scholarly journals First Report of Fruit Rot of Ridge Gourd (Luffa acutangula) Caused by Sclerotium rolfsii

2016 ◽  
Vol 17 (1) ◽  
pp. 18-19
Author(s):  
Chandrasekar S. Kousik ◽  
Jennifer Ikerd ◽  
Mihir Mandal
Keyword(s):  
United States ◽  
Sclerotium Rolfsii ◽  
The United States ◽  
Fruit Rot ◽  
Small Scale ◽  
First Report ◽  
Athelia Rolfsii ◽  
History Of ◽  
Sclerotium Rot ◽  
Luffa Acutangula

Ridge gourd is a specialty cucurbit vegetable cultivated in the United States on a small scale for select markets. We report the infection of ridge gourd fruit by Sclerotium rolfsii (teleomorph: Athelia rolfsii). This appears to be the first report of Sclerotium rot of ridge gourd. In fields with history of S. rolfsii, the gourds should be grown on trellis to prevent fruit contact with wet soil. Several fungicides are available to manage S. rolfsii and may have to be applied if and when needed. Accepted for publication 12 January 2016. Published 14 January 2016.

scholarly journals First Report of Anthracnose Caused by Colletotrichum acutatum on Persimmon Fruit in the United States

Plant Disease ◽  
2010 ◽  
Vol 94 (5) ◽  
pp. 634-634 ◽  
Author(s):  
S. M. Williamson ◽  
T. B. Sutton
Keyword(s):  
United States ◽  
Filter Paper ◽  
The United States ◽  
Grocery Store ◽  
Fruit Rot ◽  
Colletotrichum Acutatum ◽  
Diospyros Kaki ◽  
Japanese Persimmon ◽  
First Report ◽  
Persimmon Fruit

Persimmon trees are important for their fruit as well as their colorful fruit and foliage in the fall. Persimmon fruit (Japanese persimmon, Diospyros kaki cv. Fuyu) were collected in November 2008 from a tree in Windsor, NC, located in the Coastal Plain. Fruit were not symptomatic on the tree but developed dark lesions after harvest. Isolations from six fruit yielded seven isolates of Colletotrichum acutatum J. H. Simmonds. After incubation at 25°C under continuous light for 15 days on potato dextrose agar (PDA), all isolates had gray aerial mycelium, but the inverse sides of the plates of six isolates were maroon and one was beige. Masses of salmon-colored conidia were formed first in the center of the colonies, then were observed scattered across the colonies in older cultures. Conidia were hyaline, one-celled, elliptic with one or both ends pointed, and measured 8.1 to 16.3 × 3.1 to 5 μm. Setae and sclerotia were not observed. There were also dark structures measuring 1 to 10 mm that were partially embedded in the agar that contained conidia. Cultural and conidial characteristics of the isolates were similar to those of C. acutatum (3). PCR amplification was performed with the species-specific primer pair CaInt2/ITS4 (2) and genomic DNA from the original isolates and isolates obtained from inoculated fruit. An amplification product of approximately 490 bp, which is specific for C. acutatum, was observed. To fulfill Koch's postulates, persimmon fruit obtained from the grocery store were surface disinfested with 0.5% sodium hypochlorite and sterile filter paper disks dipped in conidial suspensions (1 × 105 conidia/ml) of two C. acutatum isolates (maroon and beige reverse) or sterile, deionized water were placed on the fruit. Three fruit were inoculated per treatment and the disks were placed on four locations on each fruit. Parafilm was wrapped around the diameter of the fruit to keep the filter paper disks moist and in place. Fruit were placed in moist chambers and incubated at 25°C. After 3 days, the Parafilm was removed and the fruit returned to the moist chambers. Small, dark lesions were observed on fruit inoculated with each isolate of C. acutatum when the filter paper disks were removed. Ten days after inoculation, dark lesions and acervuli with salmon-colored masses of conidia were observed on fruit inoculated with both isolates of C. acutatum and the fruit were soft. After 12 days, there were abundant masses of conidia and the inoculated areas were decayed. Control fruit remained firm and did not develop symptoms. Cultures obtained from the fruit and the conidia produced were typical of the isolates used to inoculate the fruit. C. acutatum has been reported to cause fruit rot on persimmon fruit in New Zealand (1). To our knowledge, this is the first report of C. acutatum on persimmon fruit in the United States. References: (1) R. Lardner et al. Mycol. Res. 103:275, 1999. (2) S. Sreenivasaprasad et al. Plant Pathol. 45:650, 1996. (3) B. C. Sutton. Page 523 in: Coelomycetes. Commonwealth Agricultural Bureaux, Great Britain. 1980.

scholarly journals First Report of Postharvest Fruit Rot in Persimmon Caused by Phacidiopycnis washingtonensis in Italy

Plant Disease ◽  
2010 ◽  
Vol 94 (6) ◽  
pp. 788-788 ◽  
Author(s):  
A. Garibaldi ◽  
D. Bertetti ◽  
M. T. Amatulli ◽  
M. L. Gullino
Keyword(s):  
United States ◽  
Its Region ◽  
The United States ◽  
Fruit Rot ◽  
Diospyros Kaki ◽  
Pathogenicity Test ◽  
Conidial Suspension ◽  
First Report ◽  
Pathogenicity Tests ◽  
Phacidiopycnis Washingtonensis

Persimmon (Diospyros kaki L.) is widely grown in Italy, the leading producer in Europe. In the fall of 2009, a previously unknown rot was observed on 3% of fruit stored at temperatures between 5 and 15°C in Torino Province (northern Italy). The decayed area was elliptical, firm, and appeared light brown to dark olive-green. It was surrounded by a soft margin. The internal decayed area appeared rotten, brown, and surrounded by bleached tissue. On the decayed tissue, black pycnidia that were partially immersed and up to 0.5 mm in diameter were observed. Light gray conidia produced in the pycnidia were unicellular, ovoid or lacriform, and measured 3.9 to 6.7 × 2.3 to 3.5 (average 5.0 × 2.9) μm. Fragments (approximately 2 mm) were taken from the margin of the internal diseased tissues, cultured on potato dextrose agar (PDA), and incubated at temperatures between 23 and 26°C under alternating light and darkness. Colonies of the fungus initially appeared ash colored and then turned to dark greenish gray. After 14 days of growth, pycnidia and conidia similar to those described on fruit were produced. The internal transcribed spacer (ITS) region of rDNA was amplified using the primers ITS4/ITS6 and sequenced. BLAST analysis (1) of the 502-bp segment showed a 100% similarity with the sequence of Phacidiopycnis washingtonensis Xiao & J.D. Rogers (GenBank Accession No. AY608648). The nucleotide sequence has been assigned the GenBank Accession No. GU949537. Pathogenicity tests were performed by inoculating three persimmon fruits after surface disinfesting in 1% sodium hypochlorite and wounding. Mycelial disks (10 mm in diameter), obtained from PDA cultures of one strain were placed on wounds. Three control fruits were inoculated with plain PDA. Fruits were incubated at 10 ± 1°C. The first symptoms developed 6 days after the artificial inoculation. After 15 days, the rot was very evident and P. washingtonensis was consistently reisolated. Noninoculated fruit remained healthy. The pathogenicity test was performed twice. Since P. washingtonensis was first identified in the United States on decayed apples (2), ‘Fuji’, ‘Gala’, ‘Golden Delicious’, ‘Granny Smith’, ‘Red Chief’, and ‘Stark Delicious’, apple fruits also were artificially inoculated with a conidial suspension (1 × 106 CFU/ml) of the pathogen obtained from PDA cultures. For each cultivar, three surface-disinfested fruit were wounded and inoculated, while three others served as mock-inoculated (sterile water) controls. Fruits were stored at temperatures ranging from 10 to 15°C. First symptoms appeared after 7 days on all the inoculated apples. After 14 days, rot was evident on all fruit inoculated with the fungus, and P. washingtonensis was consistently reisolated. Controls remained symptomless. To our knowledge, this is the first report of the presence of P. washingtonensis on persimmon in Italy, as well as worldwide. The occurrence of postharvest fruit rot on apple caused by P. washingtonensis was recently described in the United States (3). In Italy, the economic importance of the disease on persimmon fruit is currently limited, although the pathogen could represent a risk for apple. References: (1) S. F. Altschul et al. Nucleic Acids Res. 25:3389, 1997. (2) Y. K. Kim and C. L. Xiao. Plant Dis. 90:1376, 2006. (3) C. L. Xiao et al. Mycologia 97:473, 2005.

scholarly journals First Report of Phytophthora syringae Causing Rot on Apples in Cold Storage in the United States

Plant Disease ◽  
2002 ◽  
Vol 86 (6) ◽  
pp. 693-693 ◽  
Author(s):  
R. A. Spotts ◽  
G. G. Grove
Keyword(s):  
United States ◽  
Cold Storage ◽  
The United States ◽  
River Valley ◽  
Fruit Rot ◽  
Commonwealth Mycological Institute ◽  
Postharvest Diseases ◽  
First Report ◽  
Postharvest Decay ◽  
Wide Range

A decay of ‘Granny Smith’ apples (Malus domestica Borkh.) was observed in 1988, 1990, and 1991 on fruit grown in the lower Hood River Valley of Oregon and stored at 0°C. Harvested fruit were drenched with thiabendazole and stored in October in all years. In mid-November, fruit were sized, drenched with sodium hypochlorite, and returned to cold storage. Decay was observed in January when fruit were removed from cold storage, sorted, and packed. Decayed areas were light brown and firm with a slightly indefinite margin. Losses were less than 1% of fruit packed. Diseased fruit were surface-disinfested with 95% ethanol, and tissue pieces were transferred aseptically to potato dextrose agar acidified with lactic acid and incubated at approximately 22°C. The fungus consistently isolated was identified as Phytophthora syringae (Kleb.) Kleb. based on morphological characters (3). Sporangia were persistent and averaged 60 μm long (range 59 to 69) × 40 μm wide (range 37 to 43). Antheridia were paragynous, and oospores averaged 37 μm (range 31 to 46). ‘Golden Delicious’, ‘Granny Smith’, and ‘Gala’ apples were inoculated with mycelial plugs from a 7-day-old culture of P. syringae and incubated 12 days at 5°C and 7 to 12 days at 22°C. Twenty fruit of each cultivar were used—ten were inoculated, and ten uninoculated fruit served as controls. Lesions developed on all inoculated fruit but not on uninoculated controls. Lesions were spherical, chocolate brown, and firm with no evidence of external mycelia. Lesion morphology was similar on all cultivars. P. syringae was reisolated from lesion margins of all infected fruit. This postharvest decay of apples has not been observed in the Hood River Valley since 1991. Fruit rot of apples caused by P. syringae is known in Canada (1) and is common in the United Kingdom (2), but has not been reported previously in the United States. To our knowledge, this is the first report of postharvest decay of apples by P. syringae in the United States. References: (1) R. G. Ross and C. O. Gourley. Can. Plant Dis. Surv. 49:33, 1969. (2) A. L. Snowdon. A Color Atlas of Postharvest Diseases. CRC Press, Inc., Boca Raton, FL, 1990. (3) G. M. Waterhouse. The Genus Phytophthora. Misc. Publ. 12. The Commonwealth Mycological Institute, Kew, Surrey, England, 1956.

scholarly journals First Report of Colletotrichum scovillei Causing Anthracnose Fruit Rot on Pepper in South Carolina, United States

Plant Disease ◽  
2020 ◽  
Author(s):  
Sean M Toporek ◽  
Anthony P. Keinath
Keyword(s):  
United States ◽  
South Carolina ◽  
Average Length ◽  
The United States ◽  
Fruit Rot ◽  
Lesion Length ◽  
Pathogenicity Test ◽  
Conidial Suspension ◽  
Accession Number ◽  
First Report

Anthracnose fruit rot caused by various Colletotrichum spp. is a serious disease for pepper (Capsicum annuum) growers, resulting in extensive fruit loss (Harp et al. 2008). Samples of five pepper fruits were obtained from two commercial farms in Lexington and Pickens counties, South Carolina, in August and September 2019, respectively. All fruits had two or more soft, sunken lesions covered with salmon-colored spore masses. Pieces of diseased tissue cut from the margins of lesions were surface disinfested in 0.6% sodium hypochlorite, rinsed in sterile deionized water, blotted dry, and placed on one-quarter-strength potato dextrose agar (PDA/4) amended with 100 mg chloramphenicol, 100 mg streptomycin sulfate, and 60.5 mg mefenoxam (0.25 ml Ridomil Gold EC) per liter. Two isolates of Colletotrichum sp. per fruit were preserved on dried filter paper and stored at 10º C. One additional isolate of Colletotrichum sp. had been collected from a jalapeño pepper fruit on a farm in Charleston County, South Carolina, in 1997. Colony morphology of three isolates, one per county, on Spezieller Nährstoffarmer Agar (SNA) was pale grey with a faint orange tint. All isolates readily produced conidia on SNA with an average length of 16.4 μm (std. dev. = 1.8 μm) and a width of 2.2 μm (std. dev. = 0.2 μm). Conidia were hyaline, smooth, straight, aseptate, cylindrical to fusiform with one or both ends slightly acute or round, matching the description of C. scovillei (Damm et al. 2012). The glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and beta-tubulin (TUB2) genes from three isolates were amplified and sequenced with the primer pairs GDF1/GDR1 and T1/Bt2b, respectively. Species within the C. acutatum clade can be readily distinguished with GAPDH or TUB2 (Cannon et al. 2012). The GAPDH and TUB2 sequences for all three isolates were 100% similar to each other and strain CBS 126529 (GAPDH accession number JQ948597; TUB2 accession number JQ949918) of C. scovillei (Damm et al. 2012). GAPDH and TUB2 sequences for each isolate were deposited in GenBank under the accessions MT826948–MT826950 and MT826951-MT826953, respectively. A pathogenicity test was conducted on jalapeño pepper fruits by placing a 10-ul droplet of a 5 x 105 conidial suspension of each isolate onto a wound made with a sterile toothpick. Control peppers were mock inoculated with 10 ul sterile distilled water. A humid chamber was prepared by placing moist paper towels on the bottom of a sealed crisper box. Inoculated peppers were placed on upside-down 60 ml plastic condiment cups. Three replicate boxes each containing all four treatments were prepared. The experiment was repeated once. After 7 days in the humid chamber at 26ºC, disease did not develop on control fruits, whereas soft, sunken lesions covered with salmon-colored spores developed on inoculated fruits. Lesions were measured and C. scovillei was re-isolated onto amended PDA/4 as previously described. Lesion length averaged 15.6 mm (std dev. = 4.1 mm) by 11.5 mm (std dev. = 2.0 mm). Colletotrichum sp. resembling the original isolate were recovered from all inoculated fruit, but not from non-inoculated fruit. C. scovillei has been reported in Brazil in South America and in China, Indonesia, Japan, Malaysia, South Korea, Taiwan, and Thailand in Asia (Farr and Rossman 2020). This is the first report of C. scovillei as the casual organism of anthracnose fruit rot on pepper in South Carolina and the United States.

scholarly journals First Report of blaVIM-4- and mcr-9-Coharboring Enterobacter Species Isolated from a Pediatric Patient

mSphere ◽  
2019 ◽  
Vol 4 (5) ◽  
Author(s):  
Kalyan D. Chavda ◽  
Lars F. Westblade ◽  
Michael J. Satlin ◽  
Andrew C. Hemmert ◽  
Mariana Castanheira ◽  
...  
Keyword(s):  
United States ◽  
Pediatric Patient ◽  
The United States ◽  
Regulatory Genes ◽  
Colistin Resistance ◽  
Content Type ◽  
First Report ◽  
Insertion Elements ◽  
History Of ◽  
Enterobacter Hormaechei

ABSTRACT An Enterobacter hormaechei isolate harboring blaVIM-4 and mcr-9 was recovered from a pediatric patient in a U.S. hospital. The blaVIM-4 and mcr-9 genes are carried on the same IncH12 plasmid, pME-1a. The isolate tested susceptible to colistin, without observed induction of colistin resistance. The mcr-9 gene is located between two insertion elements, IS903 and IS1, but lacks the downstream regulatory genes (qseC and qseB) found in other isolates that harbor mcr-9. IMPORTANCE We describe the complete genome assembly and sequence of a clinical Enterobacter isolate harboring both blaVIM-4 and mcr-9 recovered from a pediatric patient in the United States with a history of travel to Egypt. Moreover, to the best of our knowledge, this is the first report of an Enterobacter isolate harboring both blaVIM-4 and mcr-9 from the United States. The blaVIM-4 and mcr-9 genes are carried on the same IncH12 plasmid, pME-1a. The isolate tested susceptible to colistin, without observed induction of colistin resistance. The mcr-9 gene is located between two insertion elements, IS903 and IS1, but lacks the downstream regulatory genes (qseC and qseB) found in other isolates that harbor mcr-9.

scholarly journals First Report of Sclerotium rolfsii on Jerusalem Cherry (Solanum pseudocapsicum) in Europe

Plant Disease ◽  
2000 ◽  
Vol 84 (9) ◽  
pp. 1048-1048
Author(s):  
A. Garibaldi ◽  
A. Minuto ◽  
M. L. Gullino
Keyword(s):  
United States ◽  
Sclerotium Rolfsii ◽  
Soil Surface ◽  
The United States ◽  
Northern Italy ◽  
Ornamental Plant ◽  
Potato Dextrose Agar ◽  
First Report ◽  
Initial Symptoms ◽  
Stem Necrosis

Jerusalem cherry (Solanum pseudocapsicum) has recently become popular as a potted ornamental plant in Italy. During the summer of 1999, a sudden wilt of 60-day-old plants was observed in the Albenga region (Northern Italy), an area of intensive floriculture. Initial symptoms included stem necrosis at the soil line and yellowing and tan discoloration of leaves. As stem necrosis progressed, infected plants wilted and died. Necrotic tissues were covered with whitish mycelium that differentiated into reddish brown, spherical (1 to 2 mm diameter) sclerotia. Sclerotium rolfsii was consistently recovered from the surface of symptomatic stem sections that were disinfected for 1 min in 1% NaOCl and then plated on potato-dextrose agar (PDA) amended with 100 ppm streptomycin sulfate. Pathogenicity of three S. rolfsii isolates was confirmed by inoculating 90-day-old S. pseudocapsicum plants grown in pots. Inoculum consisted of mycelium and sclerotia of the pathogen placed on the soil surface around the base of each plant. Noninoculated plants served as controls. All plants were kept in a growth chamber at 18 to 28°C and RH > 85%. Inoculated plants developed symptoms within 7 days, while control plants remained symptomless. Sclerotia developed on infected tissues and S. rolfsii was reisolated from symptomatic tissues. The disease has been observed in the United States (1), but this is the first report of stem blight of S. pseudocapsicum caused by S. rolfsii in Europe. Reference: (1) S. A. Alfieri, Jr., K. R. Langdon, C. Wehlburg, and J. W. Kimbrough, J. W. Index Plant Dis. Florida Bull. 11:215, 1984.

scholarly journals First Report of Stem and Root Rot of Stevia Caused by Sclerotium rolfsii in North Carolina

Plant Disease ◽  
2014 ◽  
Vol 98 (7) ◽  
pp. 1005-1005 ◽  
Author(s):  
A. Koehler ◽  
H. Shew
Keyword(s):  
United States ◽  
North Carolina ◽  
Root Rot ◽  
Mycelial Growth ◽  
Sclerotium Rolfsii ◽  
Pathogenic Fungi ◽  
The United States ◽  
Penicillin G ◽  
Stem Tissue ◽  
First Report

Stevia (Stevia rebaundia) is an emerging crop in the United States. Once established, the crop is grown for 3 to 5 years and is typically harvested twice per growing season. Stevia leaves contain multiple glycosides that are used as a natural noncaloric sweetener that was approved by the USDA in 2008 as a sugar substitute. In commercial plantings of Stevia in North Carolina, wilting and death of plants in first- and second-year plantings were observed in 2012 and 2013. Diseased plants were observed in multiple counties in the state, with first symptoms observed in May of each year and continuing through the summer months. Prior to Stevia, these fields had been planted primarily in a corn-soybean rotation. Symptoms began as moderate to severe wilting of young shoots and chlorosis of leaves, rapidly followed by death of stems and rotting of roots. White mycelial growth was frequently observed at the base of stem tissue. Theses characteristic hyphae of Sclerotium rolfsii were often accompanied by the presence of abundant white to brown sclerotia. Isolations from infected root and stem tissue were made on potato dextrose agar amended with 50 μg/ml of streptomycin sulfate and penicillin G. Isolations from diseased tissue yielded characteristic white hyphae of S. rolfsii (1,3). Numerous sclerotia 0.5 to 2 mm in diameter developed following 4 to 7 days of mycelial growth. Sclerotia were initially white and melanized turning brown with age. To verify pathogenicity, 10-week-old Stevia seedlings were transplanted in 10-cm diameter pots containing sterile 1:1:1 sand, loam, media mix. Inoculum consisted of oat grains infested with one isolate obtained from the field plants. Oats were sterilized on three consecutive days and then inoculated with colonized agar plugs of S. rolfsii. Oats were incubated at room temperature to allow the fungus to thoroughly colonize the oats. Three infested oat grains were added to each test pot and plants were then observed over a 3-week period. Symptoms were observed within 5 days on most plants and included chlorotic leaves, bleached stems, wilting, and necrotic roots. White mycelium and abundant sclerotia were found at the base of plants. Uninoculated plants did not develop any symptoms. This is the first report of S. rolfsii on Stevia in the United States. Kamalakannan et al. (2) reported a root rot disease of Stevia in India and confirmed S. rolfsii as the causal agent. References: (1) R. Aycock. N.C. Agr. Exp. St. Tech. Bull. No. 174, 1966. (2) A. Kamalakannan et al. Plant Pathol. 56:350, 2007. (3) J. E. M. Mordue. Corticium rolfsii. CMI Descriptions of Pathogenic Fungi and Bacteria No. 410. CAB International, Wallingford, UK, 1974.

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