Sclerotia Rolfsii Classification Essay

Sclerotium rolfsii Sacc.

Sclerotium rolfsii Sacc., first reported on tomato by Rolfs in Florida in year 1892 (1) is a serious fungal pathogen. It causes Southern Blight on peanut, tomato, watermelon, cowpea, sugar beet, rice and wheat (1, 3). It has a wide host range as it affects plants belonging to nearly 100 families (1).

Classification: Sclerotium rolfsii is the anamorphic stage of the pathogen which is under group Incertae sedis (5) since its classification is controversial as the teliomorph stage i.e. the sexual stage is rarely observed. The teleomorph Athelia rolfsii (Curzi) C.C. Tu & Kimbr. is a basiomycete classified in the following order:

Kingdom Fungi

Phylum Basidiomycota

Subphylum Agaricomycotina

Class Agaricomycetes

Order Atheliales

Family Atheliaceae

Genus Athelia

Species rolfsii (6)

In 2010, Binder et al. carried phylogenetic analysis of agaricomycetes based on six-locus nuclear dataset and proposed a new order Amylocorticiales. Based on sequence identity, they placed Athelia rolfsii in order Amylocorticiales (4). Taxonomic problems related to classification of Sclerotium rolfsii needs to be resolved.

Synonyms: Botryobasidium rolfsii (Curzi) Venkatar.

Corticium centrifugum (Lév.) Bres.

Pellicularia rolfsii (Curzi) E. West

Fibularhizoctonia centrifuga (Lév.) G.C. Adams & Kropp

Hypochnus centrifugus (Weinm.) Lév.

Rhizoctonia centrifuga Lév. (7)

Symptoms and Signs: The symptoms appear as wilting and yellowing of the plants (1). The decay starts from the base of the stem and progresses towards roots. In sweet potato, lesions occur on roots. In watermelon and cantaloupe, the fruits get infected as they come in contact with infested soil. In tomato, lesions occur which are later replaced by fluffy mycelia and sclerotia (3). Sclerotium rolfsii produces fluffy white mycelium on infected tissues under favorable conditions (1, 3). The mycelium turns compact and produce hard, round sclerotia measuring 0.5-2mm in diameter (2). Immature sclerotia are white but turn dark on maturation (3).

Morphology: In pure culture, the mycelium is silky white during the early growth stages and becomes dull in later stages (1). The mycelium forms fan-like structures. Sclerotia are formed after a week, but they can be observed after 4 days (8). Hyphae are hyaline (1). Dolipore septa are observed in primary septa (9).The teliomorph Athelia rolfsii produces basidiocarps and basidiospores. Basidia are 7-9 µm long and 4-5 µm wide (1). The sexual reproduction is influenced by nutrient composition of the growth media. The teliomorph stage is rarely observed under field conditions (2). Sclerotia serve as overwintering structures. They germinate in the presence of oxygen; hence, they survive better in top layer of soil (2). Sclerotia germinate either by hyphal or eruptive germination (2). The hyphae can directly penetrate the susceptible plant tissues.

Identification: Macroscopic signs like white fluffy mycelia and white or dark sclerotia indicate the presence of Sclerotium rolfsii. The species specific PCR can be used for the detection of S. rolfsii as the specific primer pairs based on sequence of Internal Transcribed Spacer region are available. PCR can detect the pathogen in infested soils (10).

Dissemination: Sclerotia spread to uninfected areas by wind, water, animals, and soil. Mycelium is carried to new places by transplants and infected seeds (1).

Ecology: Sclerotium rolfsii is a saprophytic pathogen (1). It is widely distributed in tropical and subtropical countries, as it requires high temperature and a rainy season to thrive. Geographically, it is reported from Southern US, Central America, Caribbean, South America, Africa and Asia (1). The outbreaks occur across the globe.

Epidemiology: Sclerotium rolfsii needs warm and wet weather to propagate, so the optimum temperature for mycelial growth is 8°C to 40°C (2). The sclerotia are produced as the temperature rises from 27°C to 35°C (2).

Economic Importance: It is difficult to calculate the monetary losses caused by Sclerotium rolfsii as it affects a wide range of hosts. It can cause light to severe damage and in some cases, the total destruction of the affected crops (1). According to Taubenhaus (11), it caused at least 5% annual loss of crops in South US in 1900’s. Apart from economic losses, it can prove beneficial in the near future. Eligar et al. (12) reported that Sclerotium rolfsii Lectin (SRL) inhibits the population of human ovarian cancer cells. Inamdar et al. (13) showed that SRL also plays a role in the inhibition of human colon cancer cells. These studies are still in their initial phase and needs more time.

Biochemistry: Higgins first demonstrated that oxalic acid was secreted by S. rolfsii (1). Later, Milthorpe (14) showed that pectinolytic enzymes were secreted along with oxalic acid. Bateman and Beer (15) demonstrated that pectinolytic enzymes; endo-polygalacturonase (endo-PG), endopectinmethylgalacturonase act synergistically with the oxalic acid and cause rapid destruction of the plant cells. During initial stage of infection, hyphae aggregate to form infection cushions. Infection cushions contain crystals of calcium oxalate, which lead to degradation of plant tissues (21). Infection cushions penetrate host tissues by forming penetration pegs. Later, appressoria (14) are formed at tips of individual hyphae to derive nutrition from host cells. After entering host tissues, the hyphae grow inter and intracellularly (21).

Control : Sclerotium rolfsii is difficult to manage as it has broad host range and the sclerotia can survive in soil for many years. However, there are certain measures, which can reduce the disease incidence and losses caused by the pathogen.

Chemical control: Treatment of soil with fumigants like chloropicrin is beneficial as it reduces disease incidence (16). Fumigants are applied several weeks before sowing. Commercially available strobilurin fungicides are used to control Southern Blight on vegetables and peanut (17).

Soil Solarization: Exposure of sclerotia to high temperature of 50°C for 4-6 hours and 55°C for three hours leads to death of sclerotia (18). This can be achieved by covering soil with polyethylene sheets during summer for long period. It is effective for small areas like seedbeds.

Cultural control: Deep ploughing can reduce the disease incidence to some extent. Deep ploughing reduces the germination rate of sclerotia. Soil depth of 8 cm or more prevents the germination of sclerotia (2). However deep ploughing can lead to more even and uniform spread of sclerotia in the whole field thus increasing the disease incidence (19).

Biological Control: Trichoderma harzianum and Gliocladium virens can be used as effective biological control agents against Sclerotium rolfsii . Perry et al. showed that Gliocladium virens reduces the number of sclerotia in soil resulting in reduced Southern Blight incidence on tomato (20).

Integration of cultural practices with chemical and biological control can lead to effective management of Sclerotium rolfsii .


Athelia rolfsii is a corticioid fungus in the familyAtheliaceae. It is a facultativeplant pathogen and is the causal agent of "southern blight" disease in crops.


The species was first described in 1911 by Italian mycologistPier Andrea Saccardo, based on specimens sent to him by Peter Henry Rolfs who considered the unnamed fungus to be the cause of tomatoblight in Florida. The specimens sent to Saccardo were sterile, consisting of hyphae and sclerotia. He placed the species in the old form genusSclerotium, naming it Sclerotium rolfsii. It is, however, not a species of Sclerotium in the strict sense.

In 1932, Mario Curzi discovered that the teleomorph (spore-bearing state) was a corticioid fungus and accordingly placed the species in the form genusCorticium. With a move to a more natural classification of fungi, Corticium rolfsii was transferred to Athelia in 1978.


The fungus produces effused basidiocarps (fruit bodies) that are smooth and white. Microscopically, they consist of ribbon-like hyphae with clamp connections. Basidia are club-shaped, bearing four smooth, ellipsoid basidiospores, measuring 4-7 by 3-5 μm. Small, brownish sclerotia (hyphal propagules) are also formed, arising from the hyphae.[1]

Southern blight[edit]

Athelia rolfsii occurs in soil as a saprotroph, but can also attack living plants. It has an almost indiscriminate host range, but its capacity to form sclerotia (propagules that remain in the soil) means that it particularly attacks seasonal crops. It mostly occurs in warm soils (above 15 °C) and can be a serious pest of vegetables in tropical and subtropical regions (including Florida, where it was first recognized), causing "southern blight".[2]

It can also be called mustard seed fungus.[3]

Disease Cycle[edit]

The soil-borne fungal pathogen Athelia rolfsii is a basidiomycete that typically exists only as mycelium and sclerotia (anamorph: Sclerotium rolfsii, or asexual state). It causes the disease Southern Blight and typically overwinters as sclerotia.[4] The sclerotia is a survival structure composed of a hard rind and cortex containing hyphae and is typically considered the primary inoculum.[5] The pathogen has a very large host range, affecting over 500 plant species (including tomato, onion, snapbean and pea) in the United States of America.[6] The fungus attacks the host crown and stem tissues at the soil line by producing a number of compounds such as oxalic acid, in addition to enzymes that are pectinolytic and cellulytic.[4][5] These compounds effectively kill plant tissue and allow the fungus to enter other areas of the plant.[5] After gaining entry, the pathogen uses the plant tissues to produce mycelium (often forming mycelial mats), as well as additional sclerotia.[4][5] Sclerotia formation occurs when conditions are especially warm and humid, primarily in the summer months in the United States of America.[4][5] Susceptible plants exhibit stem lesions near the soil line, and thus often wilt and eventually die.[5][7] Infection caused by Southern Blight is not considered systemic.


Athelia rolfsii typically prefers warm, humid climates (e.g. the name of the disease, Southern Blight) which is required for optimal growth (i.e. to produce mycelium and sclerotia).[8][4][7] This makes the disease an important issue in regions such as the Southern United States of America, especially for solanaceous crops.[9] In addition, oxygen rich and acidic soils have also been found to favor growth of the pathogen.[5] Southern Blight can be spread (by way of sclerotia and mycelium) by contaminated farm tools and implements, irrigation systems and infected soil and plant material.[5][10]


Thus, management of the disease is critical, especially in agricultural regions. Although historically management has been difficult, there are several practical ways to reduce disease pressure. Simply avoiding infected fields is perhaps the most straightforward management technique given the large host range and durability of survival structures (i.e. sclerotia).[5] However, when this is not possible, practicing proper sanitation and implementing effective crop rotations can help.[5] Deep tillage has also been shown to reduce Southern Blight occurrence by burying infected plant tissues and creating an anaerobic environment that hinders pathogen growth.[5] Soil solarization and certain organic amendments (e.g. composted chicken manure and rye-vetch green manure), as well as introducing certain Trichoderma spp. have also been shown to reduce plant death and number of sclerotia produced in the field in tomatoes.[6][11][12] In addition to these cultural methods, chemical methods (e.g. fungicides) can also be employed.[9][5] These methods all disrupt the production of mycelium and sclerotia, thus reducing the spread of disease.

See also[edit]

External links[edit]

Media related to Athelia rolfsii at Wikimedia Commons


  1. ^Tu CC, Kimbrough JW (1978). "Systematics and phylogeny of fungi in the Rhizoctonia complex". Botanical Gazette. 139: 454–466. doi:10.1086/337021. 
  2. ^Koike ST, Gladders P, Paulus AO (2007). Vegetable diseases: a color handbook. Gulf Professional. p. 448. 
  3. ^"Southern Blight". Retrieved 6 March 2015. 
  4. ^ abcdeAgrios, G.N. (2005). Plant Pathology. New Delhi: Academic Press. 
  5. ^ abcdefghijklMersha, Z. "Southern Blight - a disease becoming more prevalent in Missouri". Missouri Environment and Garden. Division of Plant Sciences - University of Missouri. Retrieved 11 December 2017. 
  6. ^ abFlores-Moctezuma, H.E; Montes-Belmont, R.; Jiménez-Pérez, A, A.; Nava-Juárez, R, R. (2006). "Pathogenic diversity of Sclerotium rolfsii isolates from Mexico, and potential control of southern blight through solarization and organic amendments". Crop Protection. 25: 195–201. doi:10.1016/j.cropro.2005.04.007. 
  7. ^ abMissouri Botanical Garden. "Crown Rot of Perennials (Southern Blight)". Missouri Botanical Garden. Missouri Botanical Garden. Retrieved 11 December 2017. 
  8. ^Punja, Z.K. (1985). "The Biology, Ecology, and Control of Sclerotium Rolfsii". Annual Review of Phytopathology. 23: 97–127. doi:10.1146/ 
  9. ^ abKeinath, A.P.; DuBose, V.B. (2017). "Management of southern blight on tomato with SDHI fungicides". Crop Protection (101): 29–34. 
  10. ^Joy, A; Hudson, B. "Southern Blight". University of Wisconsin-Extension. Retrieved 11 December 2017. 
  11. ^Latunde-Dada, A.O. (1993). "Biological control of southern blight disease of tomato caused by Sclerotium rolfsii with simplified mycelial formulations of Trichoderma koningii". Plant Pathology. 42: 522–529. doi:10.1111/j.1365-3059.1993.tb01532.x. 
  12. ^Liu, B.; Gumpertz, M.L.; Ristaino, J.B. (2007). "Long-term effects of organic and synthetic soil fertility amendments on soil microbial communities and the development of southern blight". Soil Biology and Biochemistry. 39: 2302–2316. doi:10.1016/j.soilbio.2007.04.001. 
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