptomatic plants collected from five different fields near Supe, 19 tested strongly positive and an additional three tested weakly positive for IYSV using double antibody sandwich-enzyme linked immunosorbent assay (DAS-ELISA) (Agdia Inc., Elkhart, IN). None of the samples tested positive for Tomato spotted wilt virus (TSWV). A number of onions with necrosis and dieback symptoms were also observed during 2004 and 2005. During September 2005, 25 plants with symptoms suspected to be caused by IYSV or TSWV in the Supe and Casma valleys were collected and screened for both viruses using DAS-ELISA. All plants screened were positive for IYSV. There was no serological indication of TSWV infection in these samples. The positive samples were blotted onto FTA cards (Whatman Inc., U.K.) to bind the viral RNA for preservation and processed according to the manufacturer's protocols. The presence of IYSV was verified by reverse transcription-polymerase chain reaction (RTPCR) using (5′-TCAGAAATCGAGAAACTT-3′) and (5′-TAATTATATCTATCTTTCTTGG-3′) as forward and reverse primers (1), respectively. The primers amplify the nucleocapsid (N) gene of IYSV, and the RT-PCR products from this reaction were analyzed with gel electrophoresis with an ethidium bromide stain in 0.8% agarose to verify the presence of this amplicon in the samples. Subsequent to the September 2005 sampling, 72 additional samples from regions in northern and southern Peru were analyzed in the same manner. The amplicons obtained were cloned, sequenced, and compared with known IYSV isolates for further verification. Onions have become a significant export crop for Peru, and more research is needed to determine the impact of IYSV on the Peruvian onion export crop. To our knowledge, this is the first report of IYSV in onion in Peru. References: (1) L. du Toit et al. Plant Dis. 88:222, 2004. (2) S. W. Mullis et al. Plant Dis. 88:1285, 2004. (3) L. Pozzer et al. Plant Dis. 83:345, 1999. (4) M. Rosales et al. Plant Dis. 89:1245, 2005.
Natural Occurrence of Chilli veinal mottle virus on Capsicum chinense in China
Authors: Wang J. , Liu Z. , Niu S. , Peng M. , Wang D. , Weng Z. , Xiong Z. 
Published: May 2007

An outbreak of a viral disease on chili pepper (Capsicum chinense Jacp. cv. Yellow Lantern) occurred in Hainan Province, China during 2003 and 2004. The disease was prevalent in five chili-producing counties surveyed. Leaves of infected plants initially displayed symptoms of dark green banding along veins and later became distorted with striking mosaic. Infected plants had reduced flower numbers and fruit set, resulting in a significant yield loss. The causative virus was characterized and identified as Chilli veinal mottle virus (ChiVMV) (3). An isolate of the virus was obtained via three single lesion passages through Chenopodium amaranticolor and was shown to reproduce the same symptoms on inoculated C. chinense cv. Yellow Lantern. Negative staining of crude extracts of the infected tissue and subsequent electron microscopy revealed flexuous rods of 12 to 13 × 750 nm, typical of a potyvirus. Pinwheel-like inclusion bodies were abundant in thin sections of infected leaves. Purified virus preparations contained one major protein of 32.8 kDa and one minor protein of 28 kDa when fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Both of these protein bands were excised and subsequently analyzed using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Multiple peptide fragments from both proteins were identified as arising from ChiVMV capsid protein (CP) (1,2). Therefore, the 32.8-kDa protein is the full-length ChiVMV CP and the 28-kDa protein is presumably a degradation product of the CP. The combined biological and molecular data provided strong evidence that the viral disease on C. chinense was caused by ChiVMV. To our knowledge, this is the first report of ChiVMV infection on C. chinense in China and the first report of C. amaranticolor as an experimental host for ChiVMV. References: (1) P. Chiemsombat et al. Arch. Virol. 143:1855, 1998. (2). J. Joseph and H. S. Savithri. Arch. Virol. 144:1679, 1999. (3) P. Siriwong et al. Plant Pathol. 44:718, 1995.