Sclerotium rolfsii (Southern blight of vegetables and melons)

Taxonomy

Domain	Eukarya
Kingdom	Fungi
Phylum	Basidiomycota
Subphylum	Agaricomycotina
Class	Agaricomycetes
Subclass	Agaricomycetidae
Order	Agaricales
Family	Amylocorticiaceae
Genus	Agroathelia

Scientific Name

Agroathelia rolfsii

Scientific Name Synonyms

Sclerotium rolfsii

Athelia rolfsii

Common Name

southern blight

Author: Garrett Ridge and Barbara Shew, North Carolina State University

Scientific Name Synonym

Athelia rolfsii (Curzi) C.C. Tu & Kimbr. [Teleomorph]

Pathogen

Sclerotium rolfsii is a necrotrophic, soilborne fungal plant pathogen that produces abundant white mycelium on infected plants and in culture. Advancing mycelium and colonies often grow in a distinctive fan-shaped pattern and the coarse hyphal strands may have a somewhat ropy appearance. Cells are hyaline with thin cell walls and sparse cross walls. Main branch hyphae may have clamp connections on each side of the septum (Figure 1). In agar plate culture, sclerotia are not formed until the mycelium covers the plate. In vitro or in vivo, sclerotia begin as small tufts of white mycelium that form spherical sclerotia 0.5 to 1.5 mm in diameter (Figure 2). Sclerotia darken as they mature, becoming tan to dark brown in color (Figure 3). Young sclerotia often exude droplets of clear to pale yellowish fluids. Mature sclerotia are hard, slightly pitted, and have a distinct rind. Although most sclerotia are spherical, some are slightly flattened or coalesce with others to form an irregular sclerotium. S. rolfsii does not form asexual fruiting structures or spores.

The teliomorph of S. rolfsii (Athelia rolfsii) is rarely observed on hosts or in culture. A. rolfsii produces basidia on an exposed hymenium and basidia produce four haploid basidiospores. The appressed hymenium develops in small, thin, irregular patches. The clavate basidia are 4 to 6 µm x 7 to 14 µm; basidiospores are hyline, 1.0 to 5 µm x 5 to 12 µm.

Hosts, Signs, and Symptoms

S. rolfsii causes disease on hundreds of plant species, including field, vegetable, fruit, and ornamental crops. Disease caused by S. rolfsii can be very destructive to numerous vegetable and fruit crops, especially tomato, pepper, melon, and watermelon.

Signs of infection include the development of coarse white strands of mycelium growing in a fan-shaped pattern on lower stems, leaf litter, and soil (Figures 4-6). Even under dry conditions, at least a trace of white mycelium should be evident on the surface of the stem or crown. In some cases, mycelium will be found only underground. After 7 to 14 days, tan-to-brown, mustard-seed-sized (0.5 to 1.5 mm) sclerotia form on the mycelial mat (Figures 7-8).

Although symptoms vary with the host affected, infection usually is restricted to plant parts in contact with the soil. Early symptoms consist of water-soaked lesions on crown and lower stem tissue. The disease usually is recognized by the yellowing and wilting of foliage, followed by a complete collapse of the plant. On tomato and pepper, dark water-soaked lesions on the lower stem at or near the soil surface are present and rapidly develop to completely girdle the stem (Figures 9-10). Infection of melon and watermelon is normally restricted to fruit lying in contact with the soil and runners where soil has been deposited over the vine (Figure 11). In watermelon, one or more runners may be affected and begin turning yellow; with cantaloupe, the melons are usually affected first.

Fruit and other fleshy organs near the soil surface may become infected with S. rolfsii. Soft, water-soaked, sunken, slightly yellowish lesions develop (Figure 12). These lesions quickly spread throughout most or all of the fruit, which will eventually become soft and collapse within 3 to 4 days of infection. The skin of the fruit often crack open and fine white mycelium and developing sclerotia spreads over the surface and quickly fills lesion cavities.

Ecology

S. rolfsii is a necrotrophic soil borne plant pathogen, killing plant tissues in advance of colonization by production of oxalic acid and cell-wall degrading enzymes. It survives as sclerotia in soil and as mycelium in crop debris. Sclerotia are known to survive several years in the absence of a host. The extremely broad host range of S. rolfsii also contributes to long-term survival between host crops. S. rolfsii thrives in highly aerobic environments and thus survives best near the soil surface. Environmental conditions that are favorable for the fungus and disease development are high temperatures (27 to 35°C), humid conditions, and acidic soil. Germination of sclerotia occurs at pH 3 to 7 and is inhibited at pH levels higher than 7. Sclerotia are disseminated through the movement of infested soil, infected transplants, and contaminated tools and machinery.

Geographic Distribution

Sclerotium rolfsii occurs worldwide but is most important in tropical and subtropical regions. In the United States it typically is restricted to the southeast but has been reported as unusual occurrences in New York, Washington, Oregon, and parts of the Midwest. Globally, this pathogen occurs in the tropical, subtropical, and warm temperate regions of Central, North, and South America, Australia, southern Europe, Africa, Asia, and Hawaii.

Management

Cultural

Management of Southern blight is difficult when inoculum levels are high and conditions are conducive to the pathogen. Avoiding the disease by selecting fields that are free of S. rolfsii is the most successful method of control. Crop rotations of two years or more to a non-host crop like corn or small grains will help to prevent build-up of inoculum and disease problems. Rotations with peanuts, soybeans, cabbage, and carrots should be avoided. Weed control must be maintained during rotations to prevent inoculum increase on susceptible species, which includes hundreds of dicots and species in several families of monocots. Certain fertilization regimes, such as high calcium levels and ammonium type fertilizers, may suppress disease under low disease pressure. Certain non-acidifying fertilizers such as calcium nitrate can be used to prevent acidifying soil and creating conditions conducive to disease development.

Close plant spacing and over-irrigation promote disease development and should be avoided. Injury during cultivation should be avoided as much as possible. Black plastic mulch and row covers can provide a barrier between fruit and soil, which greatly reduces the incidence of fruit rots. Staking plants also can prevent fruit from touching the ground. Deep plowing can be used to bury debris and sclerotia of S. rolfsii, but this is seldom practiced on a large scale due to cost and erosion concerns.

Few, if any resistant or partially resistant cultivars of cucurbits are commercially available. Six tomato breeding lines—5635M, 5707M, 5719M, 5737M, 5876M, and 5913M—resistant to Sclerotium rolfsii were released jointly from Texas A&M University Research Center, Coastal Plain Experiment Station and the University of Georgia. Useful levels of southern blight resistance also has been found in several pepper species, including in the bell-type cultivar 'Golden California Wonder.' Resistance is conferred by a single recessive gene. Grafting tomato plants onto interspecific hybrid rootstocks has also been successful in managing southern blight.

Chemical and Biological

Fungicide applications can be used to manage southern blight. Most fungicides are labeled for use on select ornamentals, vegetables, and some field crops.

Fumigants are toxic to sclerotia and mycelium in the soil. However, even after fumigation, some sclerotia survive, and treatments must be repeated annually.

The use of organic amendments, cotton gin trash, and swine manure was found to manage southern blight through the improved colonization of soil by antagonistic Trichoderma spp. Along with species of Trichoderma, other biological agents, such as Gliocladium virens, Bacillus subtilis, and Penicillium spp., were found to antagonize S. rolfsii and may aid in disease suppression. Gliocladium virens was found to reduce the number of sclerotia in soil to a depth of 30 cm, resulting in a decreased incidence of southern blight on tomato. Trichoderma koningii also reduced the number of sclerotia and the plant-to-plant spread of southern blight in tomato fields. More recently, an isolate of Streptomyces philanthi was shown to be effective at protecting chili pepper plants from infection by S. rolfsii.

Diagnostic procedures

S. rolfsii is easily diagnosed in humid weather from the abundant signs of the pathogen. Under dry conditions, signs may not be apparent on the above-ground portion of the plant. When signs are absent, incubating symptomatic stems with the top of the root system for 24 to 48 hours in a moist chamber usually results in abundant vegetative growth of the fungus and later, production of sclerotia (Figure 13). Incubation is most successful if the symptomatic tissue is placed in direct contact with a moistened paper towel. The fungus can readily be isolated on a variety of agar media, with isolation and culture on PDA being the most common. Cultures grow rapidly and should be transferred before the advancing colony margin reaches the edge of a plate. Cultures also can be obtained from surface-sterilized sclerotia. In spite of its vigorous growth, S. rolfsii frequently dies or becomes contaminated with parasites such as Trichoderma in culture. Isolates are best maintained as dried sclerotia or as mycelium on dried colonized grain.

Acknowledgments

• National Institute of Food and Agriculture, U.S. Department of Agriculture, under Agreement No. 2011-41530-30708 as part of "Diagnostic Image Series Development for Supporting IPM in the Southern Region" (USDA-NIFA-RIPM-003351)