Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


Claviceps sorghi
(sorghum ergot)



Claviceps sorghi (sorghum ergot)


  • Last modified
  • 27 September 2018
  • Datasheet Type(s)
  • Documented Species
  • Pest
  • Preferred Scientific Name
  • Claviceps sorghi
  • Preferred Common Name
  • sorghum ergot
  • Taxonomic Tree
  • Domain: Eukaryota
  •   Kingdom: Fungi
  •     Phylum: Ascomycota
  •       Subphylum: Pezizomycotina
  •         Class: Sordariomycetes
  • Summary of Invasiveness
  • C. sorghi is a pathogen of Sorghum bicolor found only in India and Southeast Asia. The more widespread Claviceps africana is predominant even in India; C. sorghi appears to be marginalized in...

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Typical elongate, cylindrical sphacelia/sclerotia of C. sorghi protruding from sorghum spikelets.
TitleSphacelia of C. sorghi
CaptionTypical elongate, cylindrical sphacelia/sclerotia of C. sorghi protruding from sorghum spikelets.
CopyrightD.E. Frederickson, INTSORMIL, Zimbabwe
Typical elongate, cylindrical sphacelia/sclerotia of C. sorghi protruding from sorghum spikelets.
Sphacelia of C. sorghiTypical elongate, cylindrical sphacelia/sclerotia of C. sorghi protruding from sorghum spikelets.D.E. Frederickson, INTSORMIL, Zimbabwe
Teleomorph of C. sorghi, note terracotta-coloured stipe and capitulum; capitulum has a white frill.
CaptionTeleomorph of C. sorghi, note terracotta-coloured stipe and capitulum; capitulum has a white frill.
CopyrightMycological Research, 95:1101-1107
Teleomorph of C. sorghi, note terracotta-coloured stipe and capitulum; capitulum has a white frill.
TeleomorphTeleomorph of C. sorghi, note terracotta-coloured stipe and capitulum; capitulum has a white frill.Mycological Research, 95:1101-1107
The first sign of infection by C. sorghi is honeydew oozing from sorghum florets.
CaptionThe first sign of infection by C. sorghi is honeydew oozing from sorghum florets.
CopyrightD.E. Frederickson, INTSORMIL, Zimbabwe
The first sign of infection by C. sorghi is honeydew oozing from sorghum florets.
HoneydewThe first sign of infection by C. sorghi is honeydew oozing from sorghum florets. D.E. Frederickson, INTSORMIL, Zimbabwe


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Preferred Scientific Name

  • Claviceps sorghi B.G.P. Kulk., Seshadri & Hegde

Preferred Common Name

  • sorghum ergot

Other Scientific Names

  • Sphacelia sorghi McRae

International Common Names

  • English: ergot; sugary disease
  • Spanish: tizon del sorgo
  • French: ergot du sorgho

Local Common Names

  • Germany: Mutterkorn: Hirse
  • India: Asali

Summary of Invasiveness

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C. sorghi is a pathogen of Sorghum bicolor found only in India and Southeast Asia. The more widespread Claviceps africana is predominant even in India; C. sorghi appears to be marginalized in its restricted range. A significant difference in invasiveness is the relative production of inoculum that spreads plant-to-plant. C. sorghi produces few to no secondary conidia from macroconidia on infected florets, whereas C.africana produces large numbers of these airborne propagules. The macroconidia of C. sorghi may themselves be transported in honeydew by wind, rain-splash, insects or direct contact between plants, but these are more limited means. Fungal sclerotia and/or the sphacelia state may be carried among harvested seed, but the seed lots can be cleaned or treated with fungicides (Bandyopadhyay et al., 1996). Alternative hosts are pearl millet (Pennisetum glaucum), wild and weedy relatives of S. bicolor, and wild grasses.

Taxonomic Tree

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  • Domain: Eukaryota
  •     Kingdom: Fungi
  •         Phylum: Ascomycota
  •             Subphylum: Pezizomycotina
  •                 Class: Sordariomycetes
  •                     Subclass: Hypocreomycetidae
  •                         Order: Hypocreales
  •                             Family: Clavicipitaceae
  •                                 Genus: Claviceps
  •                                     Species: Claviceps sorghi

Notes on Taxonomy and Nomenclature

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Ergot of sorghum with the common name ‘sugary disease’ was known worldwide by the scientific name Sphacelia sorghi until the teleomorph (sexual stage) from India was described in 1976 as Claviceps sorghi (Kulkarni et al., 1976). In 1991, when the teleomorph of a pathogen in Zimbabwe was generated (Frederickson et al., 1991), it became clear that a different pathogen was responsible for ergot disease of sorghum in Africa and that species was named Claviceps africana. However, before this distinction became known, ergot in Africa was often referred to as C. sorghi. With the arrival of sorghum ergot in the Americas during 1995-1997, confusion still prevailed because even some of these later records erroneously referred to C. sorghi instead of C. africana. Therefore, care is needed when interpreting reports of C. sorghi in the literature (see also Geographic Distribution).


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Sphacelia cream-white to grey; elongate, straight to curved, 3-14 x 1.0-2.5 mm, forming two types of spore: oblong macroconidia, with polar vacuoles and slight central constriction, 8-19 x 4-6 mm and spherical microconidia, 2.5 mm diameter. The proximal tissues form the sclerotium largely within the glumes, with distal sclerotial tissue constituting the thin, red core of the protruding sphacelium. Germination of the sclerotium gives rise to two or three stromata, stipes bronze to terracotta-coloured, 6-8 x 0.5 mm, capitulum buff 0.7 mm diameter, perithecial ostioles dark, papillate. Stipe insertion point surrounded by a white frill. Ascomata (perithecia) 130-250 x 60-125 mm diameter. Asci cylindrical 56-114 x 2.5-3.0 mm ends tapering, apical caps hyaline. Ascospores eight, 40-97 x 0.4-0.8 mm (Frederickson et al., 1991).

Muthusubramanian et al. (2006) found wider sphacelia, 4.38-4.72 x 2.94-3.06 mm, in some Indian isolates. Macroconidia were cylindrical, averaging 13.1-13.4 x 5.9-6.3 mm. Among all isolates obtained from the field, sclerotia were reddish-brown and cylindrical to conical, mean length 8.16-9.60 mm, mean thickness 1.82-2.04 mm.
In culture on a defined medium, C. sorghi isolates (from young sphacelia) grew as white, cottony to velvety, even colonies with diffuse margins and no puckering or sulcation. Macro- and microconidia were produced in pale-brown honeydew-like droplets at the centre of the colony (Muthusubramanian et al., 2006).


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McRae first found C. sorghi in India in 1915 (McRae, 1917) and Ramakrishnan recorded it in 1948, although the pathogen was then known through its anamorph as Sphacelia sorghi, until the description of the teleomorph in 1976 (Kulkarni et al., 1976). C. sorghi was assumed to be the causal agent of ergot disease of sorghum worldwide until 1991, when ergot in Zimbabwe was described as a new species, Clavicepsafricana (Frederickson et al., 1991). Any reports of C. sorghi in Africa should therefore correctly refer to C. africana. In 1998, C. africana was confirmed present in India also (Bogo and Mantle, 1999; Pazoutova et al., 2000). In retrospect, it has become clear that since the late 1980s all ergot samples from India have been of C. africana and, it was hypothesized that C. africana may have replaced, or marginalized, C. sorghi (RA Frederiksen, Texas A&M University, USA, personal communication, 1999). The earlier report of Kulkarni et al. (1976) describes both the elongate sclerotia typical of C. sorghi and small, subglobose sclerotia characteristic of C. africana, indicating that C. africana was already present in India in 1976. Bandyopadhyay (ICRISAT, India, personal communication, 1998) reported C. africana in Maharashtra, Karnataka, Andhra Pradesh, Gujarat, Tamil Nadu and Uttar Pradesh states in India. The continued presence of C. sorghi in India was confirmed by an isolation in Karnataka province (Pazoutova and Bogo, 2002) and a survey was undertaken to determine the distribution and prevalence of both C. sorghi and C. africana.  Muthusubramanian et al. (2006) reported the survey results that found C. sorghi in Andhra Pradesh and Maharashtra states, but their data showed that C. africana is, in fact, predominant in the sorghum-growing regions of India.

From the literature it is impossible to verify the reports of C. sorghi in Taiwan. The optimum temperature of conidial germination suggests C. sorghi (Chen et al., 1995b). Conversely, reports of secondary conidiation (Lin, 1993) suggest C. africana, but this trait is a feature of all sorghum ergot pathogens in vitro (Pazoutova et al., 2004). The narrow host range also suggests C. africana (Chen et al., 1995a). Records from Myanmar (CMI, 1987; specimens from the herb. IMI, c/o CABI Bioscience, Egham, UK, accession numbers 1471 and 1472) may possibly represent Claviceps sorghicola (Tsukiboshi et al., 1999b), whereas those from the Philippines and Yemen (CMI, 1987) are inconclusive and require expert verification. C. africana has been found in Yemen (CABI/EPPO, 2006). Tonapi et al. (2003a) reported that at least some ergot specimens collected in Myanmar, Thailand and Vietnam appeared to be C. sorghi.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


IndiaPresentNative Not invasive IMI Herbarium, 1981; McRae, 1917; Kulkarni et al., 1976
-Andhra PradeshPresentNative Not invasive Muthusubramanian et al., 2006
-KarnatakaPresentNative Not invasive Pazoutová and Bogo, 2002
-MaharashtraPresentNative Not invasive Frederickson and Mantle, 1988; Muthusubramanian et al., 2006
MyanmarPresentIntroducedTonapi et al., 2004a
TaiwanUnconfirmed recordChen et al., 1995a; Chen et al., 1995b; Chen et al., 1991
ThailandPresentIntroducedTonapi et al., 2004a
VietnamPresentIntroducedTonapi et al., 2004a

Risk of Introduction

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Risk Criteria Category

Economic Importance: Low
Distribution: Central and southern India and parts of southest Asia
Seedborne Incidence: Moderate
Seed Transmitted: Not recorded
Seed Treatment: Yes

Overall Risk: Low

Habitat List

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Terrestrial – ManagedCultivated / agricultural land Present, no further details Harmful (pest or invasive)

Hosts/Species Affected

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Although reports of various hosts of C. sorghi are extensive, most require substantiation by the application of Koch's postulates in properly-controlled, cross-inoculation tests. Sundaram and Singh (1975) found sugary disease on Ischaemumpilosum and managed to infect the grass with honeydew from sorghum. They similarly inoculated and infected Pennisetum ciliare (as Cenchrus ciliaris) and Pennisetum setigerum (as Cenchrus setigerus). Of 54 species tested by Chen et al. (1995a), C. sorghi would only infect Pennisetum glaucum (pearl millet) and Sorghum halepense (Johnson grass). Muthusubramanian et al. (2005) inoculated a number of grasses with conidia and found that four other species of Sorghum, as well as P. glaucum, became infected. Pazoutova et al. (2002) used molecular techniques to confirm the identity of the ergot fungus on Heteropogon triticeus in India as C. sorghi. Continued revision of grass host taxonomy must also be considered.

Growth Stages

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Individual ovaries between the glumes of some or all florets are colonized by the parasite. Infected florets become evident when sticky, orange-brown liquid droplets of spore-bearing honeydew are exuded. The soft, white, narrow and elongate growth of mycelium forming the sphacelium becomes evident soon after, appearing from between the glume tips; the glumes are barely distorted laterally. The sphacelium grows at the inner end and may achieve a length of 14 mm (Frederickson and Mantle, 1988). Honeydew droplets may coat panicles, seeds, leaves and the stalk.
In the case of colonization of the honeydew and sphacelia by the hyperparasitic fungus Cerebella andropogonis, black, spherical, convoluted growths are seen at floret tips (Mohan and Jeyarajan, 1991; Bandyopadhyay et al., 1998). Upon dissection, a discoloured sphacelium of reduced size is found underneath. Other moulds may also grow on the honeydew.

List of Symptoms/Signs

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SignLife StagesType
Fruit / honeydew or sooty mould
Inflorescence / honeydew or sooty mould
Leaves / honeydew or sooty mould
Stems / honeydew or sooty mould

Biology and Ecology

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In a study of the infection process in sorghum ergot, Frederickson and Mantle (1988) showed that macroconidia germinate on exserted stigmas of unpollinated, male-sterile sorghum ovaries within 1-2 days of inoculation. The germ tube penetrates the stigmatic surface and hyphae grow though pollen transmission tracts in the style, entering the ovary wall within 3 days. Infection via the ovary wall can occur, but is probably not a significant means of entry under natural conditions. Hyphae grow down the inner ovary wall to the base, occupying the tissues adjacent to the rachilla, which provides the necessary nutrients to support proliferation of hyphae. All but the very apex of the ovary is colonized. Six days after inoculation, hyphae of the pathogen simultaneously erupt from the lower aspect of the outer ovary wall and invade the ovule through the chalazal region. The incubation period is 8-10 days, after which time honeydew, containing large numbers of conidia, is exuded from infected florets. The sphacelium remains very small and is contained within the floret until about 15 days after germination, when it emerges from between the glume tips (Frederickson and Mantle, 1988; Frederickson, 1990). Secondary conidiation (Frederickson et al., 1989) is not a natural feature of C. sorghi infections, although it occurs readily in vitro (Frederickson, 1990; Pazoutova et al., 2004). Infected florets eventually produce typical elongated sclerotia of C. sorghi.

Ovaries resist infection and colonization by the pathogen after fertilization. For ergot diseases in general, rapid anthesis lowers the chance of infection and any factor prolonging the period from flower opening to fertilization will promote infection (Futrell and Webster, 1965). Musabyimana et al. (1995) found that each day of delay in fertilization after inoculation resulted in 8.3% more ergot. However, ovaries could be infected up to 5 days after pollination (Puranik et al., 1973). Despite various studies that have related environmental factors such as humidity, temperature and rainfall to floral infection, no definitive information is available to clarify these associations (Bandyopadhyay et al., 1996).
Spore germination occurs at 12-36°C; optimum 24-28°C (Frederickson, 1990; Chen et al., 1995b). Relative humidity >60% encourages honeydew formation (Frederickson, 1990). Chen et al. (1995a) reported that low temperatures and high rainfall were critical factors favouring infection.
Dry conditions favour development of sclerotia (Sangitrao and Bade, 1979; Mohan and Jeyarajan, 1991). Sclerotia are not separate entities, but form from within sphacelia. The proximal sclerotial tissues form an oval to cylindrical structure within the glumes; distal sclerotial tissues project into the uppermost sphacelial tissue forming a cylindrical core. However, the apex of the structure is actually all sphacelial tissue (Frederickson et al., 1991). Either sclerotia or sphacelia may facilitate survival.
Sangitrao (1982) experimentally germinated sclerotia to produce the teleomorph. Germination occurred at 5-50°C, optimum 20-30°C. At 27°C, 55% of stromata differentiated fully. Sclerotia were still viable after 10 years in storage at room temperature in the laboratory (Tonapi et al., 2003b). Frederickson et al. (1991) germinated C. sorghi sclerotia from Akola, Maharashtra, India, by incubation in moist sand in the laboratory at 24°C. Stromata were produced within 5 weeks. Germination has not been observed in the field and the significance of the teleomorph is unclear (Frederickson and McLaren, 2000).
Sclerotia may also be important as vehicles of conidia in the attached sphacelia. Conidia of ergot survived for 9 months in infected heads on the soil surface (Lakshmanan et al., 1990). Honeydew on seed may be a source of infection, but it can be eliminated by seed treatment with captan (Odvody, 1997). In the absence of secondary conidiation, it is not clear how macroconidia on seed or plant debris would infect stigmas.
Alternative hosts of C. sorghi have been reported (see Host Range), but most have not been investigated by cross-inoculation tests following Koch's postulates. Their role, if any, in the spread and survival of C. sorghi remains unclear.
Insects are known to carry ergot conidia non-specifically on their bodies after feeding on honeydew (Prom et al., 2003; Prom, 2005). Their role in specific transmission of C. sorghi has not been investigated.


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Am - Tropical monsoon climate Tolerated Tropical monsoon climate ( < 60mm precipitation driest month but > (100 - [total annual precipitation(mm}/25]))
Aw - Tropical wet and dry savanna climate Preferred < 60mm precipitation driest month (in winter) and < (100 - [total annual precipitation{mm}/25])

Seedborne Aspects

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Extensive infection of sorghum seeds by C. sorghi occurs in hybrid seed production. A 1989 survey in Taiwan of the autumn crop of cv. Taichung No. 5, indicated that 64% of the female parent (cytoplasmic male sterile line) and 12% of the male parent (restoring line) were infected (Chen et al., 1991). Seed lots may be contaminated with sclerotia, or sphacelia, and seed may be contaminated with honeydew (Bandyopadhyay et al., 1998).
Effect On Seed Quality
Ergot contamination of sorghum seed lots has a negative effect on quality standards in seed certification programmes (Bandyopadhyay, 1992).
Pathogen Transmission
Ascospore inoculum from sclerotia of C. sorghi that are planted with seeds is assumed to be a primary inoculum source, but proof is lacking. Conidia that survive on other hosts or on panicle debris in the soil were considered to be a more likely source of primary inoculum (Bandyopadhyay, 1992). Conidia carried in honeydew on seeds will not provide inoculum at the appropriate time for infection of the crop even if seeds are untreated (Dahlberg et al., 1999).
Seed Treatment
Steeping seeds in 5% salt solution is considered a practical way of removing sclerotia of C. sorghi from seed lots, but is probably not 100% effective (Bandyopadhyay, 1992). Sprays of carbendazim + tridemorph followed by carbendazim + thiram and thiophanate-methyl gave good control of C. sorghi infection and reduced contamination of seeds (Lakshmanan and Mohan, 1988). However, fungicide sprays to the seed crop have generally been considered impractical and uneconomical (Bandyopadhyay, 1992). However, captan-treatment of seed is both economic and effective against Claviceps africana conidia and presumably also against those of C. sorghi (Dahlberg et al., 1999).
Seed processing equipment such as gravity tables can separate sclerotia from seeds (Bandyopadhyay et al., 1998). See also C. africana.
Seed Health Tests
Visual examination (Bandyopadhyay et al., 1998):

Seed lots are examined for the presence of cylindrical, cream-white to grey cushions of fungal growth (sphacelia), or for thin, elongate sclerotia, mixed with the seeds. Examination at a magnification of at least x10 is recommended to avoid the problems of mis-identification frequently encountered when using the naked eye (Alderman et al., 1999).

Pathway Causes

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CauseNotesLong DistanceLocalReferences
Seed trade Yes Yes Bandyopadhyay et al., 1996

Pathway Vectors

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VectorNotesLong DistanceLocalReferences
Plants or parts of plants Yes Yes Bandyopadhyay et al., 1996
Wind Yes Frederickson, 1999

Plant Trade

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Plant parts liable to carry the pest in trade/transportPest stagesBorne internallyBorne externallyVisibility of pest or symptoms
Flowers/Inflorescences/Cones/Calyx sclerotia; spores Yes Yes Pest or symptoms usually visible to the naked eye
Leaves spores Yes Pest or symptoms usually visible to the naked eye
Stems (above ground)/Shoots/Trunks/Branches spores Yes Pest or symptoms usually visible to the naked eye
True seeds (inc. grain) sclerotia; spores Yes Pest or symptoms usually visible to the naked eye
Plant parts not known to carry the pest in trade/transport
Fruits (inc. pods)
Growing medium accompanying plants
Seedlings/Micropropagated plants

Impact Summary

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Economic/livelihood Negative


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Ergot disease is primarily an economic problem in F1 hybrid seed production. It is particularly severe in male-sterile lines (A-lines) when either nonsynchronous flowering of A-line and restorer lines (R-lines) or adverse environmental conditions result in lack of viable pollen and delayed seed set (Bandyopadhyay et al., 1998). Losses of 10-80% have been reported in hybrid seed production fields in India. However, C. sorghi has limited economic impact because of its narrow distribution.
The incidence and severity of ergot (C. sorghi and Claviceps africana) on sorghum (Sorghum bicolor) was surveyed in the Indian states Andhra Pradesh, Gujarat, Tamil Nadu, Maharashtra, Karnataka, Rajasthan and Uttar Pradesh from 1999 to 2002. Crops were examined at vegetative to physiological maturity stages, and disease incidence (number of plants infected) and severity (percentage, based on the number of florets infected within panicles) recorded in 12 m² areas. Percentage incidence of ergot infection varied with location, with Rajasthan and Gujarat having only trace infections from 1999 to 2002 and Karnataka with 27-60% infection. Disease severity followed the same pattern (Navi et al., 2002).

Risk and Impact Factors

Top of page Invasiveness
  • Has propagules that can remain viable for more than one year
  • Reproduces asexually
Impact outcomes
  • Host damage
  • Negatively impacts agriculture
Impact mechanisms
  • Pathogenic
Likelihood of entry/control
  • Difficult to identify/detect in the field

Detection and Inspection

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In the field, C. sorghi infection is usually obvious from the dripping of honeydew from infected florets, honeydew deposition on the panicle and the protruding sphacelia. The pathogen is less easily detected in seed batches, even though sclerotia are of distinct shape and size (Tonapi et al., 2003b), which poses potential problems for seed exchange. If the fungus could be cultured from seed, the description provided by Muthusubramanian et al. (2006) would be of use. See Seed Health Tests.

An assay using PCR primers and probes from the intron 3 region of the β-tubulin gene of C. sorghi is described in Tooley et al. (2010). This can be used for detecting C. sorghi in seed and grain shipments and distinguishing it from similar species.


Similarities to Other Species/Conditions

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Two other species of Claviceps, Claviceps africana (Frederickson et al., 1991) and Clavicepssorghicola (Tsukiboshi et al., 1999b) infect sorghum, but only C. africana has an overlapping distribution with C. sorghi in India. C. sorghicola is found only in central Japan (Tsukiboshi et al., 1999b). Records of C. sorghi in India go back to 1917 (McRae, 1917) and Pazoutova and Bogo (2002) confirmed its continued presence. Claviceps sorghi may have been marginalized or eradicated in places by competition with C. africana which is the most widespread of the three pathogens, present in all the major sorghum seed production areas of the world (Bandyopadhyay et al., 1998).
Both C. sorghi and C. sorghicola form elongate sphacelia and sclerotia, but those of C. sorghicola are conical rather than straight-sided. Only C. africana overlaps in geographic range and it forms subglobose sphacelia and sclerotia. Additionally, C. sorghi honeydew appears before the sphacelia are visible, so infected florets show the honeydew ooze even though the fungus is still invisible (Frederickson and Mantle, 1988). The converse is true for C. africana because the bulky sphacelium causes the glumes to bulge wide open before honeydew is produced (Frederickson, 1990; Frederickson et al., 1991). Neither conidia of C. sorghi nor those of C. sorghicola produce secondary conidia in nature, so their honeydew never appears superficially white. In contrast, secondary conidiation on the honeydew surface is a striking feature of natural C. africana infections (Frederickson et al., 1989; 1991; 1993). At the optimum temperature of 25°C, C. sorghi isolates produced few conidia from honeydew on plants in growth chambers compared to the quantities produced by Indian C. africana isolates (Muthusubramanian et al., 2006).
In the absence of the teleomorph, which is difficult to obtain, the best diagnostic test for C. sorghi is the absence of ergot alkaloids in the sclerotia. C. africana sclerotia synthesize dihydroergosine (Mantle and Waight, 1968; Frederickson et al., 1991; Mantle and Hassan, 1994; Reis et al., 1996). Sclerotia of both C.sorghicola  and C. sorghi contain trace amounts of caffeine (Bogo and Mantle, 2000; Bogo et al., 2003).
Pazoutova et al. (2000) used nucleotide sequence differences of ITS1 and part of 5.8S rDNA to distinguish between the three species. Different genetic tests were used by Tooley et al. (2006) to characterize and distinguish Indian isolates of sorghum ergot, providing molecular data to support species identifications based on morphology (Muthusubramanian et al., 2006). For a full comparison of C. sorghi and C. africana see Frederickson et al. (1991) and Muthusubramanian et al. (2006). For details of C. sorghicola, see Tsukiboshi et al. (1999b).
The sori of covered kernel smut (Sporisorium sorghi) and long smut (Tolyposporium ehrenbergii) may be confused with C. sorghi sphacelia. However, sack-like sori of the smut fungi are comprised of a smooth, cream to grey outer covering or peridium enclosing the dry, powdery-black teliospores (Frederiksen, 1986; Hilu, 1986). Spores are released by rupture of the peridium at the tip. Sphacelia of ergots are devoid of an outer covering, being solid, spongy bodies with convolutions that are spore-bearing cavities. Spores are washed-out of the sphacelium in the oozing honeydew.

Prevention and Control

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Cultural Control and Sanitary Methods
In India, early sowing reduced the incidence of C. sorghi. Planting in the first 2 weeks of June gave the best results. Planting in July, on the other hand, was recommended to facilitate screening under natural disease pressure (Singh, 1964; Sangitrao et al., 1979; Anahosur and Patil, 1982). Field practices aimed at reducing the risk or severity of all ergot pathogens include the removal of infected panicles at harvest, crop rotations and deep ploughing of crop residues. However, these methods have limited impact (Frederickson and Leuschner, 1997).
Host-Plant Resistance
There is currently no source of resistance to any species of sorghum ergot for deployment in the field in A-lines, although many workers have devised screening methodologies for C. sorghi and report variable success in finding 'resistant' lines (Khadke et al., 1979; Chandrasekaran et al., 1983; 1985; Rajkule et al., 1983; 1985; Lakshmanan et al., 1988a,b; Lakshmanan and Mohan, 1989a,b; Palanisamy et al., 1989; Anahosur et al., 1990; Hiremath and Lakshman, 1990). In trying to evaluate resistance to C. africana, McLaren (1992) concluded that simple comparisons of severity data from tests of genotypes from different localities, following either natural infection or artificial inoculation, is meaningless, and this will also be the case for C. sorghi resistance. Susceptibility to ergot is extremely sensitive to environmental factors at flowering and a few weeks before (McLaren and Wehner, 1990; 1992; McLaren, 1997). Cool nights of <12°C at 2-3 weeks before anthesis result in pollen sterility and increased ergot severity. Therefore, tolerance of low, pre-flowering minimum temperatures is important for disease avoidance (McLaren, 1997). Similarly, the mean maximum temperature 1-4 days after pollen shed affects fertilization and thus affects ergot incidence. Interactions between genotype, location and flowering date must be compared by regression analyses because differences in flowering date of even a day or two affect the severity of ergot (McLaren, 1992; McLaren and Flett, 1998).
Careful screening and selection for floral characteristics that reduce disease may prove to be one useful strategy, and results from research on C. africana are also applicable to the development of resistance to C. sorghi. For example, in Puerto Rico, Dahlberg and Bandyopadhyay (USDA-ARS-TARS, Puerto Rico, personal communication, 1999) found a male-fertile accession with glumes that tightly clasp the ovary, apparently conferring tolerance to high inoculum loads of C. africana. The line also showed potential in a male sterile background. In the USA, many A-line sorghums have a protracted stigma receptivity period, enhancing ergot susceptibility (Odvody, 1997) and disease reduction may possibly be achieved by decreasing that ergot-susceptible period of the A-line stigma. Other advantageous modifications might include reducing the floret gaping period, selecting for more rapid post-fertilization changes in the A-line, breeding for cold-temperature tolerance in R-line pollen production and extending the pollen production period.
Chemical Control
Chemical control is barely cost effective, is only feasible for controlling disease on the A-lines, and is unnecessary on the hybrids themselves. However, in India the use of fungicides has been extensively explored. In field tests, three earhead sprays of ziram and zineb were more effective than two (Gangadharan et al., 1976). Mancozeb, thiophanate-methyl and carbendazim all gave good yield increases (Anahosur, 1979; Lakshmanan et al., 1986; Lakshmanan and Mohan, 1988). Schedules involving ground applications of triazoles, such as propiconazole and tebuconazole, are effective against C. africana and, presumably, C. sorghi (Odvody, 1997). See also Seed Treatments.
Development of IPM Strategies
Ergot caused by C. sorghi is only a very limited problem in sorghum production; it is not a global problem. The survey of the distribution of C. sorghi and C. africana in India (Muthusubramanian et al., 2006; Tooley et al., 2006) indicated that serious losses from sorghum ergot in India are mostly due to the more widespread C. africana. Future combined control options such as host genetic resistance, disease prediction, manipulation of the pollination system and limited fungicide use during high risk periods are therefore likely to be useful benefits from research on the more globally important ergot pathogen, C. africana. See Control section of C. africana.



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Alderman S; Frederickson D; Milbrath G; Montes N; Narro-Sanchez J, 1999. A laboratory guide to the identification of Claviceps purpurea and Claviceps africana in grass and sorghum seed samples. Sponsored by the Seed trade Associations of Mexico, America, Oregon, Texas.

Anahosur KH, 1979. Chemical control of ergot of sorghum. Indian Phytopathology, 32(3):487-489

Anahosur KH; Lakshman M; Shivanna H, 1990. Identification of stable multiple disease resistant sorghums. Indian Phytopathology, 43(3):444-445; 5 ref.

Anahosur KH; Patil SH, 1982. Effect of date of sowing on the incidence of ergot of sorghum. Indian Phytopathology, 35(3):507-509

Bandyopadhyay R, 1992. Sorghum ergot. In: De Milliano WAJ, Frederiksen RA, Bengston G, eds. Sorghum and Millet Diseases: A Second World Review. Patancheru, India: ICRISAT, 235-244.

Bandyopadhyay R; Frederickson DE; McLaren NW; Odvody GN, 1996. Ergot - a global threat to sorghum. International Sorghum and Millets Newsletter, No. 37:1-32; 123 ref.

Bandyopadhyay R; Frederickson DE; McLaren NW; Odvody GN; Ryley MJ, 1998. Ergot: a new disease threat to sorghum in the Americas and Australia. Plant Disease, 82(4):356-367; 54 ref.

Bogo A; Mantle PG, 1999. Claviceps africana discovered in India. Plant Disease, 83(1):79; 4 ref.

Bogo A; Mantle PG, 2000. Caffeine: also a fungal metabolite. Phytochemistry, 54(8):937-939; 14 ref.

Bogo A; Mantle PG; Boff MIC; Amarante CVTdo, 2003. Production of caffeine alkaloid by Claviceps sorghi. Fitopatologia Brasileira, 28(4):446-448.

Brady LR, 1962. Phylogenetic distribution of parasitism by Claviceps species. Lloydia, 25:1-36.

CABI/EPPO, 2006. Claviceps africana. Distribution Maps of Plant Diseases, No. 715. Wallingford, UK: CAB International.

Chandrasekaran A; Palaniswamy S; Prasad MN, 1983. Sorghum disease studies in India. Sorghum Newsletter, 26:107-108.

Chandrasekaran A; Palaniswamy S; Prasad MN, 1985. Screening for resistance to sugary disease of sorghum. Sorghum Newsletter, 28:83-84.

Chen CW; Lin CY; Yeh Y; Yang TC; Tzeng DDS, 1995. Biological and ecological characteristics of Sphacelia sorghi causing ergot disease of sorghum in Taiwan. Plant Pathology Bulletin, 4(1):8-16; 24 ref.

Chen CW; Tzeng DDS; Lin CY; Yeh Y; Yang TC, 1995. Effect of temperature, light illumination, and water potential on spore germination, mycelial growth, and sporulation of sorghum ergot fungus Sphacelia sorghi. Plant Pathology Bulletin, 4(3):121-128; 23 ref.

Chen GM; Cheng QH; Yeh CC, 1991. Ergot disease of sorghum in Taiwan. Plant Protection Bulletin, Taiwan, 33(2):223-226

Dahlberg JA; Peterson GL; Odvody GN; Bonde M, 1999. Inhibition of germination and sporulation of Claviceps africana from honeydew encrusted sorghum with seed treatment fungicides. Crop Protection, 18(4):235-238; 3 ref.

Frederickson DE, 1990. Ergot Disease of Sorghum. Thesis. London, UK: University of London.

Frederickson DE, 1999. The lifecycle, spread and survival of the sorghum ergot pathogens. In: Proceedings of the global Conference on Sorghum Ergot, 1-8 June 1997, Sete Lagoas, Brazil. EMBRAPA/INTSORMIL/ICRISAT.

Frederickson DE; Leuschner K, 1997. Potential use of benomyl for control of ergot (Claviceps africana) in sorghum A-lines in Zimbabwe. Plant Disease, 81(7):761-765; 24 ref.

Frederickson DE; Mantle PG, 1988. The path of infection of sorghum by Claviceps sorghi. Physiological and Molecular Plant Pathology, 33(2):221-234

Frederickson DE; Mantle PG; Milliano WAJde, 1989. Secondary conidiation of Sphacelia sorghi on sorghum, a novel factor in the epidemiology of ergot disease. Mycological Research, 93(4):497-502

Frederickson DE; Mantle PG; Milliano WAJde, 1991. Claviceps africana sp. nov.; the distinctive ergot pathogen of sorghum in Africa. Mycological Research, 95(9):1101-1107

Frederickson DE; Mantle PG; Milliano WAJde, 1993. Windborne spread of ergot disease (Claviceps africana) in sorghum A-lines in Zimbabwe. Plant Pathology, 42(3):368-377

Frederickson DE; McLaren NW, 2000. Ergot. In: Compendium of Sorghum Diseases [ed. by Frederiksen, R. A.\Odvody, G. N.]. St Paul, Minnesota, USA: American Phytopathological Society. Second edition, unpaginated.

Frederiksen RA, 1986. Covered kernel smut. In: Frederiksen RA, ed. Compendium of Sorghum Diseases. St Paul, Minnesota, USA: American Phytopathological Society.

Futrell MC; Webster OJ, 1965. Ergot infection and sterility in grain sorghum. Plant Disease Reporter, 49:680-683.

Gangadharan K; Subramanian N; Kandaswamy TK; Sundaram NV, 1976. Control of sugary disease of sorghum. Madras Agricultural Journal, 63(5/7):411-413

Hilu O, 1986. Long smut. In: Frederiksen RA, ed. Compendium of Sorghum Diseases. St Paul, Minnesota, USA: American Phytopathological Society.

Hiremath RV; Lakshman M, 1990. Performance of high-yielding promising sorghum (Sorghum bicolor) varieties and hybrids against diseases. Indian Journal of Agricultural Sciences, 60(1):78-79; 3 ref.

IMI Herbarium, 1900-. Herbarium specimen. International Mycological Institute (now CABI Bioscience) Herbarium. Egham, UK: CABI Bioscience.

IMI, 1997. Distribution Maps of Plant Diseases, No. 715. Wallingford, UK: CAB International.

Khadke VD; More BB; Konde BK, 1979. In vitro evaluation of some fungicides and antibiotics for the control of Sphacelia sorghi an incitant of sugary disease of sorghum. Pesticides, 13(7):59-60

Kulkarni BGP; Seshadri VS; Hegde RK, 1976. The perfect stage of Sphacelia sorghi McRp. Mysore Journal of Agricultural Sciences, 10(2):286-289

Lakshmanan P; Chandrasekaran A; Palanisamy S, 1986. Chemical control of sugary disease of sorghum. Sorghum Newsletter, 29:81

Lakshmanan P; Jeyarajan R; Palaniswamy S, 1988. Sources of multiple resistance to major diseases of sorghum in Tamil Nadu, India. Tropical Pest Management, 34:106-107.

Lakshmanan P; Mohan S, 1988. Studies on the effect of various fungicides on Sphacelia sorghi. Pesticides, 22:27.

Lakshmanan P; Mohan S, 1989. Evaluation of TNAU sorghum cultures for multiple disease resistance. Madras Agricultural Journal, 76(10):588-589; 2 ref.

Lakshmanan P; Mohan S, 1989. Sources of primary inoculum and identification of resistant sorghum genotypes for Sphacelia sorghi in Tamil Nadu. Plant Disease Research, 4(2):158-159

Lakshmanan P; Mohan S; Jayarajan R, 1990. Studies on sugary disease of sorghum. Madras Agricultural Journal, 77(7-8):339-340

Lakshmanan P; Mohan S; Mohan L, 1988. Sorghum genotypes resistant to sorghum downy mildew and sugary disease. Sorghum Newsletter, 31:97

Lin CY, 1993. The occurrence of sorghum ergot disease caused by Claviceps sorghi in Taiwan. Bulletin of Taichung District Agricultural Improvement Station, 40:17-28

Loveless AR, 1964. Use of the honeydew state in the identification of ergot species. Transactions of the British Mycological Society, 47:205-213.

Mantle PG; Hassan HAG, 1994. Widening geographical distribution of Claviceps africana, an important ovary pathogen of grain sorghum. International Sorghum and Millets Newsletter, 35:97-98

McLaren NW, 1992. Quantifying resistance of sorghum genotypes to the sugary disease pathogen (Claviceps africana). Plant Disease, 76(10):986-988

McLaren NW, 1997. Changes in pollen viability and concomitant increase in the incidence of sorghum ergot with flowering date and implications in selection for escape resistance. Journal of Phytopathology, 145(5/6):261-265; 14 ref.

McLaren NW; Flett BC, 1998. Use of weather variables to quantify sorghum ergot potential in South Africa. Plant Disease, 82(1):26-29; 18 ref.

McLaren NW; Wehner FC, 1990. Relationship between climatic variables during early flowering of sorghum and the incidence of sugary disease caused by Sphacelia sorghi. Journal of Phytopathology, 130(1):82-88

McLaren NW; Wehner FC, 1992. Pre-flowering low temperature predisposition of sorghum to sugary disease (Claviceps africana). Journal of Phytopathology, 135(4):328-334

McRae W, 1917. Notes on some south Indian fungi. Madras Agricultural Yearbook, 1917:108-111.

Mohan L; Jeyarajan R, 1991. Occurrence of Cerebella andropogonis on secretions of Sphacelia sorghi on sorghum. Sorghum Newsletter, 32:43

Musabyimana T; Sehene C; Bandyopadhyay R, 1995. Ergot resistance in sorghum in relation to flowering, inoculation technique and disease development. Plant Pathology, 44(1):109-115

Muthusubramanian V; Bandyopadhyay R; Tooley PW; Reddy DJ, 2005. Inoculated host range and effect of host on morphology and size of macroconidia produced by Claviceps africana and Claviceps sorghi. Journal of Phytopathology, 153(1):1-4.

Muthusubramanian V; Ranajit Bandyopadhyay; Reddy DR; Tooley PW, 2006. Cultural characteristics, morphology, and variation within Claviceps africana and C. sorghi from India. Mycological Research, 110(4):452-464.

Navi SS; Bandyopadhyay R; Tonapi VA; Rao TGN; Tooley PW; Reddy RK; Indira S; Pande S, 2002. Prevalence of ergot of sorghum in India. International Sorghum and Millets Newsletter, 43:70-71; 2 ref.

Odvody GN, 1997. Spread and importance of ergot in the western hemisphere. In: Parker RD, Livingston SD, Falconer LL, eds. Grain Sorghum for the 21st Century: Working Together as an Industry. Texas, USA: Texas Agricultural Extension Service, 64-71.

Palanisamy S; Prasad MN; Muthaiah A; Mohanasundaram K, 1989. Co. 26 a national sorghum variety. Madras Agricultural Journal, 76(6):312-315

Pazoutová S; Bogo A, 2002. Rediscovery of Claviceps sorghi (Ascomycotina: Clavicipitaceae) in India. Mycopathologia, 153(2):99-101.

Pazoutová S; Johnson N; Kolarík M; Rajasab AH, 2002. Heteropogon triticeus, a new host of Claviceps sorghi in India. Journal of Phytopathology, 150(4/5):196-199.

Pazoutová S; Kolarík M; Kolínská R, 2004. Pleomorphic conidiation in Claviceps. Mycological Research, 108(2):126-135.

Pazoutová S; Ranajit Bandyopadhyay; Frederickson DE; Mantle PG; Frederiksen RA, 2000. Relations among sorghum ergot isolates from the Americas, Africa, India, and Australia. Plant Disease, 84(4):437-442; 36 ref.

Prom LK, 2005. Passive transmission of sorghum ergot (Claviceps africana) by four species of adult stink bugs. Southwestern Entomologist, 30:29-34.

Prom LK; Lopez JD Jr; Latheef MA, 2003. Transmission of Claviceps africana spores from diseased to non-infected sorghum by corn earworm moths, Helicoverpa zea. Journal of Sustainable Agriculture, 21(4):49-58.

Puranik SB; Padaganur GM; Hiremath RV, 1973. Susceptibility period of sorghum ovaries to Sphacelia sorghi. Indian Phytopathology, 26(3):586-587

Rajkule PN; Desai KB; Kadam JR; Chauhan GK, 1983. Sorghum Newsletter, 26:114.

Rajkule PN; Desai KB; Raja KRV, 1985. Reaction of enteries of the ISMDN to sugary disease and grain mould and sugary disease evaluation in preliminary sorghum varieties and hybrids. Sorghum Newsletter, 28:91-92.

Ramakrishnan TS, 1948. Ergot sclerotia on Sorghum vulgare Pers. Current Science, 17:218.

Reis RM; Mantle PG; Hassan HAG, 1996. First report in the Americas of sorghum ergot disease, caused by a pathogen diagnosed as Claviceps africana. Plant Disease, 80(4):463; 2 ref.

Sangitrao CS, 1982. Studies on ergot disease of sorghum in Vidarbha. Thesis. Akola, India: Punjabrao Krishi Vidyapeeth.

Sangitrao CS; Bade GH, 1979. Meteorological factors associated with honeydew development and sclerotial stage in sorghum ergot. Sorghum Newsletter, 22:107-108.

Sangitrao CS; Taley YM; Moghe PG, 1979. Effect of planting date on the appearance of sugary disease. Sorghum Newsletter, 22:111.

Singh P, 1964. Sugary disease of sorghum. In: Progress Report of the Accelarated Hybrid Sorghum Project and the Millet Improvement Programme. Indian Council of Agricultural Research and Cooperating Agencies. New Delhi, India: Indian Cooperating Council of Agricultural Research.

Sundaram NV; Singh SD, 1975. A new host for sugary disease of sorghum caused by Sphacelia sorghi. Science & Culture, 41(11):528

Tonapi VA; Navi SS; Bandyopadhyay R, 2004. Variability and viability of sorghum ergot sclerotia. International Sorghum and Millets Newsletter, 44:99-100.

Tonapi VA; Wirojwattanakul K; Dang Van Vinh; Moung Moung Thein; Navi SS; Tooley PW, 2004. Prevalence of sorghum ergot in Southeast Asia. International Sorghum and Millets Newsletter, 44:95-97.

Tooley PW; Carras MM; Sechler A; Rajasab AH, 2010. Real-time PCR detection of sorghum ergot pathogens Claviceps africana, Claviceps sorghi and Claviceps sorghicola. Journal of Phytopathology, 158(10):698-704.

Tooley PW; Ranajit Bandyopadhyay; Carras MM; Pazoutová S, 2006. Analysis of Claviceps africana and C. sorghi from India using AFLPs, EF-1alpha gene intron 4, and beta-tubulin gene intron 3. Mycological Research, 110(4):441-451.

Tsukiboshi T; Shimanuki T; Koga H, 1999. A new pathogen, Sphacelia sorghi, causing ergot of sorghum occurs in Japan. Annals of the Phytopathological Society of Japan, 65(3):318-320; 10 ref.

Tsukiboshi T; Shimanuki T; Uematsu T, 1999. Claviceps sorghicola sp. nov., a destructive ergot pathogen of sorghum in Japan. Mycological Research, 103(11):1403-1408; 14 ref.

UK CAB International, 1987. Claviceps sorghi. [Distribution map]. Distribution Maps of Plant Diseases, October (Edition 1). Wallingford, UK: CAB International, Map 582.

USDA-ARS, 2009. Germplasm Resources Information Network (GRIN). Online Database. Beltsville, Maryland, USA: National Germplasm Resources Laboratory.

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India: International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), Patancheru 502 324, Andhra Pradesh

USA: Sorghum Improvement Conference of North America, P.O. Box 530 Abernathy, Texas 79311


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10/09/09 Updated by:

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