scholarly journals Occurrence of Black Dot of Potato Caused by Colletotrichum coccodes in Central Italy

Plant Disease ◽  
2002 ◽  
Vol 86 (5) ◽  
pp. 562-562 ◽  
Author(s):  
R. Buonaurio ◽  
G. Natalini ◽  
L. Covarelli ◽  
C. Cappelli

Between 1997 and 2000, black dot of potato (Solanum tuberosum L.), caused by the polyphagous soilborne fungus Colletotrichum coccodes (Wallr.) Hughes, was observed each summer in fields located in Umbria (central Italy). Disease incidence ranged from 50 to 100%, and early potato cultivars were generally more susceptible than late-maturing ones. Disease symptoms were first observed during August as a yellowing and wilting of foliage in the tops of plants, followed by rotting of the roots and stems, which led to the premature death of 50 to 70% of plants. Setose1 sclerotia (300 to 500 mm in diameter) and acervuli of the fungus were found on roots and stems of infected plants. Acervuli produced hyaline, aseptate, cylindrical conidia (16 to 22 × 2.5 to 4.5 μm) formed on unicellular cylindrical phialidic conidiophores. The fungus was isolated from diseased stems and roots on potato dextrose agar (PDA) at pH 6.5. Pathogenicity of the fungus was confirmed by fulfilling Koch's postulates using 3- to 4-week-old potato plants of a local cultivar. A superficial 5-mm vertical cut was made with a scalpel into the base of potato stems (2 cm beneath the soil surface), and 5-mm-diameter plugs of PDA alone (control plants) or PDA plus fungal growth were placed over the cuts. The wounds were sealed with wet cotton swabs that were held in place with Parafilm. Symptoms that resembled those in the field were observed on inoculated plants 6 to 8 weeks postinoculation. Symptoms did not appear on the control plants. The same fungus was reisolated from the diseased plants. Based on morphological characteristics of sclerotia, acervuli, and conidia, as well as pathogenicity tests, the fungus was identified as C. coccodes. To our knowledge, this is the first report of C. coccodes as the causal agent of black dot of potato in central Italy. We did not observe foliar outbreaks of the disease, which were reported from the United States (2). In both 1921 (1) and 1951 (3), the fungus was reported to cause severe outbreaks of the disease in northern Italy. Since then, its presence in Italy has been rarely recorded in potato (4). The occurrence of extremely dry and hot weather conditions during the summers of 1997 to 2000, which are favorable for disease development, made the disease particularly severe. We cannot exclude the possibility that the disease may have been present in central Italy before our observations, as it can be misdiagnosed and its symptoms can be masked by the symptoms of other diseases. The significance of black dot in central Italy needs to be reappraised in terms of both yield loss and tuber quality. References: (1) C. Arnaudi. Atti Ist. Bot. Univ. Pavia. Ser. 3, 1:71, 1924. (2) A. W. Barkdoll and J. R. Davis. Plant Dis. 76:131, 1992. (3) G. Goidanich. Inf. Fitopatol. 1:5, 1951. (4) S. Vitale et al. J. Plant Pathol. 80:265, 1998.

Plant Disease ◽  
2005 ◽  
Vol 89 (5) ◽  
pp. 530-530 ◽  
Author(s):  
S. Gaetán ◽  
M. Madia

Canola (Brassica napus) was introduced as an alternative crop for wheat in Argentina. During 2003, typical symptoms of stem rot disease were observed on canola plants in two commercial fields located at Bragado, in northern Buenos Aires Province in Argentina. Average disease incidence across four canola cultivars was 21% (range = 13 to 29%). Symptoms included chlorosis and wilting of foliage and necrosis of basal stems. The disease appeared singly or in patches consisting of 4- to 5-month-old plants. The first visible symptom noticed was chlorosis and wilting of the foliage beginning from the basal leaves. Infection of the main stem at ground level typically was followed by a grayish white discoloration that progressed above the soil line to the apex. In advanced stages of the disease, stems and branches became bleached and eventually died. Black and irregularly shaped sclerotia (average size 5.5 × 2.8 mm) inside necrotic stem tissue were the typical signs of the pathogen. From September to October 2003, four samples consisting of six affected plants per sample were arbitrarily collected from two commercial fields located at Bragado. Sclerotia were taken from diseased stems, dipped in 70% ethanol, surface sterilized with 1% sodium hypochlorite for 1 min, and rinsed in sterile water. Each sclerotium was blotted dry on sterile Whatman's filter paper and placed on potato dextrose agar. Plates were incubated in the dark at 25°C for 2 to 3 days, followed by incubation under 12-h NUV light/12-h dark for 6 to 8 days. Six resulting colonies were identified as Sclerotinia sclerotiorum (Lib.) de Bary on the basis of taxonomic characteristics of the plant pathogenic species of Sclerotinia (3). Koch's postulates for three fungal isolates from infected plants were carried out on 6-week-old canola plants (cvs. Eclipse, Impulse, Master, and Mistral) by placing a colonized agar disk into wounds made in the basal stem region with a sterile scalpel. Pathogenicity tests, which included five inoculated and three control plants potted in a sterilized soil mix (soil/sand, 3:1), were conducted in a greenhouse at 23 to 26°C and 75% relative humidity with no supplemental light. Characteristic symptoms identical to the original observations developed within 12 days after inoculation on 100% of the inoculated plants for three isolates. Symptoms included wilted foliage, collapsed plants, and plant death. White mycelium and sclerotia developed on infected tissues, and the pathogen was successfully reisolated from symptomatic plants in all instances. Control plants, which were treated similarly except that the agar disk did not contain fungal growth, remained healthy. The experiment was repeated, and the results were identical to the first inoculations. Canola stem rot disease incited by S. sclerotiorum was first reported in Argentina during 1995 at experimental field plots in Buenos Aires. S. sclerotiorum, which has been reported to cause disease in canola in Canada (2) and the United States (1,4), currently represents a serious problem to the main canola cultivars grown in Argentina. To our knowledge, this is the first report of the occurrence of S. sclerotiorum causing a high incidence of stem rot in commercial crops of canola in Argentina. References: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (2) L. B. Jamaux et al. Plant Pathol. 44:22, 1995. (3) L. M. Kohn. Phytopathology 69:881, 1979. (4) D. V. Phillips et al. Phytopathology 92:785, 2002.


Plant Disease ◽  
2011 ◽  
Vol 95 (6) ◽  
pp. 775-775 ◽  
Author(s):  
V. Ayala-Escobar ◽  
V. Santiago-Santiago ◽  
A. Madariaga-Navarrete ◽  
A. Castañeda-Vildozola ◽  
C. Nava-Diaz

Bougainvillea (Bougainvillea spectabilis Willd) growing in 28 gardens during 2009 showed 100% disease incidence and 3 to 7% disease severity. Bougainvilleas with white flowers were the most affected. Symptoms consisted of light brown spots with dark brown margins visible on adaxial and abaxial sides of the leaves. Spots were circular, 2 to 7 mm in diameter, often surrounded by a chlorotic halo, and delimited by major leaf veins. Single-spore cultures were incubated at 24°C under near UV light for 7 days to obtain conidia. Pathogenicity was confirmed by spraying a conidial suspension (1 × 104 spores/ml) on leaves of potted bougainvillea plants (white, red, yellow, and purple flowers), incubating the plants in a dew chamber for 48 h and maintaining them in a greenhouse (20 to 24°C). Identical symptoms to those observed at the residential gardens appeared on inoculated plants after 45 to 60 days. The fungus was reisolated from inoculated plants that showed typical symptoms. No symptoms developed on control plants treated with sterile distilled water. The fungus produced distinct stromata that were dark brown, spherical to irregular, and 20 to 24 μm in diameter. Conidiophores were simple, born from the stromata, loose to dense fascicles, brown, straight to curved, not branched, zero to two septate, 14 × 2 μm, with two to four conspicuous and darkened scars. The conidia formed singly, were brown, broad, ellipsoid, obclavate, straight to curved with three to four septa, 40 × 4 μm, and finely verrucous with thick hilum at the end. Fungal DNA from the single-spore cultures was obtained using a commercial DNA Extraction Kit (Qiagen, Valencia, CA); ribosomal DNA was amplified with ITS5 and ITS4 primers and sequenced. The sequence was deposited at the National Center for Biotechnology Information Database (GenBank Accession Nos. HQ231216 and HQ231217). The symptoms (4), morphological characteristics (1,2,4), and pathogenicity test confirm the identity of the fungus as Passalora bougainvilleae (Muntañola) Castañeda & Braun (= Cercosporidium bougainvilleae Muntañola). This pathogen has been reported from Argentina, Brazil, Brunei, China, Cuba, El Salvador, India, Indonesia, Jamaica, Japan, Thailand, the United States, and Venezuela (3). To our knowledge, this is the first report of this disease on B. spectabilis Willd in Mexico. P. bougainvilleae may become an important disease of bougainvillea plants in tropical and subtropical areas of Mexico. References: (1) U. Braun and R. R. Castañeda. Cryptogam. Bot. 2/3:289, 1991. (2) M. B. Ellis. More Dematiaceous Hypomycetes. Commonwealth Mycological Institute, Kew, Surrey, UK, 1976. (3) C. Nakashima et al. Fungal Divers. 26:257, 2007. (4) K. L. Nechet and B. A. Halfeld-Vieira. Acta Amazonica 38:585, 2008.


Plant Disease ◽  
2011 ◽  
Vol 95 (11) ◽  
pp. 1480-1480 ◽  
Author(s):  
S. E. Cho ◽  
J. H. Park ◽  
M. J. Park ◽  
H. D. Shin

Ambrosia trifida L., commonly known as giant ragweed, is native to North America and was introduced to Korea in the 1970s (3). It is now widely naturalized, and since 1999, has been designated as one of 11 ‘harmful nonindigenous plants’ by the Korean Ministry of Environment because of its adverse effects on native plants. Various strategies to eradicate this noxious weed have been tried without any success (3). In September 2009, powdery mildew infections of giant ragweed were found for the first time in Dongducheon, Korea, and specimens were isolated and deposited in the Korea University Herbarium (KUS-F24683). White mycelial and conidial growth was present mostly on adaxial leaf surfaces with sparse growth on abaxial leaf sides. Severely infected leaves were malformed. Slight purplish discoloration occurred on the leaves contiguous with colony growth. Mycelial colonies were conspicuous, amphigenous, and epiphytic with indistinct to nipple-shaped appressoria. Conidiophores were 80 to 180 μm long and produced two to five immature conidia in chains. Conidia were ellipsoid or doliiform, 28 to 38 × 16 to 24 μm, and lacked distinct fibrosin bodies. Chasmothecia were amphigenous, scattered or partly clustered, dark brown, spherical, 95 to 130 μm in diameter, and contained 6 to 16 asci. Appendages were mycelioid, numbering 10 to 24 per chasmothecium, 0.5 to 2.5 times as long as the chasmothecial diameter, 1 to 4 septate, and were brown at the base and becoming paler toward the tip. Asci were short stalked, 50 to 75 × 32 to 42 μm and contained two spores. Ascospores were ellipsoid-ovoid with a dimension of 22 to 30 × 15 to 18 μm. On the basis of these morphological characteristics, this fungus was identified as Golovinomyces ambrosiae (Schwein.) U. Braun & R.T.A. Cook (= G. cichoracearum var. latisporus (U. Braun) U. Braun) (1). To confirm the identification, the complete internal transcribed spacer (ITS) region of rDNA from KUS-F24683 was amplified with the primers ITS5 and P3 and sequenced (4). The resulting sequence of 508 bp was deposited in GenBank (Accession No. JF907589) and was identical to the ITS sequences of G. ambropsiae on A. artemisiifolia var. elatior from Japan (AB077631) and Korea (JF919680) as well as on A. trifida from the United States (AF011292). Therefore, the sequence analysis verified the pathogen to be G. ambrosiae. To our knowledge, this is the first record of powdery mildew infections on giant ragweed outside of North America (2). Although the disease incidence is still low, the disease could be a limiting factor to suppress the expansion of this noxious weed in Korea. References: (1) U. Braun and R. T. A. Cook. Mycol. Res. 113:616, 2009. (2) D. F. Farr and A. Y. Rossman. Fungal Databases. Systematic Mycology and Microbiology Laboratory, ARS, USDA. Retrieved from http://nt.ars-grin.gov/fungaldatabases/ , May 5, 2011. (3) S. M. Oh et al. Impacts of Invasive Alien Weeds and Control Strategies of Noxious Weeds in Korea. National Institute of Agricultural Science and Technology, Suwon, Korea, 2007. (4) S. Takamatsu et al. Mycol. Res. 111:117, 2009.


2019 ◽  
Vol 20 (1) ◽  
pp. 35-37
Author(s):  
Bindu Poudel ◽  
Shouan Zhang

Phasey bean (Macroptilium lathyroides) is a member of the family Fabaceae and is native to tropical America. During the fall of 2017, the leaves of phasey bean plants in Homestead, FL, showed white powdery fungal growth. The morphological characteristics suggested that the pathogen was powdery mildew. For further identification, genomic DNA was extracted from conidia. BLAST results showed that the sequence of FL-1 shares 99% identity to an Erysiphe fallax. Phylogenetic analysis confirmed the closest proximity of FL-1 isolate to E. fallax. Koch’s postulates were performed to confirm the pathogenicity.


Plant Disease ◽  
1999 ◽  
Vol 83 (11) ◽  
pp. 1073-1073 ◽  
Author(s):  
J. E. Adaskaveg ◽  
H. Förster ◽  
J. H. Connell

A fruit rot of almond (Prunus dulcis (Mill.) D. Webb.) was observed in an orchard in Durham, CA (Butte County), in June of 1998 after an unusually wet spring with a total precipitation of 17.2 cm for April and May. Disease incidence on fully developed fruit of almond cv. Sonora was nearly 90% in the lower tree canopy by July. Almond cv. Nonpareil grown in alternate rows in the same orchard was much less affected. Fruit symptoms included extensive grayish brown discolored and shriveled hulls, often associated with a clear gum secretion and shriveled kernels. Affected fruit frequently abscised. Leaf symptoms and branch dieback were not associated with the disease in 1998. In May of 1999, however, extensive twig dieback was observed on almond cv. Sonora in the same orchard. Isolations from more than 100 symptomatic fruit were conducted from 9 sampling sites in the 9-ha orchard. Based on morphological characteristics, the same fungus was isolated from 93% of the fruit. The fungus also was isolated consistently from samples exhibiting twig dieback. During a major disease survey conducted in 1998, the fungus was only incidentally isolated from almond fruit from other California orchards. Ascomata were not observed in vivo or in vitro. The fungus produced alpha and beta spores in pycnidia when cultured on potato dextrose agar. Spore measurements were obtained from 10 spores for each of 3 isolates obtained from fruit or twig dieback of almond cv. Sonora. Conidial dimensions of fruit and twig isolates were very similar. Based on spore sizes, with alpha spores measuring 5.3 to 7.5 (to 8) × 1.7 to 2.5 μm and beta spores measuring12.8 to 29.8 × 0.6 to 0.7 μm, the fungus was tentatively identified as Phomopsis amygdali (Del.) Tuset & Portilla (2). Previous reports on this fungus (2), however, indicated that beta spores are not produced in culture, and disease symptoms have not been observed on fruit. The fungus was morphologically different from other species of Phomopsis reported from almond and other Prunus species, including P. mali Roberts, P. padina (Sacc. & Roum.) Died., P. parabolica Petrak, P. perniciosa Grove, P. pruni (Ellis & Dearn.) Wehm., P. prunorum (Cooke) Grove, P. ribetejana Camara, and P. stipata (Lib.) Sutton (3). Field inoculation studies were performed in May of 1999 on almond cvs. Carmel and Mission. Almond fruit were wounded (2 × 2 × 2 mm) or left unwounded and were sprayed with water (control) or a suspension of alpha spores (105 spores per ml). Branches were bagged for 4 days to maintain high humidity. Fruit symptoms on cv. Carmel were observed after 4 weeks on wounded and nonwounded inoculated fruit, and P. amygdali was successfully reisolated from diseased tissue. No symptoms were observed in the control treatment for almond cv. Carmel or in any treatment for cv. Mission. This is the first report of P. amygdali causing a late spring and summer fruit rot and associated branch dieback of almond in North America (1). References: (1) D. F. Farr et al. 1989. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN. (2) J. J. Tuset and M. T. Portilla. Taxonomic status of Fusicoccum amygdali and Phomopsis amygdalina. Can. J. Bot. 67:1275, 1989. (3) F. A. Uecker. 1988. A World List of Phomopsis Names with Notes on Nomenclature, Morphology, and Biology. Mycologia Memoir No. 13. J. Cramer, Berlin.


Plant Disease ◽  
2006 ◽  
Vol 90 (8) ◽  
pp. 1114-1114 ◽  
Author(s):  
A. Garibaldi ◽  
G. Gilardi ◽  
M. L. Gullino

During the summer of 2005, plants of potato (Solanum tuberosum L.) showing severe basal rot symptoms were observed in a commercial field near Alessandria (northern Italy). The first symptoms were detected during early July in correspondence with a strong increase of air temperature (as much as 38°C, with an average monthly increase of 10°C) and relative humidity. Infected plants showed dry collar rots and extensive necrosis of cortical tissues. Leaves of infected plants were chlorotic. As the disease progressed, tubers rotted and plants wilted. Infected plants appeared in patches, encompassing 10 to 15% of the cultivated area. In the presence of abundant moisture, a white mycelium occurred on infected tissues. On their surface, infected tubers showed a fan-like mycelial growth. Later, white or light-to-dark brown sclerotia (2 to 4 mm in diameter) developed from mycelium. Clamp connections were present. The diseased tissue was disinfested for 1 min in 1% NaOCl and plated on potato dextrose agar (PDA) amended with 100 mg/liter of streptomycin sulfate. Sclerotium rolfsii was consistently isolated from infected plants. Pathogenicity of one isolate obtained from infected plants was confirmed by inoculating healthy S. tuberosum plants (cv. Hermes) grown in 2:l volume pots (1 plant per pot, seven replicates). Inoculum that consisted of 1 g/pot of wheat kernels infested with mycelium and sclerotia was placed on the soil surface. Seven noninoculated plants served as controls. The inoculation trial was repeated once. Plants were kept at temperatures ranging between 25 and 32°C and watered as needed. Inoculated plants developed symptoms of leaf yellowing within 10 days, soon followed by the appearance of white mycelium and sclerotia and then eventually wilted. Control plants remained symptomless. Sclerotium rolfsii was reisolated from inoculated plants.Possible attacks of Sclerotium rolfsii on S. tuberosum were described as rarely occurring in southern Italy (3). The disease, detected at the moment in very few farms and on cvs. Hermes and Monalisa, was particularly severe on the last variety, causing 5 to 15% yield losses because of premature plant death and rotting of tubers. This disease has been reported in several countries such as India (1), Israel (2), and the United States of America (4). References: (1) N. S. Bisht. Indian Phytopathol. 35:148, 1982. (2) Y. Elad et al. Soil Biol. Biochem. 16:381, 1984. (3) R. Gigante. Ital. Agric. 87:263, 1946. (4) G. F. Weber. Phytopathology, 33:615, 1943.


Plant Disease ◽  
2004 ◽  
Vol 88 (10) ◽  
pp. 1163-1163 ◽  
Author(s):  
S. Gaetán ◽  
M. Madia

Canola (Brassica napus) is a developing oleaginous crop grown commercially in the Buenos Aires and Santa Fe provinces of Argentina. During the autumn of 2003, typical signs of powdery mildew were observed on canola plants in experimental field plots in Buenos Aires. Average disease incidence was 42% on 3- to 6-month-old canola cultivars developed in the following countries: Argentina (Eclipse, Impulse Master, Mistral, and Nolza); Australia (Oscar and Rainbow); Canada (Sentry); France (Cadillac, Camberra, and Capitol); and Sweden (Maskot, Sponsor, and Wildcat). The range of incidence on these cultivars was 35 to 93%. Other cultivars exhibited an apparent high level of resistance or escaped disease. These included: Charlton (Argentina); 46CO3, Dunkeld, Insignia, Mystic, Monty, Outback, Rivette, and Surpass 400 (Australia), and Caviar (France). Climatic conditions in Buenos Aires, especially rainfall, from March to May 2003 were apparently favorable for powdery mildew development. On susceptible cultivars, fungal growth was observed on leaves, stems, and pods that resulted in premature senescence of the tissues. The mycelium, with multilobed hausthoria, was white to gray, dense or fine, and in patches or covering the entire adaxial leaf surfaces. Appressoria were lobed and conidiophores were straight. Foot cells were cylindrical, straight, measured 35 to 42 × 7 to 10 μm, and were followed by two cells. Conidia were produced singly, cylindrical to ovoid, and measured 36 to 40 × 18 to 20 μm. The conidial length-to-width ratio was 2.0. No fibrosin bodies were observed in the conidia and conidia germinated at the ends. Cleistothecia were not observed. On the basis of mycelial, conidial, and hausthoria characteristics observed on six leaves for each affected cultivar, the fungus was identified as Erysiphe polygoni DC (1). Pathogenicity was confirmed on 5-week-old canola plants of cvs. Eclipse, Impulse, Master, Mistral, and Maskot by gently pressing (1 min) one adaxial infected leaf with abundant sporulation onto one adaxial healthy leaf. The experiment, which included five inoculated plants and three noninoculated control plants for each cultivar, was conducted in a greenhouse at 22 to 24°C and maintained at 75% relative humidity with no supplemental light. Inoculated and control plants were covered with polyethylene bags for 48 h after inoculation. Powdery mildew developed on all inoculated plants of all cultivars after 12 to14 days. The control plants did not develop disease. The experiment was repeated with similar results. E. polygoni has a worldwide distribution (2); however, the results suggest that this fungus may be a threat to the main cultivars being grown in Argentina (Eclipse, Impulse, Master, Mistral, and Nolza), since high levels of disease incidence, as much as 70%, were observed. Under propitious environments, this pathogen could cause severe yield losses in commercially grown canola in Argentina. To our knowledge, this is the first report of canola powdery mildew caused by E. polygoni in Argentina. References: (1) H. J. Boesewinkel. Rev. Mycol. Tome 41:493, 1977. (2) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St.Paul, MN, 1989.


Plant Disease ◽  
2012 ◽  
Vol 96 (7) ◽  
pp. 1068-1068
Author(s):  
A. Gaytán-Mascorro ◽  
Y. I. Chew-Madinaveitia ◽  
T. Herrera Pérez ◽  
M. A. Gallegos Robles

In 2010 and 2011, diseased watermelon plants (Citrillus lanatus [Thunb.] Matsun and Nakai) had chlorotic and wilted leaves and vines prior to harvest in three out of four sampled commercial fields in the Municipality of Matamoros, State of Coahuila, in the north-central region of Mexico known as La Comarca Lagunera. Disease incidence across the fields was 30%. Diseased plants also showed necrotic lesions and loss of secondary and tertiary roots, which can render roots unable to obtain an adequate supply of water and nutrients supporting the aboveground part of the plant before fruit maturity. Roots of affected plants contained perithecia with asci and ascospores typical of Monosporascus cannonballus Pollack & Uecker (4). This fungus has been found in hot semi-arid climates with saline and alkaline soils. Daytime temperatures above 40°C are frequent in north-central Mexico during the watermelon growing season. Small root pieces from 30 plants with disease symptoms (10 plants per field) were taken and surface-sterilized with 1.5% sodium hypochlorite, placed on potato dextrose agar (PDA) medium with 0.5 g/L of streptomycin sulfate at two petri dishes per plant and five root pieces per petri dish, and incubated for 7 days at 25°C in the dark. The fungus was isolated with a frequency of 60%. Mycelia were identified from root tissue based on morphological characteristics. DNA was also extracted in CTAB buffer followed by a phenol/chloroform purification and precipitation in isopropanol and ethanol (2). The internal transcribed spacer region was then amplified from isolate 1 using PCR, sequenced, and submitted to GenBank (Accession Number JQ599552). Pathogenicity of isolates was confirmed on watermelon plants (cv. Sweet summer 800) under greenhouse conditions at 25 to 32°C. Inoculum was produced in a sand-oat hull (Avena sativa) medium (0.5 l of sand, 45 g of oat hulls, and 100 ml of distilled water) and incubated for 50 days (1). Watermelon seeds were sown in sterile sand in 20-cm diameter and 12-cm deep polyurethane containers, where inoculum was added to reach a soil concentration of 20 CFU/g. Four seeds were sown in each of five inoculated containers; plants were thinned to two per container after emergence (each container representing a replication). Similarly, plants were also grown in four noninoculated containers and used as controls. After 50 days, all watermelon plants inoculated with M. cannonballus showed root necrosis in contrast with roots from noninoculated plants. M. cannonballus was reisolated from 80% of inoculated plants, confirming Koch's postulates. M. cannonballus causes severe damage on watermelon and other cucurbits such as cantaloupe (Cucumis melo). This fungus has been reported in the United States, Spain, Tunisia, Libya, Israel, Italy, the Netherlands (plants from Russia), Saudi Arabia, India, Japan, Taiwan, Brazil, Guatemala, and Honduras. To date, M. cannonballus has been reported on watermelon in 1996 in the State of Colima in southeastern Mexico (3). However, to the best of our knowledge, this is the first report of M. cannonballus on watermelon in northern Mexico. References: (1) B. D. Bruton et al. Plant Dis. 84:907, 2000. (2) B. R. Lovic et al. Phytopathology 85:655, 1995. (3) R. D. Martyn et al. Plant Dis. 80:1430, 1996. (4) F. G. Pollack and F. A. Uecker. Mycol. 66:346, 1974.


Plant Disease ◽  
2012 ◽  
Vol 96 (2) ◽  
pp. 291-291 ◽  
Author(s):  
S. T. Koike ◽  
S. Rooney-Latham

In April 2011, commercial garlic (Allium sativum) in Monterey County, CA showed symptoms of an undocumented disease. Bulb and stem sheaths were dark, decayed, and sloughing off the plants. Dissection of diseased sheaths revealed black hyphae between layers. Lower leaves wilted, turned tan, and dried up. Disease occurred in small patches scattered in two fields. In the patches, disease incidence was as much as 50%; however, overall field incidence was less than 1%. Isolations from 80% (16 of 20 plants) of collected plants resulted in the recovery of a dark olivaceous black fungus. Conidiophores were geniculate and brown and conidia were borne singly, brown, and ellipsoidal to cylindrical. Conidia had two to five but mostly three transverse septa. Longitudinal septa were infrequent and apical cells were rounded. Conidia measured (19.0-) 26.3 to 36.6 (-42.8) × (6.7-) 9.2 to 9.9 (-12.9) μm. Dark, intercalary chlamydospores were observed as colonies aged. DNA sequencing of the internal transcribed spacer (ITS) regions of four, single-spored isolates was completed with primers ITS1 and ITS4 (3). Sequences of all isolates (GenBank Nos. JN588614 to JN588617) were identical and 100% similar to Embellisia allii (AY278840). On the basis of morphological and molecular data, the fungus was identified as E. allii (Campanile) Simmons (1). Pathogenicity of four of the sequenced E. allii isolates and one additional E. allii isolate was tested using inoculum grown on acidified potato dextrose agar and garlic (cv. California Late) planted into 15-cm pots. A transverse incision was made at a point 2 cm above the garlic bulb so that a colonized agar plug could be inserted between the second and third sheath layer. The stem was then wrapped with Parafilm. Ten plants per isolate were inoculated and kept in a greenhouse (24 to 26°C). Seven to eight days after inoculation, the tissue around the incision turned tan and dark fungal growth was observed. Fourteen days after inoculation, the inoculated area was necrotic and dark fungal growth developed between stem layers. E. allii was reisolated from all inoculated plants and matched the morphological characteristics of the original isolates. Control plants, inoculated with uncolonized agar plugs, developed no symptoms. This experiment was repeated with similar results. In addition, one isolate was used to inoculate leek (A. porrum cv. Lancelot) and onion (A. cepa cv. Evergreen). Similar symptoms developed on these two species and E. allii was reisolated from all plants. To our knowledge, this is the first documentation of skin blotch and bulb canker caused by E. allii on garlic in California. Affected plants were of poor quality and could not be harvested. Our findings that garlic isolates of E. allii can infect leek and onion provide preliminary evidence that this pathogen is not restricted to garlic; this information may be useful to growers when considering crop rotations. E. allii has been reported on garlic in a number of places in Africa, Asia, Europe, the Middle East, and North and South America (2). The sequenced E. allii isolates are deposited in the fungal collection at the CDFA Plant Pest Diagnostics Lab (CDFA798-801). References: (1) J. C. David. Mycopathologia 116:59, 1991. (2) D. F. Farr and A. Y. Rossman. Fungal Databases. Systematic Mycology and Microbiology Laboratory, ARS, USDA. Retrieved from http://nt.ars-grin.gov/fungaldatabases/ , August 8, 2011, (3) B. M. Pryor and D. M. Bigelow. Mycologia 95:1141, 2003.


Plant Disease ◽  
1997 ◽  
Vol 81 (1) ◽  
pp. 111-111 ◽  
Author(s):  
A. Viljoen ◽  
P. S. van Wyk ◽  
D. C. Nowell ◽  
T. J. Gulya

Downy mildew, caused by Plasmopara halstedii (Farl.) Berl. & De Toni in Sacc., is an economically important disease of sunflower (Helianthus annuus L.) in Europe and the United States (1). The disease was first noticed in South Africa in a commercial field near Standerton and in a seed production field near Kroonstad during the 1993 to 1994 planting season. During the 1995 to 1996 season, downy mildew was found in experimental hybrids near Heilbron, and in commercial fields near Heil-bron, Marikana, and Potchefstroom. At Heilbron, five hybrids were infected with P. halstedii, whereas three others showed symptoms of downy mildew at Potchefstroom and Marikana. All commercially cultivated hybrids have been developed in South Africa. Disease incidence in all the fields was low, with less than 1% of plants affected by the disease. Diseased plants were dwarfed and displayed veinal chlorosis of leaves typically associated with downy mildew of sunflower. White fungal growth commonly occurred on lower leaf surfaces. Sunflower seedlings inoculated with P. halstedii produced symptoms characteristic of downy mildew. The occurrence of the disease in many geographic areas and on various hybrids in South Africa suggests that the fungus is well established. Recent outbreaks can be attributed to the cool, wet, climatic conditions of the 1993 to 1994 and 1995 to 1996 seasons. The susceptibility of local hybrids suggests that downy mildew is a potentially dangerous disease of sunflower in South Africa. Reference: (1) J. F. Miller and T. J. Gulya. Crop Sci. 27:210, 1987.


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