bluuebunny/crossref_metadata_2025_split huggingface dataset:
Absence of Oospores of Downy Mildew of Grape Caused by Plasmopara viticola as the Source of Primary Inoculum in Most Western Australian Vineyards
Authors: Killigrew B. X. , Sivasithamparam K. , Scott E. S. 
Published: May 2007

Grapevine downy mildew, caused by the obligate, oomycete pathogen, Plasmopara viticola, was first recorded in Western Australia (W.A.) in 1998 (2) and has subsequently been observed in most viticultural regions of the state. Heterothallism in P. viticola was established by Wong et al. (3), whereby more than one mating type of the pathogen is required for sexual reproduction to occur. Oospores are considered to be the source of primary inoculum for this disease with further, secondary infection being advanced by asexual inoculum. However, recent research in European vineyards suggests that the majority of infection throughout the growing season arises via sexually derived (oosporic) inoculum (1). Since downy mildew is relatively new to W.A., few surveys have been conducted to study populations of the pathogen within the state. It is also noteworthy that the incidence of oospores in Australian vineyards has not been reported. The objective of this research was to assess the occurrence and type of inoculum of P. viticola in W.A. vineyards. A total of 1,266 P. viticola-infected leaf discs (LD) from eight wine-grape (775 LD), five table-grape (450 LD), and seven unknown (41 LD) cultivars grown in 16 vineyards in 10 geographically separate regions of W.A. were collected in the growing seasons of 2001-2003. These regions range from Chittering in the north to Albany in the south and received 700 to 1,200 mm annual rainfall, mostly in winter. Each LD was cleared in 1 M KOH at 60°C for 12 to 24 h and then was assessed for the presence of oospores with light microscopy. Leaves showing “mosaic”-type lesions (older infection) late in the season were collected where possible to ensure colony maturity and an increased likelihood of oospore formation. All LD from all regions were negative for the presence of oospores except for samples from a single vineyard (approximately 1,200 mm annual rainfall), where all 140 LD from six wine-grape cultivars contained oospores. The discovery that oospores were present in only one of 16 sampled vineyards provides a rare opportunity to study gene flow in field populations of the pathogen with time and to determine sources of primary inoculum where overwintering of P. viticola may not involve oospores. References: (1) S. McKirdy et al. Plant Dis. 83:301, 1999. (2) A. Rumbou et al. Eur. J. Plant Pathol. 110:379, 2004. (3) F. P. Wong et al. Plant Pathol. 50:427, 2001.
Absence of Potato spindle tuber viroid within the Canadian Potato Industry
Authors: De Boer S. H. , DeHaan T. L. 
Published: May 2007

Potato spindle tuber viroid (PSTVd) causes a serious disease of potato, affecting yield and tuber quality. To control the disease, the Canadian seed certification program maintains a zero tolerance for the disease and a requirement that all nuclear stock, the micropropagated plantlets from which each lot of seed potatoes is initiated, is tested using reverse polyacrylamide gel electrophoresis (rPAGE) to ensure freedom from PSTVd. Moreover, seed potato fields are visually inspected during two or more annual field inspections for the presence of PSTVd and viruses. Symptoms of PSTVd have not been observed during field inspections for at least the last 25 years. Prior to 1989, seed potato stocks in the provinces of Prince Edward Island and New Brunswick were tested using rPAGE and nucleic acid dot blot hybridization for the presence of the viroid, and no infections were found (1). Similar surveys for PSTVd in Canada's western provinces of British Columbia, Alberta, and Saskatchewan also failed to detect the viroid (2). During 2000–2004, the PSTVd survey was extended to the provinces of Manitoba, Ontario, Quebec, Nova Scotia, and Newfoundland in which 211, 188, 95, 6, and 10 samples, respectively, were collected. Each sample consisted of 400 randomly selected leaves from selected potato fields representing seed lots registered in one of the four Elite seed classes or in the Foundation and Certified classes, except for a small number of samples (11%) that were from commercial nonseed fields. Leaves were tested using the dot blot procedure in composites of 50 leaves as described (2). Approximately 10% of the samples were retested using rPAGE followed by northern blotting to confirm dot blot results. All dot blot and rPAGE/northern blot results were negative for PSTVd. The cumulative results of the PSTVd surveys in all 10 Canadian provinces and the absence of the disease in the field as determined by annual visual inspection meets the International Standards of Phytosanitary Measures for the Requirements for the Establishment of Pest Free Areas (3). Hence, Canada declares that PSTVd is absent within its potato industry. A similar declaration was made by the United States recently on the basis of similar field inspection and survey data (4). References: (1) D. Coates-Milne. FAO Plant Prot. Bull. 37:130, 1989. (2) S. H. De Boer et al. Can. J. Plant Pathol. 24:372, 2002. (3) FAO. ISPM Pub. No. 4, 1996. (4) M. Sun et al. Am. J. Potato Res. 81:227, 2004.
First Report of Wheat dwarf virus in Winter Wheat in Finland
Authors: Lemmetty A. , Huusela-Veistola E. 
Published: May 2007

During June and July of 2004, several diseased plants in winter wheat (Triticum aestivum L.) were reported by agricultural advisers in the southern and southwestern coastal area of Finland. The plants showed extreme dwarfing, various yellowing symptoms, and reduced or no heading. The damage varied considerably. Yield loss estimates in direct-drilled winter wheat fields were approximately 20 to 40% and in worst cases as much as 100%. A few leafhoppers (Psammotettix alienus Dahlb.) were collected from the field with sweep nets and yellow traps. Roots and symptomatic leaves of winter wheat and the leafhoppers were first tested using a commercial polyclonal antibody (DSMZ, Braunschweig, Germany) specific for Wheat dwarf virus (WDV). For the leaf and root samples, routine double-antibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA) procedures were used. Five leafhoppers per sample were homogenized with the extraction buffer provided. The homogenate was centrifuged and the extract was evaluated using DAS-ELISA (2). The highest absorbance values were obtained from leafhoppers suspected to be viruliferous. The mean values varied from 1.002 to 1.990 after incubation in the substrate for 2 h. The absorbance values of several leaf samples exceeded the virus-positive threshold but were lower than those of the viruliferous leafhoppers. The virus was not detected in roots. Low absorbance values of virus-positive plants were confirmed using polymerase chain reaction (PCR) with primers specific for WDV (1). Total DNA extracts (DNeasy Plant Mini Kit; Qiagen, Hilden, Germany) from symptomatic leaves were tested using puRe Taq Ready-To-Go PCR beads (Amersham Biosciences, Buckinghamshire, UK). The PCR amplicon was the expected size (1,201 bp). The high absorbance value of the leafhoppers showed that the leafhoppers were carriers of the virus. These results confirmed that the causal agent of dwarfing and yellowing symptoms in winter wheat was WDV (genus Mastrevirus, family Geminiviridae). References: (1) A. Kvarnheden et al. Arch Virol 147:205, 2002. (2) J. Vacke and R. Cibulka. Plant Prot. Sci. 35:41, 2000.
First Report of Crown and Stem Rot of Orchid (Orchis palustris) Caused by Sclerotinia minor
Authors: Eken C. , Ercişli S. , Eşitken A. , Demirci E. , Yuen G. Y. 
Published: May 2007

Orchis palustris Jacq. is a wild orchid native to wetlands in eastern Anatolia. During June of 2003, near Erzurum, Turkey, a decline of this orchid was observed in several meadows that had been irrigated for forage production. Stems were chlorotic, wilted, and collapsed. There was a soft, watery rot at the crowns and lower stems. White mycelium and black sclerotia formed on necrotic stem and crown tissues. The fungus was isolated from sclerotia on potato dextrose agar (PDA) and identified as Sclerotinia minor Jagger on the basis of small sclerotia (0.5 to 2.5 mm long) scattered throughout the colonies (2). Pathogenicity was confirmed by inoculating stems of 8-week-old plants with mycelial plugs from 5-day-old PDA cultures and enclosing inoculated plants in transparent plastic bags for 3 days. After 2 weeks, symptoms similar to those in the field were observed, and S. minor was reisolated from inoculated plants. Noninoculated control plants remained asymptomatic. The disease was previously observed on O. laxiflora Lam. in Turkey (1), but to our knowledge, this is the first report of S. minor infecting O. palustris References: (1) C. Eken et al. Plant Pathol. 52:802, 2003. (2) L.M. Kohn. Phytopathology 69:881, 1979.
First Report of a Lettuce-Infecting Sequivirus in Chile
Authors: Krause-Sakate R. , Jadão A. S. , Firmino A. C. , Pavan M. A. , Zerbini F. M. , Rosales I. M. , Bustamante P. , Gall O. Le 
Published: May 2007

Sequiviruses are isometric aphidborne plant viruses. Dandelion yellow mosaic virus (DaYMV), genus Sequivirus, was isolated from dandelion and lettuce in Europe. Lettuce mottle virus (LeMoV), a putative sequivirus, is often found in mixed infections with Lettuce mosaic virus (LMV) in Brazil (3). DaYMV, LeMoV and LMV cause similar mosaics in field-grown lettuce. Differences in biology and sequence suggest that DaYMV and LeMoV are distinct species (2). Forty-two and 101 lettuce samples with mosaic symptoms collected from two locations near Santiago during a survey of lettuce viruses in Chile in 2002 and 2003, respectively, were analyzed for the presence of LeMoV using reverse transcription polymerase chain reaction (RT-PCR). Total RNA was extracted (1) and used for RT-PCR with the specific LeMoV primers pairs Lmo3 (5′ ACATGAGCACTAGTGAGG 3′) and Lmo4 (5′ AGATAGAGCCGTCT GGCG 3′) (2). One of the 42 and three of the 101 samples produced the expected 300-bp fragment. Isometric particles of 30 nm diameter, typical of a sequivirus, were visualized by transmission electron microscopy. These samples were tested using RT-PCR for the presence of LMV and Cucumber mosaic virus (CMV), but no mixed infections were observed. One isolate, Ch36, was reamplified with the degenerate primer pairs DALE 1 (5′ GARTTCAACATGCACGCCAG 3′) and DALE 2 (5′ TTTTTCTCCCCATYCGTCAT 3′) which amplify part of the putative replicase gene (2) and produced a 563-bp fragment that was cloned on pGEM-T Easy (Promega, Madison, WI) and sequenced. The Ch36 product (EMBL Accession No. AM039965) showed 97% amino acid identity with LeMoV from Brazil, 79% with DaYMV, 72% with the sequivirus Parsnip yellow fleck virus, and 34% with the waikavirus Maize chlorotic dwarf virus. To our knowledge, this is the first report of a sequivirus in field lettuce in Chile, and although the virus was found at low incidence, this report extends the range of LeMoV to the western side of the Cordillera de Los Andes. The impact of LeMoV needs to be further analyzed in Chile, Brazil, and possibly other South American countries. References: (1) Y. D. Bertheau et al. DNA amplification by polymerase chain reaction (PCR) 1998. In: Methods for the Detection and Quantification of Erwinia carotovora subsp. atroseptica on potatoes. M. C. N. Perombelon and J. M. van der Wolff, eds. Scott. Crop Res. Inst. Occasional Publ., Dundee, 1998. (2) A. S. Jadão. Caracterização parcial e desenvolvimento de oligonucleotídeos específicos para detecção de sequivirus infectando alface. Ph.D. thesis. FCA-UNESP-Botucatu, Brazil, 2004. (3) O. Stangarlin et al. Plant Dis. 84:490, 2000.
First Report of a 16SrII Group Phytoplasma Associated with Shoot Proliferation of a Cactus (Opuntia monacantha) in Lebanon
Authors: Choueiri E. , Massad R. , Jreijiri F. , Danet J. L. , Salar P. , Bové J. M. , Foissac X. 
Published: May 2007

In October 2003, during a survey to evaluate the incidence of phytoplasma diseases in Lebanon, symptoms suggestive of phytoplasma infection in Opuntia monacantha (Haworth) were observed in Saghbine, Bekaa Valley. Symptoms were excessive stem and shoot proliferation. Three symptomatic and as well as symptomless plants were collected and analyzed for the presence of phytoplasmas. Nucleic acids were extracted from 0.5 g of shoot tissue and tested using polymerase chain reaction (PCR) with universal phytoplasma primers (fU5rU3) for partial amplification of the ribosomal 16SrDNA (4). PCR resulted in amplification of an expected 881-bp rDNA fragment from the symptomatic but not from symptomless samples. For characterization, sequence of the amplified DNA was determined (Genbank Accession No. AY939815). The sequence showed a high similarity with several isolates of the 16srII group of phytoplasmas. The highest similarity has been oserved with 16S rDNA of two isolates of cactus witches'-broom phytoplasma found in China (1) and Mexico (3) (Genbank Accession Nos. AJ293216 and AF320575, respectively) (99.8%) as well as faba bean phyllody phytoplasma (Genbank Accession No. X83432) (99.7%) and “Candidatus Phytoplasma aurantifolia” (Genbank Accession No. U15442) (99.3%). The presence of phytoplasmas was confirmed using nested-PCR with primers R16mF2/R1 and R16F2n/R2 (2). The Tru9I digestion pattern of the amplified product R16F2n/F16R2 detected in O. monacantha was identical to the digestion pattern obtained from periwinkle infected by “Ca. P. aurantifolia” (subgroup 16SrII-B) and soybean phyllody phytoplasma (subgroup 16SrII-C), but different from the Tru9I digestion pattern observed for cleome phyllody phytoplasma (subgroup 16SrII-A) and tomato big bud phytoplasma (subgroup 16SrII-E). To our knowledge, this is the first report of an infection with a phytoplasma belonging to16SrII group in Lebanon. References: (1) H. Cai et al. Plant Pathol. 51:394, 2002. (2) D. E. Gundersen and I. M. Lee. Phytopathol. Mediterr. 35:144, 1996. (3) N. E. Leyva-Lopez et al. Phytopathology. (Abstr.) 89(suppl):S45, 1999. (4) B. Schneider et al. Pages 369–380 in: Molecular and Diagnostic Procedures in Mycoplasmology. Academic Press, NY, 1995.
Peach latent mosaic viroid Detected for the First Time on Almond Trees in Tunisia
Authors: Hassen I. Fekih , Roussel S. , Kummert J. , Fakhfakh H. , Marrakchi M. , Jijakli M. H. 
Published: May 2007

Almond (Prunus dulcis Mill) is an important crop in countries of the Mediterranean area. Until now, among viroids, only Hop stunt viroid (HSVd) is known to infect cultivated almond trees (2). In 2004, a survey of almond trees was carried out in orchards in different regions of Tunisia, a major producing and exporting country of almond. Symptoms such as mosaic and necrotic lesions, potentially caused by the Peach latent mosaic viroid (PLMVd), were observed on leaves of cultivated almond trees. Since PLMVd was recently detected in peach and pear trees in Tunisia (4), the presence of this viroid in almond trees was studied. The detection method on the basis of one-tube reverse transcription-polymerase chain reaction (RT-PCR) assays was previously described and validated for the detection of this viroid in fruit trees (4). Amplification products were obtained by using previously reported primer pairs of PLMVd (1). Positive controls included RNA preparations of twigs of PLMVd-infected GF 305 peach seedlings. These materials, provided by B. Pradier (Station de Quarantaine des Ligneux, Lempdes, France), were positive as revealed by chip budding on peach seedling indicator plants grown under greenhouse conditions. RT-PCR analysis of nucleic acid preparations from leaves of almond showed specific amplification products with the expected size of 337 bp for two almond trees among 17 trees tested. Nucleotide sequence analyses of cloned amplification products obtained with the PLMVd primers confirmed a size of 337 bp and revealed a sequence similar to sequences from other PLMVd isolates previously characterized. The sequences shared 94 to 98% identity with the reference isolates of PLMVd from peach (EMBL Accession No. M83545, AF170511, AF170514, and AY685181). The two infected almond trees are proximal to each other and peach trees infected with PLMVd. This suggests that one tree may have served as a source of inoculum for the other through agronomic practices such as pruning or the aphid Myzus percicae (3). Alternatively, PLMVd may have originated in an unknown host and was then transmitted to almond trees. Our investigation shows that almond is a new host for PLMVd. References: (1) N. Astruc. Eur. J. Plant Pathol. 102:837, 1996. (2) M. C. Cañizares et al. Eur. J. Plant Pathol. 105:553, 1999. (3) J. C. Desvignes et al. Phytoma 444:70, 1992. (4) I. Fekih Hassen et al. Plant Dis. 88:1164, 2004.
First Report of Leaf Spot of Spinach Caused by Stemphylium botryosum in Arizona
Authors: Koike S. T. , Matheron M. E. , du Toit L. J. 
Published: May 2007

During the winter (December through February) of 2003-2004, and again during 2004-2005, spinach (Spinacia oleracea) crops in the Yuma region of Arizona developed a foliar disease that previously had not been diagnosed in this geographic area. The problem was found on only a few acres and severity was low. The first symptoms consisted of round to oval leaf spots that were gray to olive green and visible from both adaxial and abaxial leaf surfaces. The spots were 3 to 6 mm in diameter but expanded up to as much as 10 mm. As disease progressed, leaf spots became tan and dry and papery in texture. Fungal growth was not observed on the spots. Isolations from the edges of surface-sterilized lesions onto V8 juice agar consistently resulted in fungal colonies. The fungus was identified as Stemphylium botryosum based on the following morphological characteristics of isolates incubated under fluorescent lights: dark green-to-brown mycelial growth, unbranched conidiophores with distinctly swollen apical cells that had dark bands, and dictyoconidia. The conidia were brown, ellipsoidal to ovoid, verrucose, borne singly, and measured 17 to 28 × 13 to 19 μm. To test pathogenicity, inoculum of each of five isolates (approximately 1 × 105 conidia/ml) was sprayed separately onto 20 to 25 plants each of spinach cvs. Whitney, Rushmore, Lion, Springfield, Nordic IV, and Unipak 144. Inoculated plants were incubated in a humidity chamber for 48 h and then maintained in a greenhouse (24 to 26°C). After 10 to 14 days, leaf spots resembling those seen in the field developed on all inoculated plants, and S. botryosum was reisolated from the spots. Control plants were similarly inoculated with water but did not develop symptoms. To our knowledge, this is the first report of leaf spot of spinach caused by S. botryosum in Arizona. The possibility of seedborne S. botryosum (3) may account for the development of this disease in winter spinach crops in this arid region. Leaf spot could be damaging to spinach grown in this region if rainfall is higher than normal, such as in 2004-2005. This disease has been reported in production spinach crops in California, Delaware, Florida, and Maryland (2,4) and in spinach seed crops in Washington (1). References: (1) L. J. du Toit and M. L. Derie. Plant Dis. 85:920, 2001. (2) K. L. Everts and D. K. Armentrout. Plant Dis. 85:1209, 2001. (3) P. Hernandez-Perez and L. J. du Toit. (Abstr.) Phytopathology 95:S41, 2005. (4) R. N. Raid and T. Kucharek. 2003 Florida Plant Disease Management Guide: Spinach. University of Florida, Gainesville, 2003.
Bacterial Wilt of Beans (Phaseolus vulgaris) Caused by Curtobacterium flaccumfaciens in Southeastern Spain
Authors: González A. J. , Tello J. C. , Rodicio M. R. 
Published: May 2007

Symptoms of bacterial wilt were observed on common beans (cv. Donna) in southeastern Spain. From samples collected in four different fields (coast of Granada), a bacterium was isolated with the following characteristics: gram positive, aerobic rods with yellow colonies, strictly oxidative, oxidase negative, galactose, sucrose, erythritol, mannitol, sorbitol and m-inositol were not used as a sole carbon source, and hydrolysis of casein was positive. These results coincide with what is expected for Curtobacterium flaccumfaciens pv flaccumfaciens (3). One isolate from each field was selected for pathogenicity tests using two different methods. Bacterial suspensions (approximately 108 CFU/ml) were spray inoculated on bean seedlings of cv. Andecha (10 plants with three true leaves for each isolate). Beans were covered with transparent plastic bags for 2 days and held at 25°C and 80% relative humidity with a 12-h photoperiod. In addition, 10 healthy seeds of cv. Andecha were soaked in bacterial suspensions (approximately 108 CFU/ml) for 1 h and incubated at 25°C (2). Seedlings sprayed with distilled sterile water and seeds soaked in water served as controls. With both methods of inoculation, assays were conducted twice. Results were recorded after 3 weeks. Symptoms that developed on plants after infection with the four isolates were similar to those observed in the field. They included golden yellow necrotic leaf lesions and wilting. Wilting was more pronounced in the field and when inoculation was performed by spraying seedlings rather than by soaking seeds. Control plants did not develop symptoms and grew bigger than the inoculated plants. Two pathogenic isolates were identified through sequencing of the 16S rRNA gene. The genes were amplified by polymerase chain reaction (1) and their nucleotide sequences (1,418 bp) proved to be identical (Accession No. AJ879110). Comparison of these sequences with databases showed that they were also identical to those of C. flaccumfaciens strains LMG 3645 and P 259/26 (Accession Nos. AJ312209 and AJ310414) and Curtobacterium sp. strains 2384 and 3426 (Accession Nos. AY688359 and AY688360). In Spain, the bean pathogen C. flaccumfaciens was first isolated from seeds during 2001 (4). However, to our knowledge, this is the first report of damage caused by this bacterium in the field. Bacterial wilt has been recorded, but often not substantiated, in several countries from North and South America, Africa, Asia, Oceania, and Europe. References: (1) U. Edwards et al. Nucleic Acid Res. 17:7843, 1989. (2) T. F. Hsieh et al. Plant Dis. 86:1275. 2002. (3) K. Komagata and K.-I. Suzuki. Pages 1313–1317 in: Bergey's Manual of Systematic Bacteriology. Vol. 2. Williams and Wilkins, Baltimore, MD, 1986. (4) J. L. Palomo et al. Page 154 in: XI Congreso de la Sociedad Española de Fitopatología, Almería, 2002.