Academic literature on the topic 'Eateringinna Region (S. Aust.)'

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Journal articles on the topic "Eateringinna Region (S. Aust.)"

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Litwin, Christine M., and Joel M. Johnson. "Identification, Cloning, and Expression of the CAMP-Like Factor Autotransporter Gene (cfa) of Bartonella henselae." Infection and Immunity 73, no. 7 (July 2005): 4205–13. http://dx.doi.org/10.1128/iai.73.7.4205-4213.2005.

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ABSTRACT The CAMP reaction was first described by Christie et al. (R. Christie, N. E. Atkins, and E. Munch-Petersen, Aust. J. Exp. Biol. 22:197-200, 1944) as the synergistic lysis of sheep red blood cells by Staphylococcus aureus sphingomyelinase and CAMP factor (cohemolysin), a secreted protein from group B streptococci. We observed a CAMP-like reaction when Bartonella henselae was grown in close proximity to S. aureus on 5% sheep blood agar. This study describes the cloning, sequencing, and characterization of a CAMP-like factor autotransporter gene (cfa) from B. henselae. A cosmid library of B. henselae ATCC 49793 was constructed using SuperCos1 in Escherichia coli XL1-Blue MR. Cosmids were screened for the CAMP reaction, and a quantitative cohemolysis microtiter assay was developed using purified sphingomyelinase. Cosmid clones with the strongest cohemolytic reaction had similar restriction enzyme patterns. A DNA fragment that expressed the cohemolysin determinant was subcloned in a 7,200-bp StuI-BamHI fragment which contained a 6,024-bp open reading frame. The deduced amino acid sequence showed homology to the family of autotransporters. The autotransporters are a group of proteins that mediate their own export through the outer membrane. They contain an N-terminal passenger region, the α-domain, and a C-terminal transporter region, the β-domain. The α-domain contained four, nearly identical 42-amino-acid repeats and showed homology to the family of RTX (repeat in toxin) hemolysins. The concentrated supernatant of the recombinant strain expressed a protein with a molecular mass of 180 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis consistent with the calculated molecular weight of the secreted α-domain. In conclusion, we have characterized a novel secreted cohemolysin autotransporter protein of B. henselae.
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Cronjé, C. P. R., R. A. Bailey, P. Jones, and S. Suma. "The Phytoplasma Associated with Ramu Stunt Disease of Sugarcane Is Closely Related to the White Leaf Phytoplasma Group." Plant Disease 83, no. 6 (June 1999): 588. http://dx.doi.org/10.1094/pdis.1999.83.6.588a.

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Ramu stunt disease of sugarcane (ScRS) was responsible for large yield losses in commercial sugarcane varieties (interspecific hybrids of Saccharum spp.) in the Ramu Valley in northeast Papua New Guinea during the late 1980s. Losses were total in the cultivar Ragnar; Q90 and Yasawa were also affected but Cadmus and Q107 were resistant. Since that time, replanting with resistant cultivars has kept the disease under control. The disease spreads rapidly in susceptible cultivars, where it results in severe stunting of the cane and a yellow mottled striping of the leaves. Although several attempts have been made to detect a viral pathogen, no evidence for viral etiology exists and the causal agent remains unknown. With a nested polymerase chain reaction (PCR) of general phytoplasma primers from the 16S rDNA (1), phytoplasma-specific products were consistently amplified from the leaves of field-grown sugarcane, from sugarcane with ScRS symptoms grown in the glasshouse at IACR-Rothamsted, UK, and from samples of the putative vector collected at Ramu, the delphacid plant hopper Eumetopina flavipes Muir, which had been found to transmit symptoms of Ramu stunt in pot trials (2). Digestion of the amplimers with restriction enzymes RsaI and HaeIII gave profiles that matched those of members of the sugarcane white leaf (SCWL) phytoplasma group. The DNA sequence of the intergenic spacer region of the phytoplasma associated with ScRS showed a 95.98% homology with that of SCWL, suggesting that this newly discovered phytoplasma can provisionally be placed in this group. The 16S-23S intergenic spacer sequence has been submitted to GenBank (accession no. AF 106061). References: (1) C. P. R. Cronjé et al. Ann. Appl. Biol. 133:177, 1998; (2) L. S. Kuniata et al. J. Aust. Entomol. Soc. 33:185, 1994.
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Lu, N. H., Q. Z. Huang, H. He, K. W. Li, and Y. B. Zhang. "First Report of Black Stem of Avicennia marina Caused by Fusarium equiseti in China." Plant Disease 98, no. 6 (June 2014): 843. http://dx.doi.org/10.1094/pdis-08-13-0873-pdn.

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Avicennia marina is a pioneer species of mangroves, a woody plant community that periodically emerges in the intertidal zone of estuarine regions in tropical and subtropical regions. In February 2013, a new disease that caused the stems of A. marina to blacken and die was found in Techeng Island of Zhanjiang, Guangdong Province, China. Initial symptoms of the disease were water-soaked brown spots on the biennial stems that coalesced so whole stems browned, twigs and branches withered, leaves defoliated, and finally trees died. This disease has the potential to threaten the ecology of the local A. marina community. From February to May 2013, 11 symptomatic trees were collected in three locations on the island and the pathogen was isolated as followed: tissues were surface disinfected with 75% ethanol solution (v/v) for 20 s, soaked in 0.1% mercuric chloride solution for 45 s, rinsed with sterilized water three times, dried, placed on potato dextrose agar (PDA), and incubated for 3 to 5 days at 28°C without light. Five isolates (KW1 to KW5) with different morphological characteristics were obtained, and pathogenic tests were done according Koch's postulates. Fresh wounds were made with a sterile needle on healthy biennial stems of A. marina, and mycelial plugs of each isolate were applied and covered with a piece of wet cotton to maintain moisture. All treated plants were incubated at room temperature. Similar symptoms of black stem were observed only on the stems inoculated the isolate KW5 after 35 days, while the control and all stems inoculated with the other isolates remained symptomless. An isolate similar to KW5 was re-isolated from the affected materials. The pathogenic test was repeated three times with the same conditions and it was confirmed that KW5 was the pathogen causing the black stem of A. marina. Hyphal tips of KW5 were transferred to PDA medium in petri dishes for morphological observation. After 48 to 72 h, white, orange, or brown flocculence patches of KW5 mycelium, 5.0 to 6.0 cm in diameter, grew. Tapering and spindle falciform macroconidia (11 to 17.3 μm long × 1.5 to 2.5 μm wide) with an obviously swelled central cell and narrow strips of apical cells and distinctive foot cells were visible under the optical microscope. The conidiogenous cells were intertwined with mycelia and the chlamydospores were globose and formed in clusters. These morphological characteristics of the isolate KW5 are characteristic of Fusarium equiseti (1). For molecular identification, the ITS of ribosomal DNA, β-tubulin, and EF-1α genes were amplified using the ITS4/ITS5 (5), T1/T2 (2), and EF1/EF2 (3) primer pairs. These sequences were deposited in GenBank (KF515650 for the ITS region; KF747330 for β-tubulin region, and KF747331 for EF-1α region) and showed 98 to 99% identity to F. equiseti strains (HQ332532 for ITS region, JX241676 for β-tubulin gene, and GQ505666 for EF-1α region). According to both morphological and sequences analysis, the pathogen of the black stem of A. marina was identified as F. equiseti. Similar symptoms on absorbing rootlets and trunks of A. marina had been reported in central coastal Queensland, but the pathogen was identified as Phytophthora sp. (4). Therefore, the disease reported in this paper differs from that reported in central coastal Queensland. To our knowledge, this is the first report of black stems of A. marina caused by F. equiseti in China. References: (1) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual, 1st ed. Wiley-Blackwell, Hoboken, NJ, 2006. (2) K. O'Donnell and E. Cigelnik. Mol. Phylogenet. Evol. 7:103, 1997. (3) K. O'Donnell et al. Proc. Natl. Acad. Sci. USA. 95:2044, 1998. (4) K. G. Pegg. Aust et al. Plant Pathol. 3:6, 1980. (5) A. W. Zhang et al. Plant Dis. 81:1143, 1997.
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Garibaldi, A., D. Bertetti, M. T. Amatulli, and M. L. Gullino. "First Report of Septoria Spot of Clementine Caused by Septoria citri in Italy." Plant Disease 95, no. 7 (July 2011): 873. http://dx.doi.org/10.1094/pdis-03-11-0241.

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In January 2010, a fruit spot of “Clementine” (Citrus clementina Hort. ex Tan.) was observed on Italian-grown fruit in a market in northern Italy. The surface of the peel of infected fruits had black, irregular, necrotic areas that were slightly depressed, 10 mm in diameter, and surrounded by chlorotic halos. No pycnidia were observed on the necrotic spots. Tissues beneath the necrotic spots, which included the albedo (white pith), appeared dark and a black rot affected the external part of the juice vesicles. Small sections (approximately 3 mm2) of infected internal tissues were cultured on potato dextrose agar (PDA) amended with 25 ppm of streptomycin and maintained at 22 to 24°C. A slow-growing fungus with dark colored mycelium that produced pycnidia was consistently isolated. Conidia were hyaline, elongate, straight or slightly curved, unicellular, but sometimes with one septum, and measured 9.0 to 25.4 × 1.0 to 2.7 (average 17.7 × 1.8) μm. Preliminary morphological identification of the fungal isolates resembling Septoria spp. was confirmed by PCR using genomic DNA extracted from the mycelia of pure cultures. The internal transcribed spacer (ITS) region of rDNA was amplified using the primers ITS4/ITS6 and sequenced. BLAST analysis of the 508-bp segment showed a 99% homology with the sequence of Septoria citri (GenBank Accession No. DQ897650). The nucleotide sequence has been assigned the GenBank Accession No. HQ176410. Pathogenicity of one isolate was tested by inoculating 10 fruits. These were wounded at the equatorial level (three wounds per fruit, 5 mm depth) and dipped for 10 s in a conidial suspension (1.2 × 107 conidia/ml). Ten wounded noninoculated fruits were dipped in sterilized water and served as control. Fruits were kept at 10 ± 1°C. After 50 days, dark, sunken necrosis appeared around the wounds of inoculated fruits and the same symptoms first observed were present into the tissues beneath the wounds. S. citri was consistently reisolated from the inoculated fruits. Noninoculated fruits remained healthy. The pathogenicity test was carried out twice. The same disease was observed on other fruits belonging to the Rutaceae family, such as lemon in Greece (3) and on orange and lemon in Australia (1). In Italy, S. citri has been reported on lemon (2) fruit. To our knowledge, this is the first report of the presence of this pathogen on clementine in Italy as well in the world. The presence of Septoria spot on clementine fruits is currently sporadic in Italy; however it is necessary to monitor the incidence of this disease with field and postharvest surveys. References: (1) T. G. B. Osborn and G. Samuel. Trans. R. Soc. Aust. 46:166, 1922. (2) P. Petri. Boll. Stn. Patol. Veg. Roma N.S. 16:1, 1936. (3) D. G. Zachos. FAO Plant Prot. Bull. 6:41, 1957.
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Lee, E., S. J. Wylie, and M. G. K. Jones. "First Report of ‘Candidatus Phytoplasma aurantifolia’ Associated With Severe Stunting and Necrosis on the Invasive Weed Pelargonium capitatum in Western Australia." Plant Disease 94, no. 10 (October 2010): 1264. http://dx.doi.org/10.1094/pdis-07-10-0477.

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Pelargonium capitatum (rose pelargonium) is a plant indigenous to southern Africa, originally brought to Western Australia for its ornamental qualities. It has since become naturalized in the Southwest Australian Floristic Region, recognized for its high level of species endemism, where it is a serious invasive weed in bushlands and coastal dunes. Since P. capitatum outcompetes native species it is listed among the top 10 most important coastal weeds of the region (3). In 2008, large patches of stunted, dying, and dead P. capitatum plants were observed within a population covering coastal dunes at Woodman Point, Western Australia (GPS coordinates 32°07′40.51″S, 115°45′28.39″E). Diseased plants had small misshapen leaves in clumps that were often chlorotic or pink, shortened internodes, and exhibited phylloidy typical of infection by a phytoplasma. From August 2009 to January 2010, samples from symptomatic and asymptomatic plants were collected from the site and from plants of an asymptomatic population at another site located on the Murdoch University campus nearby. DNA was extracted from 15 samples collected from symptomatic and asymptomatic plants at the dune site and from five at the campus site. Briefly, 2 to 5 g of leaf and stem tissue was cut into 5-mm pieces and shaken overnight in 30 ml of phosphate-buffered saline buffer. Supernatant was filtered and a pellet was collected by centrifugation. After resuspension in 500 μl of extraction buffer (200 mM Tris-HCl [pH 7.5] 250mM NaCl, 25mM ethylenediaminetetraacetic acid, 0.5% sodium dodecyl sulfate, and 2% polyvinylpyrrolidone), DNA was precipitated in 500 μl of cold isopropanol. Samples were tested for the presence of phytoplasma ribosomal 16S DNA by nested PCR using phytoplasma universal primers P1/P7 followed by amplification with primers Tint, R16mF2, and R16mR1 (1,2,4). Phytoplasma-specific DNA sequences were synthesized directly from amplicons using the above primers. Phytoplasma was detected from both symptomatic and asymptomatic plant samples collected from the dune site but not from the campus site. Analysis of the nine sequences obtained (GenBank Accession Nos. HM583339, HM583340, HM583341, HM583342, HM583343, HM583344, HM583345, HM583346, and HM583347) revealed high sequence identity between isolates (~99%) and with the ‘Candidatus Phytoplasma aurantifolia’ (16SrII) group of phytoplasmas (1,4). Presence of phytoplasma in symptomatic plants was confirmed by histological examination of stem sections stained with Dienes' stain. This finding is significant because there is potential for utilizing this phytoplasma to control P. capitatum where it has invaded ecologically significant sites, although its effect on indigenous plants must be determined first. Although phytoplasmas within the 16SrII group have been identified in Australia previously (1,4), to our knowledge, this is the first report of it infecting P. capitatum. References: (1) K. S. Gibb et al. Phytopathology 85:169, 1995. (2) D. E. Gundersen and I.-M. Lee. Phytopathol. Mediterr. 35:144, 1996. (3) B. M. J. Hussey et al. Western Weeds. A Guide to the Weeds of Western Australia. 2nd ed. Plant Protection Society of Western Australia, Victoria Park, 2007. (4) M. Saqib et al. J. R. Soc. West. Aust. 90:175, 2007.
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Mathew, F. M., R. S. Goswami, S. G. Markell, L. Osborne, C. Tande, and B. Ruden. "First Report of Ascochyta Blight of Field Pea Caused by Ascochyta pisi in South Dakota." Plant Disease 94, no. 6 (June 2010): 789. http://dx.doi.org/10.1094/pdis-94-6-0789a.

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Tan lesions approximately 1.7 × 0.8 cm with distinct dark brown margins and small pycnidia were observed on leaves of field peas (Pisum sativum L. ‘Agassiz’) growing in Campbell County, South Dakota (45°45.62′N, 100°9.13′W) in July 2008. Small pieces of symptomatic leaves were surface sterilized (10% NaOCl for 1 min, 70% EtOH for 1 min, and sterile distilled H2O for 2 min) and placed on potato dextrose agar (PDA) for 7 days under fluorescent lights with a 12-h photoperiod to induce sporulation. A pure culture was established by streaking a conidial suspension on PDA and isolating a single germinated spore 3 days later. The culture was grown on clarified V8 media for 10 days. Conidia were 10 to 16 × 3 to 4.5 μm and uniseptate with a slightly constricted septum, similar to those of Ascochyta pisi Lib. The exuding spore mass from pycnidia growing on the medium was carrot red. No chlamydospores or pseudothecia were observed (1,2). To confirm the identity of A. pisi, DNA was extracted from the lyophilized mycelium of the 10-day-old culture with the DNeasy Plant Mini Kit (Qiagen, Valencia, CA). Internal transcribed spacer (ITS) regions I and II were amplified with PCR primers ITS 5 and ITS 4 (3). PCR amplicons were cleaned and directly sequenced in both directions using the primers. A BLASTN search against the NCBI nonredundant nucleotide database was performed using the consensus sequence generated by alignment of the forward and reverse sequences for this region. The consensus sequence (GenBank Accession No. GU722316) most closely matched A. pisi var. pisi strain (GenBank Accession No. EU167557). These observations confirm the identity of the fungus as A. pisi. A suspension of 1 × 106 conidia/ml of the isolate was spray inoculated to runoff on 10 replicate plants of 2-week-old, susceptible green field pea ‘Sterling’. Plants were incubated in a dew chamber for 48 h at 18°C and moved to the greenhouse bench where they were maintained at 20 to 25°C with a 12-h photoperiod for 1 week. Tan lesions with dark margins appeared 7 days after inoculation and disease was assessed after 10 days (4). No symptoms were observed on water-treated control plants. A. pisi was reisolated from lesions and confirmed by DNA sequencing of the ITS region, fulfilling Koch's postulates. Currently, states bordering South Dakota (North Dakota and Montana) lead the United States in field pea production. Although acreage is limited in South Dakota, the identification of A. pisi in this region is serious. The disease is yield limiting and foliar fungicides are used for disease management (1). To our knowledge, this is the first report of Ascochyta blight on P. sativum caused by A. pisi occurring in South Dakota and the MonDak production region (the Dakotas and Montana). References: (1) T. W. Bretag et al. Aust. J. Agric. Res. 57:88, 2006. (2) A. S. Lawyer. Page 11 in: The Compendium of Pea Diseases. D. J. Hagedorn, ed. The American Phytopathological Society, St Paul, MN, 1984. (3) T. J. White et al. Page 315 in: PCR Protocols: A Guide to Methods and Applications. M. A. Innis et al., eds. Academic Press, San Diego, 1990. (4) J. M. Wroth. Can. J. Bot. 76:1955, 1998.
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Zhao, S., G. Xie, H. Zhao, H. Li, and C. Li. "First Report of a Leaf Spot on Snow Lotus Caused by Alternaria carthami in China." Plant Disease 92, no. 2 (February 2008): 318. http://dx.doi.org/10.1094/pdis-92-2-0318b.

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Snow lotus (Saussurea involucrata Karel. & Kir. ex Sch. Bip.) is an economically important medicinal herb increasingly grown in China in recent years. In June of 2005, a leaf spot disease on commercially grown plants was found in the QiTai Region, south of the Tianshan Mountain area of Xinjiang, China at 2,100 m above sea level. Disease incidence was approximately 60 to 70% of the plants during the 2006 and 2007 growing seasons. Initial symptoms appeared on older leaves as irregularly shaped, minute, dark brown-to-black spots, with yellow borders on the edge of the leaflet blade by July. As the disease progressed, the lesions expanded, causing the leaflets to turn brown, shrivel, and die. A fungus was consistently isolated from the margins of these lesions on potato dextrose agar. Fifty-eight isolates were obtained that produced abundant conidia in the dark. Conidia were usually solitary, rarely in chains of two, ellipsoid to obclavate, with 6 to 11 transverse and one longitudinal or oblique septum. Conidia measured 60 to 80 × 20 to 30 μm, including a filamentous beak (13 to 47 × 3.5 to 6 μm). According to the morphology, and when compared with the standard reference strains, the causal organism of leaf spot of snow lotus was identified as Alternaria carthami (1,4). Pathogenicity of the strains was tested on snow lotus seedlings at the six-leaf stage. The lower leaves of 20 plants were sprayed until runoff with conidial suspensions of 1 × 104 spores mL–1, and five plants sprayed with sterile distilled water served as controls. All plants were covered with a polyethylene bag, incubated at 25°C for 2 days, and subsequently transferred to a growth chamber at 25°C with a 16-h photoperiod. Light brown lesions developed within 10 days on leaflet margins in all inoculated plants. The pathogen was reisolated from inoculated leaves, and isolates were deposited at the Key Oasis Eco-agriculture Laboratory of Xinjiang Production and Construction Group, Xinjiang and the Institute of Biotechnology, Zhejiang University. No reports of a spot disease caused by A. carthami on snow lotus leaves have been found, although this pathogen has been reported on safflower in western Canada (3), Australia (2), India (1), and China (4). To our knowledge, this is the first report of a leaf spot caused by A. carthami on snow lotus in China. References: (1) S. Chowdhury. J. Indian Bot. Soc. 23:59, 1944. (2) J. A. G. Irwin. Aust. J. Exp. Agric. Anim. Husb. 16:921, 1976. (3) G. A. Petrie. Can. Plant Dis. Surv. 54:155, 1974. (4) T. Y. Zhang. J. Yunnan Agric. Univ.17:320, 2002.
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Khangura, R., and M. Aberra. "First Report of Charcoal Rot on Canola Caused by Macrophomina phaseolina in Western Australia." Plant Disease 93, no. 6 (June 2009): 666. http://dx.doi.org/10.1094/pdis-93-6-0666c.

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In the spring of 2006, canola (Brassica napus L.) plants suffering from wilt were observed in an experimental plot at Merredin, Western Australia. Symptoms on the affected plants were tan-brown, longitudinal streaks along the main stem and on some lateral branches. Lesions on the stem were predominantly unilateral but sometimes covered the entire stem. Some of the lateral branches were completely wilted, and if present, pods were either shriveled or contained small seed. At the base of the stem, the lesions were grayish brown streaks that caused longitudinal splitting of the stem base. Small spherical (55 to 75 μm in diameter) and elongated (75 to 120 μm long) microsclerotia were seen in the pith and vascular region. Roots appeared to be symptomless, but upon removing the epidermis, grayish streaks were also seen on the roots and small sclerotia were observed in the pith and the vascular region of roots. One hundred and four small pieces (1 to 2 cm) of stem and root from 10 symptomatic plants were surface sterilized with 1.25% NaOCl, rinsed twice in sterile distilled water, and plated on potato dextrose agar (PDA) supplemented with 10 ppm of aureomycin. These were incubated under a blacklight at 22°C. Macrophomina phaseolina (Tassi) Goid. was isolated from 80% of the pieces as identified by colony morphology and the size of microsclerotia that ranged between 50 and 190 μm (3). Eight-three isolates were obtained. None of the isolates produced pycnidia on PDA. However, pycnidia (100 to 190 μm) with pycnidiospores (17.5 to 30 × 7.5 to 10 μm) were produced on the affected stems collected from the field. Pathogenicity tests with one of the isolates were conducted on seven 2-week-old canola plants (cv. Stubby). Three uninoculated plants served as the control. Roots of 2-week-old plants were dipped in an aqueous conidial suspension (1 × 104 conidia/ml) of M. phaseolina for an hour while roots of control plants were dipped in sterile water. Inoculated and control plants were repotted in separate pots and transferred to a glasshouse. A week after inoculation, M. phaseolina produced chlorosis of the leaves, and subsequently, complete wilting and death of the inoculated plants. M. phaseolina was successfully reisolated from roots and stems of symptomatic plants. No symptoms developed on the control plants. Pathogenicity was also tested by soaking seeds of cv. Stubby with an aqueous conidial suspension of M. phaseolina for one-half hour and incubating on agar media after drying. Germinating seeds were colonized by the growing mycelium and seedlings were completely killed within a week. Abundant microsclerotia were produced on the dead seedlings. M. phaseolina has been previously reported on canola in the United States (1) and Argentina (2) and more recently has been reported on canola in eastern Australia (4). To our knowledge, this is the first record of occurrence of M. phaseolina on canola in Western Australia and its impact on canola yield needs to be determined. References: (1) R. E. Baird et al. Plant Dis. 78:316, 1994. (2) S. A. Gaetán et al. Plant Dis. 90:524, 2006. (3) P. Holliday and E. Punithalingam. Macrophomina phaseolina. No. 275 in: Descriptions of Plant Pathogenic Fungi and Bacteria. CMI, Kew, Surrey, UK, 1970. (4) M. Li et al. Aust. Plant Dis. Notes 2:93, 2007.
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Ramdial, H. A., and S. N. Rampersad. "First Report of Fusarium solani Causing Fruit Rot of Sweet Pepper in Trinidad." Plant Disease 94, no. 11 (November 2010): 1375. http://dx.doi.org/10.1094/pdis-06-10-0433.

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In Trinidad, sweet pepper (Capsicum annuum L.) is an important crop that is produced for local markets and regional export. From February to April 2010, severe fruit rot was observed in 9 of 11 commercial fields located in North Trinidad in the major production areas of North and South Aranguez. All fields were in the late harvesting stage and the most commonly grown cultivars were Aristotle and Canape. Disease incidence for each field was estimated to be 80% with a yield loss of 40 to 60%. Symptoms appeared on mature red fruits but growers reported that disease can also occur on green fruit. Symptoms began as soft lesions that turned dark brown to black. Lesions usually originated at the calyx end of the fruit and extended down the sides. Fruits were surface sterilized by rinsing with 70% ethanol for 2 min, followed by three rinses with sterile distilled water. Two 4-mm3 blocks of tissue from the opposite sides of fruit lesions were transferred to water agar and incubated for 5 to 7 days at 25 ± 1°C. A 4-mm3 agar block consisting of the leading mycelial edge was then transferred to potato dextrose agar (PDA) and incubated under the same conditions. Colonies on PDA were fast growing with white, fluffy, aerial mycelia; hyphae were septate and hyaline; conidiophores were unbranched; microconidia were abundant, thin walled, hyaline, ovoid, one to two celled, and measured 6 to 10 × 2 to 4 μm. Macroconidia were hyaline, three to four celled, curved, thick walled, and measured 20 to 30 × 4 to 6 μm. PCR amplification was carried out utilizing universal primers ITS4/5 and translation elongation factor primers EF1/2 (2). Sequence comparisons of the internal transcribed spacer (ITS) region (HM157262) and EF-1α gene (HQ014854) with cognate sequences available in GenBank and the FUSARIUM-ID databases revealed 100 and 99.6% sequence identity, respectively, to Fusarium solani (Mart.) Sacc. Pathogenicity tests were conducted by drop inoculating 10-μl of spore suspension (106 spores/ml) of each of four isolates on wounded and unwounded sites of mature sweet pepper fruits (five per isolate of cvs. Aristotle, Canape, Century, Destra, and Paladin). Control fruits were inoculated with sterile distilled water. Inoculated fruits were kept at 25 ± 1°C in loosely sealed plastic containers and monitored for the onset of symptoms for 6 days. The experiment was conducted twice. Lesions (8.0 to 15.2 mm in diameter) developed on wounded fruit of Aristotle, Canape, and Century. No symptoms were seen on Destra, Paladin, or the water controls. No symptoms developed on nonwounded fruits. Koch's postulates were fulfilled by reisolating the pathogen from infected tissues. Fruit rot caused by F. solani has been reported to be a serious constraint to sweet pepper production in Canada (4), the United Kingdom (1), and New Zealand (3). To our knowledge, this is the first report of Fusarium fruit rot of sweet pepper in Trinidad. References: (1) J. T. Fletcher. Plant Pathol. 43:225, 1994. (2) D. M. Geiser et al. Eur. J. Plant Pathol. 110:473, 2004. (3) J. L. Tyson. Aust. Plant Pathol. 30:375, 2001. (4) R. Utkhede and S. Mathur. Plant Dis. 87:100, 2003.
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Bratsch, S., D. Mollov, B. Lockhart, D. Johnson, and S. Ehlenbeck. "First Report of Cucumber mosaic virus Infection in Pachysandra in the United States." Plant Disease 99, no. 3 (March 2015): 422. http://dx.doi.org/10.1094/pdis-09-14-0974-pdn.

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Pachysandra terminalis Siebold & Zucc. (Japanese pachysandra, spurge) is widely used as a groundcover. In early 2012, Japanese pachysandra plants from Missouri, which originated in Pennsylvania, showed symptoms of light and dark green mosaic, leaf deformation, concentric ringspots, and stunting. Initial screening of symptomatic leaf tissue by transmission electron microscopy (TEM) using partially purified extracts confirmed the presence of spherical (~28 nm) and bacilliform (18-nm diameter, 35- to 58-nm length) virus particles. Immunosorbent electron microscopy (ISEM) using antisera to a clover isolate of Alfalfa mosaic virus (AMV) (PVAS 92) and to Cucumber mosaic virus (CMV) (ATCC PVAS-30) obtained from the American Type Culture Collection, Manassas, VA, confirmed the presence of AMV and CMV. No other type of virus-like particles were observed by TEM. After 6 months, nearly 20% of the 4,000 pachysandra cuttings exhibited the described symptoms. However, it is possible that more than 20% of the cuttings were infected with both viruses and not yet exhibiting symptoms. Reverse-transcription PCR (RT-PCR) was done using total RNA extracted with a Qiagen RNeasy kit and Ready-To-Go RT-PCR beads (GE Healthcare, UK Limited, UK). The primer pair CMV-1 (5′-GCCGTAAGCTGGATGGACCA) and CMV-2 (5′-TATGATAAGAAGCTTGTTTTCGCG) were used (3) to obtain a 502-bp amplicon from the coat protein (CP) region of CMV RNA 3. The product was ligated and cloned (pGEM-T Easy Vector System; Promega, USA). Three clones were sequenced (UMGC, USA), and the consensus sequence (Sequencher 5.1, Gene Codes Corp., USA) was deposited in GenBank (Accession No. JX227938). The sequence obtained had 100% identity with a homologous CP CMV sequence (AFQ94058) and 99% identity with several other homologous CP CMV sequences (CAX62443, CCK24369, and 15 others). It also contained an EcoRI site at nucleotides 332 to 337, characteristic of CMV Type II isolates (3). The primer pair AMV1F (5′-ATCCACCGATGCCAGCCTTA) and AMV1R (5′-TTCCGCCTCACTGCTGCTG) generated a 1,047-bp product from AMV RNA1 that was deposited in GenBank (JX227937). This product had 100% identity with a homologous AMV sequence (AFQ94057), and 99% identity with several other homologous AMV sequences (AGV15824, ADO85715, CBX36144). From the data presented here, it was concluded that the pachysandra had a mixed infection of AMV and a Type II isolate of CMV. Occurrence of AMV in pachysandra was first reported in New Jersey in 1982 (2) and reported for the first time in France and Germany in 2000 (1). The presence of CMV infection in pachysandra has not been reported in the present literature. Some of the symptoms associated with AMV infection in pachysandra in New Jersey (2) and Europe (1) were similar to the symptoms produced by pachysandra plants infected with both viruses (ring spots, mosaic, and line patterns). However, some symptoms were unique to the mixed infection in pachysandra by AMV and CMV (leaf deformation, stunting). A potential source of this co-infection could occur when plants are grown near alfalfa fields (AMV infection by aphids) and undergo vegetative propagation (CMV infection by contaminated tools). This is the first report of pachysandra co-infected by AMV and CMV in the United States. References: (1) L. Cardin and B. Moury. Plant Dis. 84:594, 2000. (2) D. E. Hershman and E. H. Varney. Plant Dis. 66:1195, 1982. (3) S. Wylie et al. Aust. J. Agric. Res. 44:41, 1993.
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Dissertations / Theses on the topic "Eateringinna Region (S. Aust.)"

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Conor, Colin H. H. "The geology of the Eateringinna 1:100 000 sheet area, eastern Musgrave Block, South Australia /." Title page, contents and abstract only, 1987. http://web4.library.adelaide.edu.au/theses/09SM/09smc753.pdf.

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Layton, Ronald A. "Sustainability issues in the Central Mount Lofty Ranges." Title page, table of contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09ENV/09envl429.pdf.

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Bibliography: leaves 78-83. "The dissertation brings together discourses relating to sustainability with that of the environment, at least in terms of its meaning and responses to it being culturally constructed. The Central Adelaide Hills provides the locality for achieving this, which a peri-urban environment is subject to the power exerted by urban Adelaide as well as the tension arising out of land use conflict and attitudes to the environment."
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Barrett, Brian Edward. "Water-borne geophysics for Murray River salt-load detection." Title page, contents and abstract only, 2003. http://web4.library.adelaide.edu.au/theses/09SM/09smb2741.pdf.

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Includes bibliographical references (leaves 112-115) Towed DC Resistivity and Transient Electromagnetic arrays have been trialled for suitability in monitoring salt-loads on the Murray River at Waikerie, South Australia.
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Puckridge, James Terence. "The role of hydrology in the ecology of Cooper Creek, Central Australia : implications for the flood pulse concept /." Title page, abstract and contents only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09php9774.pdf.

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Higginson, Gareth Edward. "The ecotourism potential of the Barber Inlet Wetlands, South Australia." Title page, table of contents and abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09ENV/09envh637.pdf.

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Bibliography: leaves 127-134. This thesis argues for the expansion of ecotourism in the Adelaide metropolitan Barker Inlet Wetlands, currently used for small scale ecotourism. Through analysing current literature and evaluating a range of ecotourism strategies, it demonstrates that the potential for and offers guidelines for ecotourism in the Barker Inlet Wetlands. Opprtunities for expansion lie primarily in environmental education, with a particular focus on Adelaide secondary schools.
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French, Rachel. "Modelling urban runoff : volume and pollutant concentration of the Barker Inlet Wetland Catchment." Title page, abstract and contents only, 1999. http://web4.library.adelaide.edu.au/theses/09ENS/09ensf875.pdf.

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Bibliography :leaves 158-171. A monitoring program, funded by the South Australian government (through the former MFP Development Corporation), was established to monitor the quality and quantity of storm water entering and leaving the wetland. This study formed part of the funded program. Simple regression models were developed; and will assist in the monitoring of performance of the wetland to alleviate the pollutant load into the Barker Inlet.
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Rea, Naomi. "The influence of water regime on the population ecology of two emergent macrophytes in South Australia /." Title page, contents and summary only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phr281.pdf.

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Spriggs, Shelley. "Participatory decision making : new democracy or new delirium? /." [Richmond, N.S.W.] : Faculty of Environmental Management & Agriculture, University of Western Sydney, Hawkesbury, 1999. http://library.uws.edu.au/adt-NUWS/public/adt-NUWS20030505.110740/index.html.

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Dwyer, Brian James. "Aspects of governance and public participation in remediation of the Murray-Darling Basin /." View thesis, 2004. http://library.uws.edu.au/adt-NUWS/public/adt-NUWS20060517.130206/index.html.

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Thesis (Ph.D.) -- University of Western Sydney, 2004.
"A thesis submitted for the degree of Doctor of Philosophy of the University of Western Sydney, Sydney, January 2004." Includes bibliography : leaves 359 - 369.
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Conor, Colin H. H. (Colin Hugh Holford). "The geology of the Eateringinna 1:100 000 sheet area, eastern Musgrave Block, South Australia." 1987. http://web4.library.adelaide.edu.au/theses/09SM/09smc753.pdf.

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Books on the topic "Eateringinna Region (S. Aust.)"

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Hayk, Khachʻatryan. Hazaragitaran: Teghekatu hushamatyan. Erevan: "Amaras", 2003.

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