scholarly journals First Report of Sclerotinia Blight of Peanut Caused by Sclerotinia minor in Arkansas

Plant Disease ◽  
2014 ◽  
Vol 98 (7) ◽  
pp. 1013-1013 ◽  
Author(s):  
T. R. Faske ◽  
M. Emerson ◽  
K. Hurd

In September, 2013, symptoms similar to Sclerotinia blight caused by Sclerotinia minor were observed on Runner peanut (cv. FloRun 107) in a commercial field near Pocahontas, Arkansas, in Randolph County (2). Blighted plants with wilted leaves were observed in several small (30 × 30 cm) clustered foci located near the end of a 20-ha, furrow-irrigated field. Peanut stems within the lower canopy of symptomatic plants had straw-colored lesions, with white fluffy mycelium and small (<2.0 mm diam.), black, irregularly shaped sclerotia. Stems on plants with severe symptoms were shredded in appearance, with small black sclerotia inside the stem tissue (2). Final disease incidence near harvest in mid-October was less than 1% of the field. Sclerotinia blight symptoms were also observed in 2013 on Runner (cvs. FloRun 107, Georgia 09B, and Florida 07) and Spanish peanut (cvs. OLin and OL06) research plots near Newport, AR, in Jackson County. Disease incidence among cultivars in these research plots was <1% for all cultivars except FloRun 107, which had a disease incidence of 2.6% for a 849.8 m2 plot. Isolations from surface-disinfected leaves on potato dextrose agar (PDA) consistently yielded white, fluffy mycelia with small (0.5 to 2.0 mm diam.), black, irregularly shaped sclerotia typical of S. minor (2). Six-week-old peanut plants (cv. FloRun 107) growing in pots were used to test pathogenicity. Each plant was inoculated by placing an agar plug (5 mm diam.), collected from the edge of an actively growing S. minor culture, on the main peanut stem. Plants (n = 5) were incubated for 8 days in a humidity chamber where temperatures ranged from 24 to 30°C and relative humidity remained >95%. Characteristic symptoms of Sclerotia blight were observed on all inoculated peanut plants whereas none of the plants (n = 3) inoculated with sterile PDA agar plugs expressed symptoms. Pathogenicity tests were repeated on peanut cvs. Flavor Runner 458 and Georgia 09B with similar results. S. minor was consistently isolated from symptomatic tissue on PDA, fulfilling Koch's postulates. To our knowledge, this is the first report of S. minor on peanut or any host in Arkansas or the Mid-South region. The two peanut fields with Sclerotinia blight had a history of soybean production, and S. minor may have gone undetected on soybean or one of many host weed species (1). Since S. minor is a major economic pathogen of peanut, commonly causing yield losses of 10% (2), it will likely be a significant factor in Arkansas and Mid-South peanut production. References: (1) M. S. Melzer et al. Can. J. Plant Pathol. 19:272, 1997. (2) D. M. Porter and H. A. Melouk. Sclerotinia blight. Page 34 in: Compendium of Peanut Diseases, 2nd ed. N. Kokalis-Burelle et al., eds. The American Phytopathological Society, St. Paul, MN, 1997.

Plant Disease ◽  
2008 ◽  
Vol 92 (3) ◽  
pp. 482-482 ◽  
Author(s):  
J. E. Woodward ◽  
M. A. Batla ◽  
P. A. Dotray ◽  
T. A. Wheeler ◽  
T. A. Baughman

Sclerotinia blight, caused by the soilborne fungus Sclerotinia minor Jagger, is a major disease of peanut (Arachis hypogaea L.) in parts of west Texas. Previous reports have indicated that annual weed species may serve as collateral hosts for S. minor (2). Several Ipomoea spp. are commonly found in peanut fields throughout the region. In September of 2007, Ipomoea hederacea and I. coccinea plants with bleached, shredded stems, and signs of black sclerotia were collected from a field known to be infested with S. minor. Symptomatic stem sections were rinsed in tap water, surface disinfested in 0.5% sodium hypochlorite for 1 min, air dried, and plated on potato dextrose agar (PDA). Pure cultures of S. minor consisting of white, fluffy mycelia and small (<2 mm), black, irregular sclerotia were consistently recovered. Pathogenicity tests were conducted by wound-inoculating healthy I. hederacea and I. coccinea transplants (n = 3) with agar plugs obtained from the edges of actively growing S. minor cultures. Plants were incubated in a dew chamber at 20°C and 95% relative humidity for 5 days. Plants inoculated with sterile PDA plugs served as controls (n = 3). A similar test was conducted using the susceptible peanut cultivar Flavorunner 458. Characteristic symptoms of Sclerotinia blight (3) were observed on all inoculated weed and peanut plants; whereas, the controls remained healthy. Pathogenicity tests were repeated with similar results. Cultures of S. minor were obtained from all symptomatic tissues, fulfilling Koch's postulates. These results indicate that I. hederacea and I. coccinea are additional hosts of S. minor and that sclerotia produced on infected plants can significantly augment soil inoculum. S. minor has been observed to infect I. batatas seedlings in New Jersey (1); however, this to our knowledge is the first report of S. minor infecting Ipomoea spp. in Texas. Therefore, weed management should inevitability be a part of disease management strategies for the control of Sclerotinia blight in peanut. References: (1) Anonymous. Index of Plant Diseases in the United States. USDA Handb. No. 165, 1960. (2) J. E. Hollowell et al. Plant Dis. 87:197, 2003. (3) D. M. Porter and H. A. Melouk. Sclerotinia blight. Page 34 in: Compendium of Peanut Diseases. 2nd ed. N. Kokalis-Burelle et al., eds. The American Phytopathologicial Society, St. Paul, MN, 1997.


Plant Disease ◽  
2003 ◽  
Vol 87 (2) ◽  
pp. 197-199 ◽  
Author(s):  
J. E. Hollowell ◽  
B. B. Shew ◽  
M. A. Cubeta ◽  
J. W. Wilcut

Bleached stems and sclerotia were observed on winter annual weed species growing in harvested peanut fields in northeastern North Carolina in March 2001. Each field had a history of Sclerotinia blight caused by Sclerotinia minor. Symptomatic plants were collected and brought back to the laboratory for identification and isolation. S. minor was isolated and Koch's postulates were fulfilled to confirm pathogenicity of S. minor on nine weed species. They included Lamium aplexicaule (henbit), Cardamine parviflora (smallflowered bittercress), Stellaria media (common chickweed), Cerastium vulgatum (mouse-ear chickweed), Coronopus didymus (swinecress), Oenothera laciniata (cutleaf eveningprimrose), Conyza canadensis (horseweed), Brassica kaber (wild mustard), and Arabidopsis thaliana (mouse-ear cress). This is the first report of these species as hosts of S. minor in the natural environment. All isolates of S. minor obtained from the weed species were pathogenic to peanut.


Plant Disease ◽  
2013 ◽  
Vol 97 (12) ◽  
pp. 1658-1658 ◽  
Author(s):  
T. R. Faske ◽  
T. N. Spurlock

In early September 2012, symptoms similar to aerial blight were observed on runner peanut (cv. Georgia 09B) in a commercial field in Randolph County, Arkansas (3). Leaves within the canopy closest to the soil had water-soaked, gray to green lesions or tan to brown lesions. Localized areas of matted leaves with mycelium occurred on stems and hyphae extended along stems and newly affected leaves. Dark brown spherical sclerotia (1.5 to 4 mm diam.) were produced on the surface of symptomatic peanut tissue (3). Aerial blight symptoms were observed in two peanut fields (~4 to 6 ha) that were furrow irrigated. Symptomatic plants were localized in a single circular pattern (~20 × 25 m) near the lower end of each field with the final disease incidence of less than 5%. Isolations from surface-disinfected leaves on potato dextrose agar consistently yielded light brown to brown colonies with sclerotia typical of Rhizoctonia solani AG1-IA. The fungus was confirmed to be R. solani AG1 by anastomosis reaction (2) with known cultures of AG1-IA isolated from soybean and rice in Arkansas. Sequencing of the rDNA ITS region 5.8s with primers ITS1 and ITS4 (1) supported the identification of the R. solani isolates as AG1-IA. The BLAST search revealed that the sequence had a 96 to 97% maximum sequence identity to several R. solani AG1-IA isolates collected from rice sheaths in China and Arkansas. Eight-week-old peanut plants (cv. Georgia 09B) growing in pots were sprayed until runoff (2 ml/plant) with a solution containing approximately 1 × 105 hyphal fragments/ml. Five inoculated plants were placed in a humidity chamber within a greenhouse where temperatures ranged from 28 to 33°C. After 14 days, water soaked, gray to green or light brown lesions developed on all inoculated plants along with hyphal strands along inoculated sections of the peanut with dark brown sclerotia. None of the plants inoculated with sterile water expressed symptoms. Rhizoctonia solani was consistently reisolated from symptomatic tissue plated on PDA. Inoculations were repeated on peanut cv. Flavor Runner 458, Florida 07, FloRun 107, and Red River Runner with similar results. Although R. solani AG1-IA is a common pathogen on rice and soybean, causing sheath blight and aerial blight, respectively, to our knowledge this is the first report of aerial blight of peanut in the region. Currently, there is a renewed interest in peanut production in the state. Production practices include furrow irrigation, which can distribute floating sclerotia to peanut vines and the rotation practiced with soybean and, less frequently, rice, could potentially increase inoculum for the subsequent crop. Thus, this may be a significant disease problem in the region or Mid-South where peanut is planted after rice or soybean and furrow irrigated. References: (1) S. Kuninaga et al. Curr. Genet. 32:237, 1997. (2) G. C. MacNish et al. Phytopathology 83:922, 1993. (3) H. A. Melouk and P. A. Backman. Management of soilborne fungal pathogens. Pages 75-85 in: Peanut Health Management. H. A. Melouk and F. M. Stokes, eds. The American Phytopathological Society, St. Paul, MN, 1995.


2010 ◽  
Vol 37 (1) ◽  
pp. 1-11 ◽  
Author(s):  
J. P. Damicone ◽  
C. C. Holbrook ◽  
D. L. Smith ◽  
H. A. Melouk ◽  
K. D. Chamberlin

Abstract In 2001, entries from the peanut core collection, a subset of the USDA peanut germplasm collection, were planted in non-replicated plots in a field with a history of Sclerotinia blight caused by Sclerotinia minor. Variability existed among entries for reaction to Sclerotinia blight. Of the 744 entries evaluated, 11% had no disease, nearly 30% had &lt;10% disease incidence, and only 21% had 50% disease incidence or more. Most of the resistant entries had an upright growth habit and were in early and mid-maturity groups. Many of the early maturing entries were susceptible to the foliar disease pepper spot which occurred throughout the study. Entries were selected for further evaluation in replicated plots based on a nil to low (&lt;10%) incidence of Sclerotinia blight, adaptation and/or vigor, and other desirable characteristics such as an intermediate to prostrate growth habit and pepper spot resistance. Selected entries were retested in both 2002 and 2003 (n  =  62) and compared to resistant (Tamspan 90), moderately resistant (Tamrun 96), and susceptible (Okrun) reference cultivars. Most entries (55 in 2001 and 46 in 2003) had disease incidence less than Tamrun 96 and similar to Tamspan 90. In 2003 when disease incidence was highest, all 46 entries with resistant reactions similar to that of Tamspan 90 had erect plant growth habits except for entries 208 and 582 which were prostrate, and entries 273, 128, and 804 which were intermediate. Resistance to Sclerotinia blight and yield similar to Tamspan 90, plant habit, and/or reactions to pepper spot and web blotch were used to select the best entries. Entries 208, 128, 804, 582, and 273 combined resistance to Sclerotinia blight, pepper spot, and web blotch with less than erect growth habits. Entry 103 had good Sclerotinia blight resistance and yield, but an upright growth habit. Entry 92 had an upright growth habit and low yield, but good Sclerotinia blight resistance. Entries 92 and 103 had upright growth habits but were among the best entries for resistant to pepper spot and web blotch. Entries 426, 184, and 562 were upright and susceptible to pepper spot, but had resistance to web blotch and the best resistance to Sclerotinia blight. These entries appear to be useful sources of resistance to Sclerotinia blight for breeding programs and for increasing the probability of finding additional sources of resistance in clusters of germplasm identified within the entire USDA collection.


Plant Disease ◽  
2009 ◽  
Vol 93 (5) ◽  
pp. 550-550 ◽  
Author(s):  
A. M. Alippi ◽  
A. C. López

During May of 2008 (austral autumn), an uncharacterized disease was observed on Dieffenbachia picta (Lodd.) Schott and Aglaonema commutatum Schott in commercial greenhouses in Pontevedra (34°45′6″S, 58°42′42″W), Argentina. Affected plants showed irregular, brown lesions on leaves, approximately 15 to 20 mm in diameter, surrounded by water-soaked haloes that progressed inward from the margins. Water-soaked rotting symptoms were also observed in petioles. Disease incidence approached 80%. Abundant bacterial streaming was observed from lesions when examined at ×100. Bacteria consistently isolated from lesions formed cream-colored, glistening, convex colonies on sucrose peptone agar and produced a yellowish green, diffusible, nonfluorescent pigment on King's medium B. Four isolates from different symptomatic plants were selected for further study. All were aerobic, gram-negative rods that accumulated poly-β-hydroxybutyrate inclusions. In LOPAT tests, all induced a hypersensitive response in tobacco plants, caused soft rot of potato tubers, and were positive for levan, negative for arginine dihydrolase, and variable for oxidase. All isolates oxidized glucose, did not hydrolyze starch and were able to rot onion slices. Colonies developed at 41°C but not at 4°C. With the API 20NE test strips and database (bioMerieux, Buenos Aires, Argentina), all isolates matched (99% identity) Burkholderia cepacia, but their inability to metabolize cellobiose and sucrose further identified them as B. gladioli. For molecular identification, 23S rDNA was amplified by PCR using B. gladioli-specific primers LP1 and LP4, which yielded a 700-bp product (3), and PCR-restriction fragment length polymorphism of 16S rDNA using AluI (2). PCR products were identical to those from the type strain for B. gladioli, ICMP 3950, isolated from Gladiolus spp. that had been included in all tests for comparison. Pathogenicity was verified on D. picta and A. commutatum by spraying the plants with bacterial suspensions in sterile distilled water at 108 CFU/ml with and without wounding the leaves with a sterile needle and also by injection-infiltration of bacterial suspensions at 105 CFU/ml. In addition, another host plant, Gladiolus communis L., was inoculated in the same manner. Controls were sprayed or infiltrated with sterile distilled water. After 48 h in a humidity chamber, plants were kept at 25 ± 3°C in a greenhouse. In all hosts, symptoms were first detected 3 days after inoculation and lesions expanded to resemble natural infections within 4 to 7 days. All strains caused necrosis around the inoculation sites and lesions were identical to those induced by the ICMP reference strain. Bacteria were reisolated from each host tested and then the original and reisolated strains were compared by enterobacterial repetitive intergeneric consensus-PCR (1); DNA fingerprints of the reisolated strains were identical to those of the original strains, thereby fulfilling Koch's postulates. No lesions were observed on controls or on plants inoculated by spraying without wounding, suggesting that bacteria gain entry through wounds. On the basis of PCR and physiological tests the pathogen was identified as B. gladioli (2–4). To our knowledge, this is the first report of B. gladioli on Dieffenbachia and Aglaonema spp. References: (1) F. J. Louws et al. Appl. Environ. Microbiol. 60:2286, 1994. (2) C. Van Pelt et al. J. Clin. Microbiol. 37:2158, 1999. (3) P. W. Whitby et al. J. Clin. Microbiol. 38:282, 2000. (4) E. Yabuuchi et al. Microbiol. Immunol. 36:1251, 1992.


Plant Disease ◽  
2002 ◽  
Vol 86 (6) ◽  
pp. 697-697
Author(s):  
M. L. Molinero-Ruiz ◽  
J. M. Melero-Vara

In 2001, sunflower (Helianthus annuus L.) plants with symptoms of stem and root rot and wilt were observed in Soria, Spain. Light brown, water-soaked lesions developed on the collar of infected plants and extended along the stem, affecting the pith and causing early and sudden wilt. White mycelium and sclerotia (0.5 to 2 mm long) formed in the pith of stems. The sclerotia were disinfested in NaClO (10% vol/vol) for 1 min, transferred to potato dextrose agar (PDA), and incubated at 20°C. The fungus consistently obtained was identified as Sclerotinia minor Jagger (1). Pathogenicity was confirmed in a greenhouse experiment (15 to 25°C, 13 h light). Seven-week-old plants of six genotypes of sunflower (‘Peredovik’, HA89, HA821, HA61, RHA274, and HA337) were inoculated by placing one PDA disk with active mycelial growth adjacent to each basal stem just below the soil line and covering it with peat/sand/silt (2:2:1, vol/vol). Six plants of each genotype were inoculated without wounding, and another six were inoculated immediately after stem base wounding with a scalpel; six wounded and uninoculated plants were used as controls. First symptoms (wilting) appeared 4 days after inoculation in all genotypes. Two weeks after inoculation, the percentage of dead plants ranged from 33 to 92% (depending on cultivar), white mycelium was observed at the base of affected plants, and sclerotia were present in the pith of diseased plants. There was no effect of plant wounding on disease incidence or severity, and the fungus was reisolated from inoculated plants. To our knowledge, this is the first report of S. minor in Spain. Reference: (1) L. M. Kohn. Mycotaxon IX 2:365, 1979.


2017 ◽  
Vol 18 (4) ◽  
pp. 219-220
Author(s):  
J. E. Woodward ◽  
P. A. Dotray ◽  
J. M. Cason ◽  
T. A. Baughman

Symptomatic Eclipta prostrate plants exhibiting symptoms of Sclerotinia blight were collected from a peanut field near Stephenville, TX. Pathogenicity tests demonstrated that isolates obtained were pathogenic on both E. prostrate and peanut. While E. prostrate has been reported as a weed host of Sclerotinia minor, this to our knowledge is the first reported occurrence of the disease in Texas.


Plant Disease ◽  
2013 ◽  
Vol 97 (9) ◽  
pp. 1250-1250 ◽  
Author(s):  
S. T. Koike

Mexican sunflower (Tithonia rotundifolia) is a plant in the Asteraceae that is grown commercially as a cutflower commodity and also as a beneficial insectary plant. In June 2012 in coastal California (Santa Cruz County), several fields of organic lettuce (Lactuca sativa) were interplanted with direct-seeded rows of Mexican sunflower (cv. Torch) in order to attract beneficial insects. When approximately 2 to 3 weeks from harvest, lettuce plants began to wilt and collapse. Lettuce crowns were decayed and covered with white mycelium and small (0.5 to 3 mm diameter), irregularly shaped, black sclerotia. These plants were confirmed to have lettuce drop disease caused by Sclerotinia minor (2). In addition, Mexican sunflower plants began to wilt and eventually died. Initial symptoms on crowns and bases of the main stems in contact with soil consisted of a light tan discoloration. These discolored areas turned darker brown, became necrotic, and later were covered with white mycelium and sclerotia that were identical to those found on lettuce. Symptomatic sunflower stems were surface disinfested and small pieces from the margins of necrotic areas were placed into petri plates containing acidified potato dextrose agar. Resulting fungal colonies were white, produced profuse numbers (approx. 39 sclerotia/cm2) of small black sclerotia, and were identified as S. minor. Six-week-old Mexican sunflower plants grown in a peat moss-based rooting medium in 5-cm square pots were used to test the pathogenicity of four isolates. Isolates were grown on cubed and autoclaved potato pieces and resulting sclerotia were recovered and dried (1). For each isolate, 12 plants for each of three cultivars (cvs. Fiesta del Sol, Torch, and Yellow Torch) were inoculated by placing 3 to 5 sclerotia 1 cm below the soil level and adjacent to the plant crowns/stem bases. Sterile sand was placed next to crowns of the control plants. Plants were maintained in a greenhouse at 22 to 24°C. Symptom development was rapid and after 6 to 7 days, inoculated Tithonia plants exhibited brown necrosis at inoculated areas. After 10 days, Tithonia crowns were decayed and plants wilted. S. minor was reisolated from selected necrotic crown and stem tissues. Diseased plants that were not used for reisolations later supported the growth of the characteristic white mycelium and black sclerotia. There were no significant differences between the Tithonia cultivars, and overall disease incidence ranged from 74 to 100%. Non-inoculated plants were asymptomatic. The experiment was repeated and results were similar. In addition, the sclerotia of the four Tithonia isolates were similarly inoculated onto sets of 12 romaine lettuce plants (cv. Green Towers). After 5 to 6 days, all plants developed lettuce drop disease and the pathogen was reisolated. To my knowledge, this is the first report of Mexican sunflower as a host of S. minor. These findings indicate that Mexican sunflower and lettuce are susceptible to the same lettuce drop pathogen, and that this beneficial insectary plant could increase soilborne inoculum of S. minor. Growers should therefore be aware of the host status of beneficial insectary and other plants interplanted with crops. References: (1) P. Chitrampalam et al. Phytopathology 101:358, 2011. (2) K. V. Subbarao. Plant Dis. 82:1068, 1998.


Plant Disease ◽  
2004 ◽  
Vol 88 (3) ◽  
pp. 312-312
Author(s):  
J. E. Hollowell ◽  
B. B. Shew

The soilborne fungus Sclerotinia minor Jagger is a major pathogen of peanut (Arachis hypogaea L.) in North Carolina and overwinters in soil, on crop debris, or on winter annual weed species (1). Bleached stems and small, black sclerotia are typically seen on peanut plants infected by S. minor. Carolina geranium (Geranium carolinianum L.) is one of several winter annual weed species found during winter fallow in peanut production areas of northeastern North Carolina. During a March 2002 survey of previously harvested peanut fields, plants of Carolina geranium were observed with typical signs and symptoms of infection caused by S. minor. Symptomatic plants with bleached stems and signs of small, black sclerotia were collected in the field and returned to the laboratory. Pathogen isolation and fungal identification were performed from the symptomatic tissues by placing 1- to 2-cm sections of stems on potato dextrose agar after rinsing with tap water and towel drying. Pure cultures of S. minor were obtained and observed to have white, fluffy mycelium and small, black irregular-shaped sclerotia (<2 mm) produced abundantly and scattered over the culture surface. Pathogenicity was tested by inoculating stems of three symptom-free Carolina geranium plants with 2-day-old fungal mycelium from pure isolation. Mycelial agar plugs, 4 mm in diameter, were held in place with self-sticking bandaging gauze. Plants were misted, enclosed in plastic bags, and incubated at ambient temperature (24°C) on the laboratory counter top. Bleached water-soaked lesions developed on the stems, and leaves became chlorotic after 8 days. Following 8 days of incubation, S. minor was reisolated from all inoculated plants. Three noninoculated plants remained healthy over the incubation period. The performance of Koch's postulates confirmed that Carolina geranium is a host of S. minor. To our knowledge, this is the first report of S. minor on G. carolinianum. These results indicate that G. carolinianum is a potential overwintering host for S. minor in peanut fields. Infected weed hosts allow reproduction of the fungus in the winter, potentially resulting in more disease on peanut planted in the spring. Reference: (1) J. E. Hollowell et al. Plant Dis. 87:197, 2003.


1923 ◽  
Vol 14 (1-10) ◽  
pp. 291-377 ◽  
Author(s):  
Robert Miller

The forest area in Illinois to which this report applies is bounded by the Mississippi River on the west and the thrid principal meridian on the east, and extends in a north and south direction from Thebes, in Alexander county, to Chester, in Randolph county. It comprises all of Jackson county and portions of Union, Alexander, Pulaski, and Randolph counties, a total of 697,286 acres. It forms the western part of the Ozark highlands of southern Illinois (Colyer, '22), a region which extends across the state for 75 miles, with an average width of about 25 miles, from the mouth of the Big Muddy on the Mississippi to Shawneetown on the Ohio.


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