Fitness Attributes of Pythium aphanidermatum with Dual Resistance to Mefenoxam and Fenamidone.

Pythium aphanidermatum is the predominant species causing Pythium root rot on commercially grown poinsettias in North Carolina. Resistance to mefenoxam is common in populations of P. aphanidermatum but resistance to fenamidone and other quinone outside inhibitor fungicides has only just been reported in greenhouse floriculture crops. The in vitro sensitivity to the label rate of mefenoxam (17.6 µl active ingredient [a.i.]/ml) and fenamidone (488 µl a.i./ml) was determined for 96 isolates of P. aphanidermatum. Isolates were assigned to four fungicide phenotypes: mefenoxam-sensitive/fenamidone-sensitive (MefS, FenS), mefenoxam-sensitive/fenamidone-insensitive (MefS, FenR), mefenoxam-insensitive/fenamidone-sensitive (MefR, FenS), and mefenoxam-insensitive/fenamidone-insensitive (MefR, FenR). In all, 58% of isolates were insensitive to one (MefR, FenS = 36% and MefS, FenR = 16%) or both fungicides (MefR, FenR = 6%). A single point mutation in the cytochrome b gene (G143A) was identified in fenamidone-insensitive isolates. Mycelial growth rate at three temperatures (20, 25, and 30°C), in vitro oospore production, and aggressiveness on poinsettia were evaluated to assess relative fitness of sensitive and insensitive isolates. Isolates with dual insensitivity to mefenoxam and fenamidone had reduced radial hyphal growth at 30°C and produced fewer oospores than isolates sensitive to one or both fungicides. Isolates sensitive to both fungicides produced greater numbers of oospores. Aggressiveness on poinsettia varied by isolate but fungicide phenotype was not a good predictor of aggressiveness. These results suggest that populations of P. aphanidermatum with dual resistance to mefenoxam and fenamidone may be less fit than sensitive populations under our imposed experimental conditions but populations of P. aphanidermatum should continue to be monitored in poinsettia production systems for mefenoxam and fenamidone insensitivity.

Mefenoxam Sensitivity, Aggressiveness, and Identification of Pythium Species Causing Root Rot on Floriculture Crops in North Carolina.

Herbaceous ornamental plants exhibiting symptoms of Pythium root rot were collected from 26 greenhouses in 21 counties in North Carolina (NC) from 2010 to 2012. Plant symptoms ranged from mild stunting to severe wilting, root rot, and death. Roots were plated on selective media, and 356 isolates of Pythium were recovered from 34 host species. Selected isolates were identified by sequencing of the internal transcribed spacer (ITS) rDNA gene region. Seventeen Pythium species were identified, with P. aphanidermatum, P. irregulare, and P. myriotylum comprising 75% of the 320 isolates sequenced. Twelve of the 26 greenhouses had more than one species present. Mefenoxam sensitivity was tested in vitro by growing isolates in wells of microtiter plates containing clarified V8 agar amended with 100 µg a.i./ml mefenoxam. Colonization was scored after 24 to 48 h using a scale of 0 (no growth) to 5 (entire well colonized). Fifty-two percent of the isolates were resistant to mefenoxam (mean score ≥4). All 32 isolates of P. myriotylum were sensitive, whereas sensitivity varied among isolates of P. aphanidermatum and P. irregulare. Resistant and sensitive isolates of the same species were found within the same greenhouses. The aggressiveness of P. aphanidermatum and P. irregulare isolates was evaluated on poinsettia, Gerbera daisy, and petunia. P. aphanidermatum was more aggressive than P. irregulare on poinsettia and petunia; symptoms were mild and no differences in aggressiveness were observed on Gerbera daisy. Sensitivity to mefenoxam was not related to aggressiveness.

Sclerotinia blight resistance in Virginia-type peanut transformed with a barley oxalate oxidase gene.

Transgenic peanut lines expressing oxalate oxidase, a novel enzyme to peanut, were evaluated for resistance to Sclerotinia blight in naturally infested fields over a 5-year period. Area under the disease progress curve (AUDPC) for transgenic lines in single rows planted with seed from single-plant selections averaged 78, 83, and 90% lower than nontransgenic parents in 2004, 2005, and 2006, respectively. In addition, AUDPC in 14 transgenic lines planted with bulked seed in two-row plots averaged 81% lower compared with nontransgenic parents in 2005 and 86% lower in 16 transgenic lines in 2006. Six transgenic lines yielded 488 to 1,260 kg/ha greater than nontransgenic parents in 2005, and 10 lines yielded 537 to 2,490 kg/ha greater in 2006. Fluazinam (0.58 kg a.i./ha) fungicide sprays in 2008 and 2009 reduced AUDPC in transgenic and nontransgenic lines but AUDPC was lowest in transgenic lines. Without fluazinam, yields of transgenic lines averaged 1,133 to 1,578 kg/ha greater than nontransgenic lines in 2008 and 1,670 to 2,755 kg/ha greater in 2009. These results demonstrated that the insertion of barley oxalate oxidase in peanut conveyed a high level of resistance to Sclerotinia blight, and negated the need for costly fungicide sprays.

Evaluation of Microbial, Botanical, and Organic Treatments for Control of Peanut Seedling Diseases.

Diseases affecting stand establishment are a major obstacle to organic production of peanut (Arachis hypogaea). Stand losses of 50% or more are possible with untreated seed. Biological, botanical, and organic seed treatments or soil amendments were tested for efficacy against pre- and postemergence damping-off of peanut in greenhouse, microplot, and field plot trials. Seed of the lines Perry, GP-NC 343, and Bailey (tested as N03081T) were used in all trials. Commercial formulations of Bacillus subtilis (Kodiak), B. pumilus (Yield Shield), Trichoderma harzianum (T-22 PB and Plantshield HC), Muscodor albus, and Coniothyrium minitans (Contans); activated charcoal; two separate soil amendments of dried herbage of Monarda didyma cultivars; a commercial fungicide control (Vitavax PC); and an untreated control were tested in natural soil in the greenhouse. Vitavax PC and Kodiak were the only treatments that resulted in higher percent emergence and survival than in untreated seed. A separate greenhouse experiment was conducted in natural soil or natural soil infested with field isolates of Aspergillus niger. Seed were treated with Kodiak, copper hydroxide (Champion), Plantshield HC, Kodiak + Plantshield HC, Streptomyces griseoviridis (Mycostop), hot water, Vitavax PC, or were left untreated. Seedling emergence and survival was much lower in infested versus uninfested soil. Seed treatment with Kodiak increased percent emergence and survival compared to untreated seed, but was not as effective as Vitavax PC. Field microplot studies in 2007 and 2008 at Clayton, NC, evaluated four seed treatments on the peanut lines following small grain cover crops, soil amendment with M. albus, or no cover. Cover crops did not affect emergence or interact with seed treatments. In field studies in 2007 and 2008 at Lewiston, NC, the peanut lines were planted with M. albus infurrow, with Kodiak or T. harzianum seed treatments, or were untreated. In the 2007 trial, none of the treatments improved stands compared to the untreated check. In 2008, the highest stand counts were produced by seed treated with Kodiak. In both years, Bailey produced the greatest stand counts. A. niger was strongly associated with postemergence damping-off in the field. Regardless of peanut line, in many trials, Kodiak seed treatment increased emergence and survival over untreated seed.

A Site-Specific, Weather-Based Disease Regression Model for Sclerotinia Blight of Peanut.

In North Carolina, losses due to Sclerotinia blight of peanut, caused by the fungus Sclerotinia minor, are an estimated 1 to 4 million dollars annually. In general, peanut (Arachis hypogaea) is very susceptible to Sclerotinia blight, but some partially resistant virginia-type cultivars are available. Up to three fungicide applications per season are necessary to maintain a healthy crop in years highly favorable for disease development. Improved prediction of epidemic initiation and identification of periods when fungicides are not required would increase fungicide efficiency and reduce production costs on resistant and susceptible cultivars. A Sclerotinia blight disease model was developed using regression strategies in an effort to describe the relationships between modeled environmental variables and disease increase. Changes in incremental disease incidence (% of newly infected plants of the total plant population per plot) for the 2002-2005 growing seasons were statistically transformed and described using 5-day moving averages of modeled site-specific weather variables (localized, mathematical estimations of weather data derived at a remote location) obtained from SkyBit (ZedX, Inc.). Variables in the regression to describe the Sclerotinia blight disease index included: mean relative humidity (linear and quadratic), mean soil temperature (quadratic), maximum air temperature (linear and quadratic), maximum relative humidity (linear and quadratic), minimum air temperature (linear and quadratic), minimum relative humidity (linear and quadratic), and minimum soil temperature (linear and quadratic). The model explained approximately 50% of the variability in Sclerotinia blight index over 4 years of field research in eight environments. The relationships between weather variables and Sclerotinia blight index were independent of host partial resistance. Linear regression models were used to describe progress of Sclerotinia blight on cultivars and breeding lines with varying levels of partial resistance. Resistance affected the rate of disease progress, but not disease onset. The results of this study will be used to develop site- and cultivar-specific spray advisories for Sclerotinia blight.

Analysis of Factors That Influence the Epidemiology of Sclerotinia minor on Peanut.

In North Carolina, sclerotia of Sclerotinia minor germinate myceliogenically to initiate infections on peanut. The effects of soil temperature and soil matric potential (ψM on germination and growth of S. minor have not been well characterized, and little is known about relative physiological resistance in different parts of the peanut plant. Laboratory tests examined the ability of the fungus to germinate, grow, and infect detached peanut leaflets at soil temperatures ranging from 18 to 30°C at ψM of -100, -10, and -7.2 kPa. In addition, detached pegs, leaves, main stems, and lateral branches from three peanut lines varying in field resistance were examined for resistance to infection by S. minor. Sclerotial germination was greatest at 30°C and ψM of -7.2 kPa. Final mycelial diameters decreased with decreasing ψM, whereas soil matric potential did not affect lesion development. Mycelial growth and leaflet lesion expansion were maximal at 18 or 22°C. Soil ψM did not affect leaflet infection and lesion expansion. Lesions were not observed on leaves incubated at temperatures of 29°C or above, but developed when temperatures were reduced to 18 or 22°C 2 days after inoculation. Pegs and leaflets were equally susceptible to infection and were more susceptible than either main stems or lateral branches. Results of this work, particularly the effects of temperature on S. minor, and knowledge of peanut part susceptibility has application in improving Sclerotinia blight prediction models for recommending protective fungicide applications.

First Report of Sclerotinia minor on Allium vineale in North Carolina.

Allium vineale L. (wild garlic) is a bulbous perennial that emerges in early spring in many agricultural fields. The soilborne fungus Sclerotinia minor Jagger is a major pathogen found in many peanut (Arachis hypogaea L.) production areas of northeastern North Carolina. During September 2002, symptoms of bleached, water-soaked foliage and wilting were observed on several wild garlic plants growing in a 0.8-ha (2-acre) peanut research plot in Perquimans County, NC. We had previously observed similar symptoms on wild garlic at another location. Two symptomatic wild garlic plants were collected from the field. In the laboratory, symptomatic tissues were excised into 1- to 2-cm sections, rinsed in tap water, towel dried, and placed on potato dextrose agar (PDA) for fungal isolation and identification. Pure cultures with small, black, irregular-shaped sclerotia (<2 mm) scattered abundantly over the culture surface were distinctive of S. minor. Pathogenicity of isolates was tested by inoculating leaf blades near the leaf axils of two symptom-free wild garlic plants (vegetative stage, 4 cm high) with fungal mycelium from 2-day-old cultures. 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 an ambient temperature (24°C) on the laboratory countertop. Fluffy mycelium developed on leaves within 2 days. Plants wilted and bleached water-soaked lesions formed within 6 days after inoculation. Sclerotia were produced on leaf blades after approximately 14 days. Following the incubation period, S. minor was reisolated from the inoculated plants. Two plants treated similarly with plugs of pure PDA remained healthy over the incubation period. The performance of Koch's postulates confirmed that wild garlic is a host of S. minor. Although few monocots have been reported as hosts of S. minor, the fungus has been reported on two other species of Allium (A. cepa and A. satium), Gladiolus spp., and Cyperus esculentus (1,2). Weed hosts may support populations of S. minor during rotations to nonhosts, serve as reservoirs of inoculum, or act as infection bridges in peanut fields. References: (1) D. F. Farr et al. Fungal Databases. Systematic Botany and Mycology Laboratory. On-line publication. ARS, USDA, 2005. (2) M. S. Melzer et al. Can. J. Plant Pathol. 19:272, 1997.

First Report of Sclerotinia minor on Sida spinosa in North Carolina.

The soilborne fungus Sclerotinia minor Jagger is a major pathogen of peanut (Arachis hypogaea L.) in North Carolina, Virginia, Oklahoma, and Texas. The pathogen attacks several winter annual weed species (1). Economic crops that are hosts to S. minor are seldom grown in rotation with peanut; therefore, its pathogenicity on weed species is of importance in understanding how inoculum densities are maintained between peanut crops. During September 2004, signs of fluffy, white mycelium, small, black sclerotia, and symptoms of bleached leaves and stems were observed on prickly sida (Sida spinosa L.) in a peanut field in Bertie County, NC. Plants of prickly sida with similar signs and symptoms were observed previously in a Chowan County, NC peanut field. Prickly sida is one of several weed species commonly found in peanut fields and rotational crops in agricultural areas of northeastern North Carolina. Cultivation and herbicides usually keep prickly sida under control in the early part of the growing season, but as the summer progresses into early fall, it can become prevalent, as was true in the two fields reported here. Symptomatic tissues were excised into 1- to 2-cm sections, rinsed in tap water, blotted dry, and placed on potato dextrose agar (PDA). The pure cultures with small, black irregular-shaped sclerotia (<2 mm) scattered abundantly over the culture surface were distinctive of S. minor. Pathogenicity was determined by inoculating stems of two symptom-free prickly sida plants with 2-day-old fungal mycelium. 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 countertop. Fluffy mycelium developed on the stems in 2 days and water-soaked leaves and bleached lesions formed within 6 days after inoculation. Following the incubation period, S. minor was reisolated from the inoculated plants. Two plants treated similarly with plugs of pure PDA remained healthy over the incubation period. The performance of Koch's postulates confirmed that prickly sida is a host of S. minor. To our knowledge, this report of S. minor on prickly sida is also the first report of a plant in the family Malvaceae as a host of S. minor (2). Reference: (1) J. E. Hollowell et al. Plant Dis. 87:197, 2003. (2) M. S. Melzer et al. Can. J. Plant Pathol. 19:272, 1997.

First Report of Stem and Leaf Blight Caused by Sclerotinia minor on Geranium carolinianum in North Carolina.

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.

First Report of Sclerotium rolfsii on Common Chickweed in North Carolina.

Common chickweed (Stellaria media (L.) Cyrillo) is a common weed species found in agricultural fields of northeastern North Carolina. Symptomatic plants of common chickweed were observed during a March 2001 survey of winter annual weed species in Perquimans County, NC. The plants were growing in a harvested peanut field with a known history of southern stem rot caused by Sclerotium rolfsii Sacc. Water-soaked, bleached stems and chlorotic leaves were collected from plants and brought to the laboratory for isolation. Small portions (1 to 2 cm) of symptomatic stems and entire leaves were rinsed with tap water and placed on potato dextrose agar (PDA). Developing colonies were transferred to obtain pure cultures. The rapidly growing cultures had coarse, white mycelium typical of S. rolfsii and produced abundant, small, round, brown sclerotia approximately 2.0 mm in diameter on the surface of the culture. Clamp connections were observed with microscopic examination of mycelia. Pathogenicity of isolates was tested by placing 4-mm-diameter agar plugs of 2-day-old fungal mycelium on stems of three mature, nonsymptomatic chickweed plants. Agar plugs without fungal mycelium were used for the control treatment. Plugs were held in place with self-sticking bandage gauze. Plants were misted with water, enclosed in plastic bags, and incubated on a laboratory counter top at ambient temperature (24°C). Abundant mycelia developed, and water-soaked lesions and necrotic stems were observed. Noninoculated plants remained healthy and free of signs and symptoms during the incubation period. The fungus was reisolated on PDA, and pure cultures of S. rolfsii were obtained. Koch's postulates confirmed common chickweed was a host of S. rolfsii. To our knowledge, this is the first report of common chickweed as a host of S. rolfsii. Crop species commonly used in peanut rotations (corn, small grains, sorghum, and cotton) do not support populations of S. rolfsii. Many dicotyledonous weed species have been reported as hosts of S. rolfsii, but our observation of active disease on a winter weed species was unexpected. Colonization of winter weed, if prevalent, may enhance survival of S. rolfsii between crops of susceptible hosts such as peanut.

Weed Species as Hosts of Sclerotinia minor in Peanut Fields.

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.

Evaluating Isolate Aggressiveness and Host Resistance from Peanut Leaflet Inoculations with Sclerotinia minor.

Sclerotinia minor is a major pathogen of peanut in North Carolina, Virginia, Oklahoma, and Texas. Partial resistance to S. minor has been reported based on field screening, but field performance is not always correlated with laboratory or greenhouse evaluations of resistance. More efficient screening methods and better understanding of the mechanisms contributing to Sclerotinia blight resistance are needed, and a detached leaf assay was developed and evaluated. Detached leaflets of 12 greenhouse-grown peanut lines were inoculated on the adaxial surface with a 4-mm-diameter mycelial plug of a single isolate of S. minor. Leaflets were incubated in the dark at 20°C in Nalgene utility boxes containing moistened sand. Lesion length 3 days after inoculation ranged from 11 to 24 mm, with a mean of 19 mm. Lengths differed significantly among the entries, with GP-NC WS 12, an advanced breeding line derived from a cross of NC 6 × (NC 3033 × GP-NC WS 1), being the most resistant. Forty-eight isolates of S. minor obtained from peanut were inoculated on leaflets of the susceptible cultivar NC 7 and aggressiveness was assessed by measuring lesion-length expansion. Three days after inoculation, lesion length differed among the isolates and ranged from 2 to 24 mm, with a mean of 15 mm. Finally, the potential for specific interactions between peanut lines and S. minor isolates was evaluated. A subset of S. minor isolates was selected to represent the observed range of aggressiveness and a subset of peanut entries was selected to represent the range of resistance or susceptibility. Nine-week-old greenhouse- or field-grown plants were compared for five peanut entries. Main effects of isolates and entries were highly significant, but isolate-entry interactions were not significant. The most resistant peanut entry (GP-NC WS 12) performed consistently with all isolates regardless of plant source.

Resistance of Peanut to Sclerotinia Blight and the Effect of Acibenzolar-S-methyl and Fluazinam on Disease Incidence.

Sclerotinia minor, a soilborne fungal pathogen of peanut, can cause serious yield loss in North Carolina. A field test was implemented to study genotype reaction, and the effect of aciben-zolar-S-methyl (a plant activator) and the fungicide fluazinam on disease incidence. In all, 13 genotypes in 1997 and 12 genotypes in 1998 were evaluated. Three applications of acibenzolar-S-methyl (0.14 kg a.i./ha) or fluazinam (0.58 kg a.i./ha) were made on a calendar-based schedule. Disease ratings were made weekly in 1997 and every other week in 1998. Fluazinam suppressed disease at all sites and increased yield at two of three locations. Acibenzolar-S-methyl had no effect on disease incidence or yield. The advanced breeding line N92056C and cvs. Tam-run 98 (TX 901417) and Perry (N93112C) had moderate to high levels of resistance to S. minorand produced high yields compared with susceptible cv. NC 7. Lines derived from wild species also demonstrated moderate to high levels of resistance relative to NC 7 and represent potential breeding lines.

Wheat Straw Mulch and Its Impacts on Three Soilborne Pathogens of Peanut in Microplots.

Experiments were conducted in 1992, 1993, and 1994 to determine the effects of surface residue on incidence of Cylindrocladium black rot (CBR), Sclerotinia blight, and Southern stem rot of peanut in microplots in North Carolina. Soil was infested with either Cylindrocladium parasiticum, Sclerotium rolfsii, or Sclerotinia minor and plots were planted with the peanut cultivars NC 7 or NC 10C. Wheat straw was applied to establish 80 to 90% soil-surface coverage. Disease incidence data were collected every 2 weeks in 1992 and weekly in 1993 and 1994. Southern stem rot incidence did not increase with straw amendment but final inoculum density of Sclerotium rolfsii was highest in straw-amended plots. Straw amendment enhanced CBR incidence in 1992, but had minimal effects in 1993 and 1994. Neither root rot severity nor inoculum density of C. parasiticum was affected by straw treatment. Straw application reduced Sclerotinia blight in 1992 and 1993 but not in 1994 compared with unamended plots. Initial inoculum density had the greatest impact on final Sclerotinia minor populations. Soil temperature and moisture were monitored in 1993 and 1994. Soil at 0 to 2 cm of depth in strawamended microplots was 1 to 2°C cooler than in unamended plots.

Yellow Nutsedge (Cyperus esculentus L.) as a Host of Sclerotinia minor.

Sclerotinia minor Jagger is a major pathogen of peanut (Arachis hypogaea L.) in North Carolina, Virginia, Oklahoma, and Texas. Economic crops that are hosts to S. minor are seldom grown in rotation with peanut, and the pathogenicity of S. minor to most weed species commonly found in peanut fields is unknown. In September 2000, signs and symptoms of Sclerotinia infection were observed on plants of yellow nutsedge growing in peanut fields in Bertie County, NC. Fluffy white mycelium, water soaked and bleached areas of the leaves were observed on basal portions of plants. Isolations were made from a symptomatic plant growing in a peanut field at the Peanut Belt Research Station at Lewiston-Woodville, NC. Small portions (1 to 2 cm) of symptomatic leaves were placed on potato dextrose agar (PDA) and pure cultures typical of S. minor were obtained. Small black irregular-shaped sclerotia (<2 mm) were produced abundantly and scattered over the culture surface (1). Pathogenicity was tested by placing agar plugs of mycelium of the fungus between the leaf blades of potted mature yellow nutsedge plants. Plants were misted with water, enclosed in plastic bags, and incubated on a lab counter top at ambient temperature (˜24°C). Mycelia developed after 3 to 4 days and chlorotic leaves appeared by day 7. Sclerotia were observed in 11 days on seedheads, which were distal from the site of inoculation. Uninoculated plants did not develop symptoms. The fungus was reisolated on PDA, and typical cultures of S. minor with small sclerotia were obtained. The nutgrass isolate was inoculated onto detached peanut leaves and typical symptoms developed. This is the first report of yellow nutsedge as a host of S. minor. Reference: (1) L. M. Kohn. Mycotaxon 9:365-444, 1979.

Occurrence of Pod Rot Pathogens in Peanuts Grown in North Carolina.

Pod rot diseases historically caused significant losses in peanut production in North Carolina. Advances in the understanding of pod rot diseases and changes in cultural practices minimized losses in the years since 1979. By the early 1990s, however, some peanut growers began to observe pod rot that apparently was not associated with infection by common soilborne pathogens. Incidence of pod rot also was high in research plots used to study conservation tillage methods. Selected farms were surveyed in the fall of 1994, 1995, and 1996 to identify the fungi associated with pod rot symptoms in North Carolina. Over the three years of the study, more than 6,000 symptomatic pods from 125 peanut fields were assayed for Rhizoctonia spp., Pythium spp., Cylindrocladium parasiticum, Sclerotium rolfsii, and Sclerotinia minor. All five pathogens were isolated during the field survey, with Pythium spp. and Rhizoctonia spp. isolated most frequently. Rhizoctonia spp. were the dominant pathogen in the majority of fields in 1994, whereas Pythium spp. predominated in 1995 and 1996. Combinations of pathogens were identified from 12 to 15% of pods; Rhizoctonia spp. + Pythium spp. and Pythium spp. + C. parasiti-cum were the most frequent combinations. The mean estimated incidence of pod rot was 6.6% in 1995 and 5.9% in 1996. The effects of cover crops and tillage on pod rot incidence were studied in microplots in 1995 and 1996. In 1995, winter cover crops (wheat, oat, rye, and fallow soil) did not affect pod rot incidence, but incidence was greater in no-till treatments compared to plots with conventional tillage. Pod rot incidence did not differ among infestation treatments and no interactions among pathogen, cover crop, or tillage treatments were significant. In contrast, significant (P = 0.04) interactions among winter cover crops and tillage occurred in 1996. Tillage did not affect pod rot incidence following wheat or oats, but incidence following rye was much greater in no-till than in tilled plots.