Search PMN  


PDF version
for printing

Peer Reviewed

© 2006 Plant Management Network.
Accepted for publication 27 March 2006. Published 31 May 2006.

Sclerotinia Blight in Georgia and Evidence for Resistance to Sclerotinia sclerotiorum in Runner Peanuts

Jason E. Woodward, Graduate Research Assistant, Timothy B. Brenneman, Professor, Robert C. Kemerait, Jr., Associate Professor, and Albert K. Culbreath, Professor, Coastal Plain Experiment Station, Department of Plant Pathology, University of Georgia, Tifton 31793; and James R. Clark, Extension Coordinator, University of Georgia Cooperative Extension, Baxley 31515

Corresponding author: Jason E. Woodward.

Woodward, J. E., Brenneman, T. B., Kemerait, R. C., Jr., Culbreath, A. K., and Clark, J. R. 2006. Sclerotinia blight in Georgia and evidence for resistance to Sclerotinia sclerotiorum in runner peanuts. Online. Plant Health Progress doi:10.1094/PHP-2006-0531-01-RS.


Sclerotinia blight (Sclerotinia sclerotiorum (Lib.) de Bary) was recently identified in a commercial peanut (Arachis hypogaea L.) field in Appling County, GA. Symptoms were first observed on the cultivars Tifrunner and Georgia 02C. Plant inoculations and a detached leaflet assay were conducted to determine the susceptibility of the cultivars Georgia Green, Georgia 02C, Georgia 03L, AP-3, Georgia 01R, Hull, C-99R, and Tifrunner. For plant inoculations, lesion lengths were greatest for Okrun, the susceptible control, and Georgia 02C; lesion lengths for C-99R and Georgia 01R did not differ significantly from Tamspan 90, the resistant control. Georgia Green, the current commercial standard, exhibited intermediate lesion lengths. Similar results were obtained from the detached leaflet assay. These results suggest that differing levels of resistance to S. sclerotiorum are available in runner cultivars used in the southeastern United States.


Sclerotinia blight, caused by the soilborne fungus Sclerotinia minor Jagger, is a destructive disease of peanut (Arachis hypogaea L.). The disease was first identified in the Virginia-North Carolina region in 1971 (16) and has since become established in Oklahoma (22) and Texas (26). Although S. minor is typically associated with Sclerotinia blight, S. sclerotiorum (Lib.) de Bary has also been shown to incite the disease (14,18). While S. sclerotiorum is rarely found causing disease on peanut in the United States, it is more prevalent in Australia (4) and Argentina (13).

Sclerotinia sclerotiorum causes severe disease on various members of the family Brassicaceae in the southeastern United States (1). In the mid to late 1980s, canola (Brassica napus L.) was being evaluated as a winter crop in Georgia. Severe epidemics of stem rot, caused by S. sclerotiorum, were observed and isolates were found to be pathogenic to peanut in vivo (3); however, attempts at field inoculations with S. sclerotiorum were unsuccessful, presumably due to unfavorable environmental conditions. Also, S. sclerotiorum generally infects via ascospores produced in apothecia, which are only observed during the winter months in south Georgia (T. Brenneman, unpublished data). Previous reports for S. minor suggest that cool air and soil temperatures along with available moisture are required for disease development (8,15). In vitro studies have found that the optimum temperature range for germination of sclerotia is 18 to 26°C (26) and 21°C for mycelial growth (17). Such environmental conditions are generally not experienced in the southeastern United States during the peanut growing season.

Tomato spotted wilt, caused by Tomato spotted wilt tospovirus (TSWV), is an increasingly important disease throughout the peanut-growing areas of Alabama, Florida, and Georgia. The development and release of spotted wilt resistant cultivars has resulted in the suppression of spotted wilt epidemics (5,23); however, cultivars with improved resistance to spotted wilt are often late-maturing. These cultivars require 150 to 160 days to reach optimum maturity in the southeast, whereas the more commonly grown mid-maturing cultivars, such as Georgia Green, require approximately 135 days to reach maturity (2). As the later-maturing cultivars gain popularity, peanut producers in the southeast could be faced with additional disease problems later in the season.

Sclerotinia blight (S. sclerotiorum) was identified in a commercial peanut field in Appling County, GA in October of 2004 (27,28). Dense tufts of white mycelium (Fig. 1) and water-soaked lesions were prevalent near the soil surface in diseased areas. Infected tissues were bleached and had a shredded appearance. Large, irregular-shaped sclerotia were found on the surface and imbedded in the pith cavity of stems (Fig. 2). Currently, little information is available regarding Sclerotinia blight resistance in runner cultivars, and that information is limited to S. minor (6,7,10). The objectives of this research were to (i) document through field observations the susceptibility of commercially available peanut cultivars to S. sclerotiorum, and (ii) verify the susceptibility of the cultivars with in vitro inoculations.


Fig. 1. Active mycelium and sclerotial initials of Sclerotinia sclerotiorum on peanut.


Fig. 2. Shredding of an infected peanut mainstem caused by Sclerotinia sclerotiorum with sclerotia on and within the infected tissue.

Field Observations of S. sclerotiorum on Runner Cultivars

The field site where the disease was observed had a long history of corn (Zea maydis L.) production, and cotton (Gossypium hirsutum L.) had been planted in field the previous two seasons (2002 and 2003). This location was initially chosen to evaluate the response of eight peanut cultivars to reduced fungicide programs for the management of early leaf spot, caused by Cercospora arachidicola Hori; late leaf spot, caused by Cercosporidium personatum (Berk. & M.A. Curtis) Deighton; and stem rot, caused by Sclerotium rolfsii Sacc. (29).

Soils at the location were a Tifton fine-loamy sand with less than 2% organic matter. Cultivars evaluated in this trial included Georgia Green, Georgia 02C, Georgia 03L, AP-3, Georgia 01R, Hull, Tifrunner, and C-99R. Bradyrhizobium sp., were applied in-furrow as Lift (Nitragin Corp., Brookfield, WI) at a rate of 1.2 liter/ha. Peanuts were strip-tilled into a heavy rye (Secale cereale L.) cover on 11 June 2004 in a single row pattern. Glysophate (Roundup 4 EC; Monsanto, Kansas City, MO) at a rate of 1.28 kg/ha was applied to kill the cover crop two weeks prior to planting. The strip-till implement (Kelly Manufacturing Company, Tifton, GA) had a subsoil shank to loosen the plow pan 30 cm beneath the row, and tilled a strip 20 cm wide. Cultivars were planted at 19.7 seed/m of row on 91-cm row spacing. This was a non-irrigated field, and planting was delayed until adequate soil moisture was present. Regional weather data were obtained from a University of Georgia system located approximately 15 mi south of the field site (12).

Cultivars were planted in three separate trails to evaluate their performance to a standard 7-spray program (Trial 1), a reduced 3-spray program (Trial 2), and a non-treated control program (Trial 3). The fungicide programs evaluated at this location included propiconazole plus chlorothalonil, azoxystrobin and tebuconazole. None of the aforementioned compounds are registered for control of Sclerotinia spp. in peanut; however, chlorothalonil has been shown to increase Sclerotinia blight at least with S. minor (9). Chlorothalonil rates included in these trials were 0.84 kg ai/ha applied as Bravo WeatherStik (Syngenta Crop Protection, Greensboro, NC) with the standard and reduced program receiving 3 and 1 application, respectively. Plots were a single bed 1.8 m wide and 61 m long with two rows per bed. Because of planter constraints, cultivars were blocked by maturity and planted in alternating strips for each of the three trials. Pod development was monitored using the hull scrape method (24). The mid-maturing cultivars were fully mature and inverted on 1 November; whereas late-maturing cultivars were inverted on 11 November, approximately 10 to 14 days premature, to avoid frost. The incidence of Sclerotinia blight was assessed 24 h after digging by determining the number of disease loci per plot (<30 cm per locus) (19). Disease incidence was determined for each plot and data were pooled across the three trials.

The 2004 growing season was unique in that several tropical storm systems impacted the area late in the season. In addition to ample rainfall, mean air temperatures below 20°C were recorded over several periods prior to the disease being observed and harvest (Fig. 3). Because the cultivars could not be randomized, only average disease incidences and their respective standard deviations are presented (Table 1). Differences in reaction to S. sclerotiorum were observed in the cultivars evaluated. Disease incidence was substantially lower for the mid-maturing cultivars when compared to the late-maturing cultivars. For the mid-maturing cultivars, disease incidence ranged from 0% for Georgia 03L to 3.5% for Georgia 02C, with an overall mean of 1.9% and median of 1.7%, while disease incidence for the late-maturing cultivars ranged from 4.3% for Hull to 22.7% for Tifrunner with an overall mean of 10.1% and median of 7.7% (Table 1).


Fig. 3. Daily rainfall (bars) and mean daily temperature (squares) during the 2004 growing season. Data were obtained from a regional weather station located in Alma, Georgia. Symbols denote initial disease observation (arrow), and disease rating date for mid-maturing (asterisk) and late-maturing (double asterisks) cultivars.


Table 1. Mean Sclerotinia blight incidence in field plantings of mid- and late-maturing runner peanut cultivars in 2004x.

Cultivar Maturity Growth habit  Ny Disease
incidence ± S.E.
Georgia Green Mid Upright 6 1.0 ± 0.6       
Georgia 02C Mid Upright 4 3.5 ± 1.0       
Georgia 03L Mid Upright 4 0.0 ± 0.0       
AP-3 Mid Upright 2 2.5 ± 0.7       
C-99R Late Mod. Prostrate 4 6.0 ± 3.4       
Georgia 01R Late Prostrate 8 7.3 ± 4.1       
Hull Late Prostrate 4 4.3 ± 3.8       
Tifrunner Late Upright 4 22.7 ± 2.9       

 x Incidence per 61 m of row.

 y N = the number of observations.

Screening for Resistance

Greenhouse tests were conducted on the eight cultivars from the field test. The cultivars Okrun and Tamspan90 were included for comparison and served as susceptible and resistant controls, respectively (7). Seeds were planted in 10-cm pots containing a sand:peat (2:1) potting mix, placed in a growth chamber and maintained at 28°C with a 12-h photoperiod for 10 weeks. Plants were then removed from the growth chamber and stems were wound inoculated 3 cm below the second fully expanded leaf. Pots were placed in a dew chamber, arranged in four randomized complete blocks and incubated at 20°C and 95% relative humidity. This experiment was repeated for a total of eight replications.

An additional assay used leaflets excised from the second fully expanded leaf of 10-week-old greenhouse grown plants (10). Pairs of leaflets were placed in plastic petri plates (25 × 30 mm) lined with sterile filter paper, which was moistened with 2.5 ml of sterile, distilled water. Potato dextrose agar plugs (4-mm-diameter) were taken from the leading edge of actively growing cultures of S. sclerotiorum and placed mycelia side down in the center of each leaflet. Petri plates were arranged in a randomized complete block design, and placed in a dew chamber. Plates were incubated as described above for 72 h. Lesion area was calculated by measuring lesion and width. There were a total of four replications, and the experiment was repeated once. Data from the whole plant inoculation tests and the detached leaflet assays were subjected to analysis of variance and Fisher’s protected least significant differences were calculated for the separation of means (21). Subsequent references to significant differences among means are at the P ≤ 0.05 level.

Cultivar × trial interactions for the whole plant inoculations and detached leaflet assays were not significant; therefore, data from both trials were pooled for analysis. Symptoms appeared three days after stem inoculations. Lesion length at five days after inoculation ranged from 7.7 to 14.8 cm (Fig. 4). All mean lesion lengths were significantly less than those on Okrun, the susceptible control. Mean lesion lengths for the cultivars C-99R and Georgia 01R did not differ from Tamspan 90, the resistant control cultivar, whereas lesion lengths of Georgia Green were intermediate.


Fig. 4. Mean lesion lengths caused by stem inoculations of Sclerotinia sclerotiorum on 10 peanut cultivars. Bars with the same letter are not significantly different according to Fisher’s Protected LSD (P ≤ 0.05). Cultivars evaluated included Okrun, Georgia 02C, Tifrunner, Georgia Green, Georgia 03L, AP-3, Hull, C-99R, Tamspan 90, and Georgia 01R.


Similar results were observed in the detached leaflet assays (Fig. 5). Lesions were largest on the cultivars Okrun and Georgia 02C with areas of 388 and 314 mm2, respectively. Lesion areas for AP-3, Hull, C-99R, and Georgia 01R did not differ significantly from Tamspan 90 and ranged from 45.6 to 93.7 mm2. Georgia Green and Georgia 03L expressed intermediate levels of resistance with lesion areas of 198 and 196 mm2, respectively.


Fig. 5. Mean lesion area caused by Sclerotinia sclerotiorum on detached leaflets of 10 peanut cultivars. Bars with the same letter are not significantly different according to Fisher’s Protected LSD (P ≤ 0.05). Cultivars evaluated included Okrun, Georgia 02C, Tifrunner, Georgia Green, Georgia 03L, AP-3, Hull, C-99R, Tamspan 90, and Georgia 01R.



Sclerotinia blight is an economically important disease throughout peanut-producing regions of Oklahoma, Texas, and Virginia and North Carolina (18). Although S. sclerotiorum is commonly recovered from soils in Georgia, Sclerotinia blight of peanut has never previously been found there. One explanation for this could be that typical environmental conditions during the peanut growing season are not conducive for growth of the fungus. Phipps (15) has speculated that activity of S. minor is inhibited when soil temperatures exceed 28°C. The average soil temperatures during the growing season in south Georgia ranges from 25.1 to 31.3°C (unpublished data). Although, S. sclerotiorum typically infects following carpogenic germination, the authors have not observed apothecia within the peanut growing season. Infections within the field all developed at the soil surface and appeared to have originated from myceliogenic germination of sclerotia, supporting previous reports that mycelia are capable of causing basal infections in other hosts (25).

Ample precipitation and unseasonably low temperatures during the latter part of the 2004 growing season were favorable for development of Sclerotinia blight (8,15). Results from the field observations suggested that varying levels of resistance to S. sclerotiorum may be present in the cultivars evaluated. Overall, less disease was observed in the earlier-maturing cultivars at harvest than in the later-maturing cultivars; however, the earlier-maturing cultivars had less exposure to favorable environmental conditions at the end of the season. The cultivars evaluated reacted differently to S. sclerotiorum in the field than in the growth chamber experiments, although the resistant and susceptible control cultivars separated out as previously reported (7) in both in vivo assays. In the field, the cultivar Tifrunner exhibited the highest level of disease incidence, whereas Georgia Green and Georgia 02C had substantially less disease. Results from growth chamber experiments indicated that disease development for Tifrunner, Georgia Green, and Georgia 02C was similar to Okrun, the susceptible control. These findings are consistent with field resistance data for S. minor (7). Damicone et al. (6) reported that the majority of highly resistant entries from a core collection of peanut accessions exhibited an upright growth habit whereas two of the moderately resistant entries had a prostrate growth habit. In addition, resistance to Sclerotinia blight appeared to be associated with earlier maturity.

Detached leaf and leaflet inoculations have been used to evaluate host resistance to S. minor in peanut (10) and S. sclerotiorum in common bean (20). Results from leaf and plant inoculations were highly correlated (R2 = 0.76, P = 0.003), suggesting that either method can be used to identify differences in reaction to Sclerotinia blight. Results from both assays indicated that C-99R and Georgia 01R possess levels of resistance similar to Tamspan 90, even though the two cultivars were not originally selected for Sclerotinia blight resistance. Despite these findings, little information is available regarding S. sclerotiorum on peanut; therefore, additional studies are required to further define the levels of resistance to S. sclerotiorum in runner cultivars used in the southeast.

The long-term implications of these findings are uncertain. The excessive moisture and cool temperatures late in the season compounded by late harvest may have been unique to the 2004 season. The field had a history of winter weeds belonging to the Brassicaceae family (J. Clark, personal observation), which could have served as a source of initial inoculum (11). Field experiments were repeated in an adjacent field in 2005, but environmental conditions were not conducive for Sclerotinia blight. No further occurrences of the disease have been reported since the initial observation. It is unlikely that Sclerotinia blight will become a problem in the southeastern production region unless planting late-maturing cultivars to minimize losses associated with TSWV becomes a common practice. In that case, Sclerotinia blight-related losses could be incurred when peanuts are planted in infested fields and exposed to prolonged cool, wet periods late in the fall.


The authors would like to express their appreciation to Kent Fountain and Roger Branch from Southeastern Gin and Peanut Inc. for supplying the land used in this study and for their cooperation during this project. We thank H. A. Melouk for providing seed of the susceptible and resistant controls. The contributions of Reid Turner, Hugh Lightsey, Mitchel Bryant, Jimmy Mixon, and Lewis Mullis are gratefully acknowledged.

Literature Cited

1. Alfieri, S. A., Jr., Langdon, K. R., Wehlburg, C., and Kimbrough, J. W. 1984. Index of Plant Diseases in Florida (Revised). Fla. Dep. Agric. Consum. Serv. Bull. 11:1-139.

2. Branch, W. D. 1996. Registration of ‘Georgia Green’ peanut. Crop Sci. 36:806.

3. Brenneman, T. B., Sumner, D. R., and Phillips, D. V. 1991. Sclerotinia sclerotiorum on canola in Georgia and its potential as a pathogen on peanut. Plant Dis. 75:319.

4. Cruickshank, A. W., Cooper, M., and Ryley, M. J. 2002. Peanut resistance to Sclerotinia minor and S. sclerotiorum. Aust. J. Agric. Res. 53:1105-1110.

5. Culbreath, A. K., Todd, J. W., Gorbet, D. W., Brown, S. L., Baldwin, J., Pappu, H. R., and Shokes, F. M. 2000. Reaction of peanut cultivars to spotted wilt. Peanut Sci. 27:35-39.

6. Damicone, J. P., Jackson, K. E., Dashiell, K. E., Melouk, H. A., and Holbrook, C. C. 2003. Reaction of the peanut core collection to Sclerotinia blight and Pepper spot. (Abstr.) Proc. Am. Peanut Res. Educ Soc. 35:55-56.

7. Damicone, J. P., and Jackson, K. E. 2004. Cultivar responses to fungicide programs for control of Sclerotinia blight. Pages 48-51 in: Results of field trials on control of peanut diseases in 2003. Oklahoma State Univ., Oklahoma Agric. Exp. Sta. Res. Rep. P-10031.

8. Dow, R. L., Porter, D. M., and Powell, N. L. 1988. Effects of environmental factors on Sclerotinia minor and Sclerotinia blight of peanut. Phytopathology 78:672-676.

9. Hau, F. C., and Beute, M. K. 1983. Effects of chlorothalonil on the virulence and physiology of a nontargeted pathogen, Sclerotinia minor. Phytopathology 73:475-479.

10. Hollowell, J. E., Shew, B. B., and Isleib, T. G. 2002. Evaluating isolate aggressiveness and host resistance from peanut leaflet inoculations with Sclerotinia minor. Plant Dis. 87:402-406.

11. Hollowell, J. E., Shew, B. B., Cubeta, M. A., and Wilcut, J. W. 2003. Weed species as hosts of Sclerotinia minor in peanut fields. Plant Dis. 87:197-199.

12. Hoogenboom, G. 2005. Georgia Automated Environmental Monitoring Network. Online. Univ. of Georgia, Griffin.

13. Marinelli, A., March, G. J., Rago, A., and Giuggia, J. 1998. Assessment of crop losses in peanut caused by Sclerotinia sclerotiorum, S. minor, and Sclerotium rolfsii in Argentina. Int. J. Pest Manag. 44:251-254.

14. Melouk, H. A., Jackson, K. E., and Damicone, J. P. 2003. First report of Sclerotinia blight on peanut in Nebraska. (Abstr.) Proc. Am. Peanut Res. Educ Soc. 35:77.

15. Phipps, P. M. 1995. An assessment of environmental conditions preceding outbreaks of Sclerotinia blight of peanut in Virginia. Peanut Sci. 22:90-93.

16. Porter, D. M., and Beute, M. K. 1974. Sclerotinia blight of peanut. Phytopathology 64:263-264.

17. Porter, D. M., and Phipps, P. M. 1985. Effects of three fungicides on mycelial growth, sclerotium production, and development of fungicide-tolerant isolates of Sclerotinia minor. Plant Dis. 69:143-146.

18. Porter, D. M., and Melouk, H. A. 1997. Sclerotinia blight. Pages 34-36 in: Compendium of Peanut Diseases. 2nd ed. N. Kokalis-Burelle, D. M. Porter, R. Rodriquez-Kabana, D. H. Smith, and P. Subrahmanyam, eds. American Phytopathological Society, St. Paul, MN.

19. Rodriguez-Kabana, R., Backman, P. A., and Williams, J. C. 1975. Determination of yield losses to Sclerotium rolfsii in peanut fields. Plant Dis. Rep. 59:855-858.

20. Steadman, J. R., Powers, K., and Higgins, B. 1997. Screening common bean for white mold resistance using detached leaves. Annu. Rep. Bean Improv. Coop. 4:140-141.

21. Steel, R. G. B., and Torrie, J. H. 1980. Principles and Procedures of Statistics. McGraw-Hill, New York.

22. Wadsworth, D. F. 1979. Sclerotinia blight of peanuts in Oklahoma and occurrence of the sexual stage of the pathogen. Peanut Sci. 6:77-79.

23. Wells, M. L., Culbreath, A. K., Todd, J. W., Brown, S. L., and Gorbet, D. W. 2002. A regression approach for comparing field resistance of peanut cultivars to tomato spotted wilt tospovirus. Crop Prot. 21:467-474.

24. Williams, E. J., and Drexler, J. S. 1981. A non-destructive method for determining peanut pod maturity. Peanut Sci. 8:134-141.

25. Willetts, H. J., and Wong, J. A. L. 1980. The biology of Sclerotinia sclerotiorum, S. trifoliorum, and S. minor with emphasis on specific nomenclature. Bot. Rev. 46:101-165.

26. Woodard, K. E., and Simpson, C. E. 1993. Characterization of growth and sclerotial production of Sclerotinia minor from peanut in Texas. Plant Dis. 77:576-579.

27. Woodward, J. E., Brenneman, T. B., Kemerait, R. C., and Clark, J. R. 2005. First occurrence of Sclerotinia blight of peanut in Georgia. (Abstr.) Phytopathology 78:1025.

28. Woodward, J. E., Brenneman, T. B., Kemerait, R. C., Culbreath, A. K., and Clark, J. R. 2006. First report of Sclerotinia blight of peanut caused by Sclerotinia sclerotiorum in Georgia. Plant Dis. 90:111.

29. Woodward, J. E., Brenneman, T. B., Kemerait, R. C., Culbreath, A. K., Smith, N. B. and Clark, J. R. 2005. Impact of variety selection and reduced fungicide inputs in peanut fields with low fungal disease risk. Pages 65-70 in: 2004 Georgia Peanut Research and Extension Report. J. P. Beasley and W. Faircloth eds. University of Georgia Cooperative Extension Service and the U.S. Department of Agriculture, Tifton, GA. In press.