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Diagnostic Fact Sheet for Claviceps fusiformis

Invasive and Emerging Fungal Pathogens - Diagnostic Fact Sheets

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Ergot of pearl millet - Claviceps fusiformis

Claviceps fusiformis is widespread in Africa and India, where the host crop, pearl millet (Pennisetum glaucum (L.) R. Br.), has been grown for thousand of years. This disease became a major yield constraint in India with the introduction of open-pollinated hybrid lines of pearl millet (Thukar & Rai, 2003). Conidia are spread from plant to plant by wind, rainsplash, and insects. Wild species of Pennisetum and related grasses are hosts that may serve as reservoirs of inoculum. Ergot infection can have a significant impact on yields, with up to 70% loss in susceptible varieties (Natarajan et al, 1974). The use of clean seed and cultivation under particular climate conditions may prevent ergot from appearing as a significant problem in the Americas.

Claviceps fusiformis Loveless

Sclerotia elongate to globose, 3.6–6.1 x 1.3—1.6 mm, pale to dark brown, with or without conidia-containing cavities (Thakur et al., 1984). Germination by 1-16 fleshy purplish stalks, 6–26 mm long, each bearing apical, globular capitulum, light to dark brown with numerous perithecial ostioles.

Perithecia immersed in head of stalked stroma developed from sclerotia. Asci interspersed with paraphyses, emerge through ostioles. Ascospores hyaline, filiform,non-septate, 103–176 x0.5 µm (Thakur et al., 1984).

Conidia of two types, macroconidia and microconidia, developing both in culture and in honeydew on infected pearl millet panicles. Macroconidia hyaline, fusiform, unicellular, 12.0–26.5 x2.5–6.0 µm, producing 1–3 germ tubes from ends or sides. Microconidia hyaline, globular, unicellular, 2.5–11.0 x`1.0–5.0 µm, producing only one germ tube. Both macroconidia and microconidia are able to produce additional microconidia in chains from conidiophores formed by the germ tubes (Prakash et al., 1983).

See also Loveless, 1967; Siddiqui and Khan, 1973; Thakur et al., 1984; Chahal et al., 1985; Verma and Pathak, 1985b.

Host range: Primarily known on cultivated pear millet, Pennisetum glaucum divisum but also reported on related grasses, specifically Panicum antidotale (elbow grass), P. curviflorum (= P. trypheron), Pennisetum ciliare (? Cenchrus ciliaris), P. diversum, P. massaicum , P. squamulatum, and Setaria verticillata

Geographic distribution: Widespread in most African and Asian countries where pearl millet is grown. Although not reported on pearl millet in the western hemisphere, there is one report of the species on Pennisetum ciliare as Cenchrus ciliaris in Mexico (San Martin et al., 1997)

NOTES ON TAXONOMY/SYSTEMATICS

Loveless (1967) first identified the fungus Claviceps fusiformis in feed grain as the causal agent of an agalactia of sows in Africa. For quite some time the name Claviceps microcephala, that of the pathogen of Pennisetum hohenackeri in India, had been misapplied to the pearl millet ergot pathogen. Siddiqui and Khan (1973) confirmed the identity of the fungus on bajra (pearl millet) as C. fusiformis. Subsequent studies by Bhat (1977), Kumar and Arya (1983), Thakur et al. (1984) and Chahal et al. (1985) supported these findings from morphological studies of the fungus.

More recently, Tooley et al. (2001) distinguished five species of Claviceps (C. africana, C. sorghicola, C. purpurea, C. fusiformis and C. paspali) using the beta-tubulin gene intron 3 region and intron 4 of the EF-1alpha gene. PCR primers designed from unique sequences within the beta-tubulin intron 3 region can be used to differentiate the five Claviceps species.

Nomenclature for the primary economic host of the fungus, Pennisetum glaucum (L. ) R. Br., commonly called “pearl millet”, has also undergone changes. Loveless (1967) referred to it as P. americanum Stapf & C.E. Hubb. In the literature on this disease, the names P. typhoides (L.) Leeke or P. typhoideum L.C. Rich. are also used for the grass species. Other synonyms are P. spicatum (L.) Kom. and Setaria glauca (L.) P. Beauv. (USDA/ARS). Another host Cenchrus ciliaris is now considered Pennisetum ciliare (L.) Link.

HOST RANGE

Claviceps fusiformis was isolated from infected panicles of Pennistum ciliare, a host that may serve as the source of inoculum. This host may have been the source of inoculum that led to a sudden large-scale epidemic of pearl millet ergot in Rajasthan, India (Singh et al., 1983). Earlier, Dwarakanath Reddy et al. (1969) reported P. squamulatum and P. massaicum as grass hosts inTamil Nadu, India. The poaceous weeds Setaria verticillata (Rathi and Panwar 1993) and Pennisetum divisum (Dhindsa et al., 1986) also were found to be infected in India. Cross inoculations indicate that Panicum antidotale may be another host for C. fusiformis (Pahil et al., 1986).The sphacelial state of C. fusiformis was reported on Pennisetum ciliare (as Cenchrus ciliaris) in Mexico (San Martin et al., 1997). Macroconidial shape and size agreed with the description of Thakur et al. (1984). Pandemics of ergot on this species in Texas, where the grass has also been introduced for production of forage, had been reported earlier, although the identity of the fungus was not determined (Craig and Hignight, 1991). Claviceps paspali was common in the area on another panicoid grass. Conidial shape and size reported by Alderman et al. (2004) for C. paspali do not match those of the Mexican fungus, but their list of Claviceps specimens in the United States also includes some from Setaria spp. in the southwest that are identified only as “Claviceps sp.”. Velasquez-Valle et al. (1998) reported further on Claviceps species appearing in Mexico and Texas. Grassed found with honeydew containing macroconidia fitting the description of C. fusiformis were identified as P. glaucum in Texas, Pennisetum ciliare (as Cenchrus ciliaris) in Mexico and Texas, Dichanthium annulatum in Mexico, and Eriochloa sericea in Texas. An ergot fungus resembling C. maximensis was also found on pearl millet in Texas. No inoculations of the wild grass isolates to pearl millet were reported. Therefore, whether C. fusiformis is present in North America or there is another species that attacks pearl millet and wild grasses remains to be determined.

GEOGRAPHIC DISTRIBUTION

Claviceps fusiformis occurs in most African and Asian countries where pearl millet is grown (Ramakrishnan, 1971; Rachie and Majumdar, 1980; Rothwell, 1983). However, it has not been reported on pearl millet in the western hemisphere (Thakur and King, 1988b). There is one report of the species on Pennisetum ciliare ( ? Cenchrus ciliaris in Mexico (San Martin et al., 1997)The distribution map published by CABI/EPPO in 2006 includes records based on specimens of C. fusiformis from the collection in the herbarium (herb. IMI) at CABI Bioscience, Egham, UK

BIOLOGY AND ECOLOGY

Life Cycle: The life cycle of Claviceps fusiformis begins when the sclerotia germinate to produce stalked stromata bearing asci and ascospores in perithecia. The ejected airborne ascospores infect the stigmas of flowering pearl millet panicles before pollination. Honeydew oozes out of the infected florets 5-7 days after infection. This honeydew contains numerous macroconidia and microconidia that serve as secondary inoculum for the disease (Thakur et al., 1984). The conidia are disseminated from one panicle to another by rain splash, wind currents, contact and also by insects. Both types of conidia initiate infection when they land on the stigmas of flowering pearl millet. Optimal conditions for conidial germination in the laboratory were found to be a temperature of 25 C and 100% relative humidity. Germination of at least 60% was obtained with temperatures between 20 and 30 C and with relative humidity greater than 80% (Verma and Pathak, 1985a)..

Dense brown fusiform sclerotia form in the infected florets within 15-20 days of the appearance of honeydew. These sclerotia are the survival form of the fungus and may fall to the ground or be included with harvested seed. The following season, sclerotia germinate by forming 1-16 fleshy stipes, each with a globular capitulum containing pyriform perithecia. Thakur et al. (1984) reported that the conidia to conidia cycle of plant to plant transmission took 4-6 days, with mature sclerotia observed 20-25 days after inoculation.

Prakash et al. (1983) studied the germination and nuclear behaviour of sexual and asexual propagules of C. fusiformis. The uninucleate ascospores germinated to produce conidia. The nucleus of most ascospores migrated into the conidium In some ascospores the nucleus divides into two resulting in two primary conidia. The conidial nuclei could then migrate into secondary conidia without undergoing any division. Likewise, the asexual conidia in honeydew germinated to provide secondary, tertiary and quaternary conidia. The nucleus migrated into successive conidia without division. Inoculation studies showed that only the nucleated, last-formed conidia were infective to pearl millet whether they were of ascosporic or conidial origin. Thus, apparently, the infectiousness of ascospores and conidia falling on unsuitable substrates may be sustained over time. Pazoutova et al. (2004) have shown that iterative (secondary) sporulation also occurs in the macroconidia from honeydew of this and other species of Claviceps.

Conidial infection occurs through the stigma, style or ovary wall (Prakash et al., 1980). Hyphae are located below the ovary wall three days after inoculation and subsequently the fungus shows preferential growth towards the ovary wall. The whole ovary is replaced by hyphae by ten days after infection. Fungal spread is always intercellular. Honeydew production begins five days after inoculation and persists for one week.Although direct infection by ascospores has been considered to initiate the disease in a growing season (Chal et al., 1989), another primary source of infection in field tests was found to be the conidia produced by sclerotia left on the soil from the previous season (Verma and Pathak, 1986), whereas the main source of secondary infection was the conidia from infected spikelets (Sharma and Chauhan, 1982; Roy and Kumar, 1988a).

Epidemiology: An overcast sky, drizzling rain (>80% RH), moderate temperatures (20-25°C) and air movement during crop flowering favour the development and spread of ergot. Heavy rainfall combined with high relative humidity gave the highest incidence of the disease. Multiple regression analysis revealed that maximum and minimum temperatures, morning and evening relative humidity, total rainfall and sunshine all influence the incidence of ergot (Dakshinamoorthy and Sivaprakasam, 1988).

A temperature range of 14 to 35°C, with 8 hours/day at <20°C and 4.6 hours/day at >30°C, was more favourable to ergot infection than a temperature range of 21 of 35°C, with 6.4 hours/day at >30°C. The minimum temperature was more critical for ergot infection than the maximum temperature, with higher minimum temperatures resulting in less disease. Ergot infection was favoured by a panicle wetness duration of 16-24 h. Maximum ergot severity and minimum latent period were obtained at a 30°C day/25°C night temperature regime with 24-96 h of panicle wetness (Thakur et al., 1991a).Ergot severity on pearl millet cultivars NHB-3, PSB-8 and 7042 was highest when there were 12 rainy days during the flowering period and lowest when there was no rain. Large differences were recorded in the ratio of ascospores + conidia to pollen grains collected on greased slides placed at earhead level in a millet crop in 1981 (1:13) and 1983 (1:3) indicating that a large amount of pollen was washed down by rain showers. A reduction in the pollen available to inhibit stigma infection (see below) increased ergot severity (Chahal and Dhindsa, 1985).

The concentration of C. fusiformis spores influences the level of disease. The percentage disease index was increased from 10 to 87 by increasing the concentration of spores used to inoculate P. glaucum from 250,000 to 1250,000 spores/ml. Disease development was optimal at 25-30°C and 86-88% RH (Roy and Kumar, 1987). Continuous air sampling used in pearl millet fields at two locations in Marathwada, India, during July-October showed maximum spore concentrations in July (5026 spores/m³ air) at Parbhani and in September (1972 spores/m³) at Aurangabad. At both places, a rise in spore concentration was associated with rainfall and high relative humidity (Tilak and Rao, 1987).

Sclerotia germinated in sterilized field soil after 40 d at 28°C with continuous high moisture. The percentage germination was higher in partially buried sclerotia and those at a depth of 1 cm; those placed below 4 cm failed to germinate (Chahal et al., 1989). A good rate of sclerotial germination from infected millet ears was obtained by alternate wetting and drying, and by incubation at 23°C under moist conditions. Ascospores germinated directly by germ tubes or by producing conidia at the germ tube tips (Prakash et al., 1981).

Sclerotia placed in the soilproduced mycelium and conidia, which were then trapped on glass slides at a height of 2 m. P. glaucum plants grown in field plots containing sclerotia became infected, indicating that sclerotia in the soil at the time of sowing can produce conidia which may become air-borne and cause infection (Verma and Pathak, 1986).

Production of Toxins: Loveless (1967) reported the production of water-soluble alkaloids from sclerotia of C. fusiformis in pearl millet. The alkaloids differed from those produced by Claviceps purpurea on rye and wheat. Two groups of alkaloids, agroclavine and elymoclavine, have been identified in the sclerotia of C. fusiformis and their concentration varies between sclerotia (Bhat et al., 1976). A diet containing 2-3% sclerotia prevented mice from raising litters due to agroclavine-induced toxicity which inhibited normal mammary gland development (Mantle, 1968). Agroclavine has also been reported to cause agalactia (milklessness) in sows (Loveless, 1967) and dropping of feathers and weakening of legs in chicks (Bhat et al., 1976).

The alkaloids present in honeydew and sclerotia from 20 millet varieties were identified as setoclavine, agroclavine, penniclavine, elymoclavine, an unidentified alkaloid and chanoclavine. Ergometrine was not found. Symptoms of ergot poisoning in animals and man (giddiness, diarrhoea, nausea and vomiting, followed by dehydration) from contaminated millet grain have been reported in Rajasthan and Maharashtra, India (Kumar and Arya, 1978). A sclerotial filtrate inhibited the germination of pearl millet seeds and also elongation of the root compared to the plumule (Kumar, 1980).

A gene (cpd1) coding for the dimethylallyltryptophan synthase (DMATS), which catalyses the first specific step in the biosynthesis of ergot alkaloids, has been cloned from a strain of C. purpurea. The derived gene product (CPD1) showed 70% similarity to a gene previously isolated from Claviceps strain ATCC 26245 (probably an isolate of C. fusiformis) suggesting that some of the genes of ergot alkaloid biosynthesis in C. purpurea are clustered (Tudzynski et al., 1999). De Vries et al. (1999) have identified and characterized a new type of hydrophobin encoded by an abundant mRNA of C. fusiformis.

MEANS OF MOVEMENT AND DISPERSAL

Natural dispersal (non-biotic) - Pearl millet ergot can spread more than 18 m from the source of infection, but the intensity of disease generally decreases with increasing distance from the source. Wind direction during flowering also influences the spread of the pathogen in the field (Kumar S et al., 1997b).

Insect-borne spread - Insects, including various bees, flies, ants and hemipteran bugs, can be non-specific vectors of the ergot fungus. Eight species were found to be contaminated with conidia: Apis indica (=A. cerana indica) and Tabanus rubidus carried the heaviest conidial loads. Others involved in the spread of conidia are, Dysdercus cingulatus, Monomorium salomonis, Musca domestica, Syrphus confractor (=Metasyrphus confractor), , Vespa orientalis and V. tropica (Sharma et al., 1983; Verma and Pathak, 1984). Dakshinamoorthy et al. (1988) reported several other species: Apis florea, Camponotus compressus, Dolycoris indicus, Oxycetonia versicolor, Syrphus sp. and Tachina fallax (=Exorista fallax).

Seedborne spread - Seed contaminated with the sclerotia of C. fusiformis plays a major role in the spread of the pathogen (Thakur, 1984).

Agricultural practices - The movement of sclerotia with seed and with soil adhering to farm implements makes it possible to transport the pathogen from one field to another.

Movement in trade - Sclerotial contamination of seed and food grain can transport the fungus through trade.

Plant parts liable to carry the pest in trade/transport

- Flowers/Inflorescences/Cones/Calyx: Spores, Hyphae; borne internally; borne externally; visible to naked eye as wet or dry accumulations (“honeydew”).

- Leaves: Spores, Hyphae borne externally; visible to naked eye.

- True Seeds (inc. Grain): Spores, Hyphae; borne externally; invisible unless in accumulations causing seeds to cohere in masses ((Sharma, 1990).

Plant parts not known to carry the pest in trade/transport

- Bark

- Bulbs/Tubers/Corms/Rhizomes

- Fruits (inc. Pods)

- Growing Medium Accompanying Plants

- Seedlings/Micropropagated Plants

- Roots

- Stems (above Ground)/Shoots/Trunks/Branches

- Wood

SEEDBORNE ASPECTS

Incidence: Claviceps fusiformis is not truly seedborne but the sclerotia and honeydew can contaminate seed lots (Chahal et al.,1994).

Effect on Seed Quality

Claviceps fusiformis does not affect seed quality. Seed lots contaminated with sclerotial bodies can be cleaned and sclerotia-free seed can be used for planting (Pathak et al., 1984).

Pathogen Transmission

The transmission of C. fusiformis occurs mainly through the contamination of seed lots with sclerotia. In some cases, seeds coated with the honeydew form clumps of abortive and healthy seeds and such seeds could act as a source of infection (Sharma, 1990).

Seed Treatments

No seed treatment is required.

Seed Health Tests

No seed health test is required, but according to the international rules for seed testing (ISTA, 1993), the minimum required sample for purity analysis should be equal to the weight of at least 2500 seeds, and sclerotia and their parts should be removed from seed samples.

Sclerotia are best removed from pearl millet seed using the Specific Gravity Table. Cleaning by this method is convenient, rapid and cost-effective. Cleaning may also be achieved by dipping samples in a 20% salt solution and scooping away the sclerotia. This method is slow, cumbersome, expensive and reduces seed germination and seedling growth (Pathak et al., 1984).

NATURAL ENEMIES

Natural enemies listed in the database: The list of natural enemies has been reviewed by a biocontrol specialist and is limited to those that have a major impact on pest numbers or have been used in biological control attempts; generalists and crop pests are excluded. For further information and reference sources, see About the data. Additional natural enemy records derived from data mining are presented as a separate list.

IMPACT

Claviceps fusiformis can cause heavy reductions in grain yield of pearl millet. In hybrids HB 3 and HB 4, yield losses due to the disease were estimated at 58-70% (Natarajan et al., 1974). In a field experiment in India, Thakur et al. (1989a) recorded grain yield losses of 55% in open-pollinated varieties of pearl millet and 65% in hybrids. A field survey carried out in the pearl millet-growing areas of Haryana, India, during the rainy season in 1993, revealed the widespread occurrence of ergot with disease intensity ranging from 9 to 16% (mean 12.5%) resulting in considerable yield losses (Kumar R et al., 1997). A popular hybrid, HHB 67, was recorded as exhibiting 7-10% ergot in 1992 and 1993 crop seasons in two districts in Harayana (Kumar S et al., 1996). Of 11 districts surveyed in Rajasthan, India, maximum ergot (53%) was recorded in Dholpur with maximum grain yield losses of 7.64 g/ha. Disease intensity was more severe on the popular hybrid BJ 104 than on local cultivars (Bansal and Siradhana, 1988b).Yield losses in the highly susceptible male sterile line, 843A, were calculated by correlating the number and weight of sclerotia produced with the reduction in grain yield, at different disease intensities. A significant negative correlation was observed between the number and weight of sclerotia and the number and weight of grains. A regression equation was developed to predict losses in grain yield due to the disease (Kumar R et al., 1997).

PRODUCTIVE USES AND MANAGEMENT

Ergot of bajra (pearl millet) is reported to have been used in traditional medicine in India (Vaidya and Rabba, 1993).

PHYTOSANITARY SIGNIFICANCE

There is no serious quarantine risk because proper seed cleaning removes all sclerotial bodies that can transmit the fungus from one place to another with seeds.

SYMPTOMS

On panicles, droplets of creamy to pink, mucilaginous fluid are seen exuding from the infected florets. The sticky fluid called 'honeydew' contains numerous conidia, When excessive amounts of honeydew are produced, it drops on to the foliage and the ground. The droplets on the panicle become darker and coalesce to form compact patches. Infected florets do not produce grains because the ovaries are replaced by compact, dark, hard fungal masses known as sclerotia. These sclerotia are often larger than the grains and protrude out of the glumes.

DETECTION AND INSPECTION

Disease symptoms, both honeydew and sclerotial phases, are clearly visible in the field on infected panicles of pearl millet. Sclerotia mixed with grains/seeds are easily seen but a magnifying lens may be needed to detect broken sclerotia mixed with grain.

DIAGNOSIS

Conidia can be easily detected in honeydew droplets by mixing them with a drop of water on a glass slide followed by examination under a microscope for their presence. Both macroconidia and microconidia may be present in abundance. The fungus can be cultured on various media, although growth is slow ( Kumar and Arya, 1984;Sharma RK et al, 1984; Verma and Pathak, 1985b; Bansal and Siradhana, 1988a).

CONTROL

Host-Plant Resistance

Mechanism of resistance: Infection occurs mainly through the stigmas, so pollination protects the plant against infection, because it induces rapid withering of stigmas (Thakur and Williams, 1980). Ergot resistance is based on a pollen escape phenomenon linked to the normal events that occur during pollination (Willingale et al., 1986). Disease escape is mediated through the development of a localized stigmatic constriction, which occurs 6 h after self-pollination.The susceptibility of pearl millet F1 hybrids is closely associated with events in flowering that govern resistance in A lines and their hybrids (Thakur et al., 1991b). Protogyny (the period between stigma initiation and anthesis), the time between full protogyny and the initiation of anthesis, and stigma length are shorter, self-pollination is quicker and seed set is higher, in resistant and intermediate cultivars than in susceptible cultivars (Thakur et al., 1992). High ergot susceptibility of pearl millet hybrids has often been associated with the A1 cytoplasm of male-sterile lines (A-lines). Although the A1 cytoplasm has a significant effect on increasing ergot severity in hybrids, the contribution of nuclear genetic factors of female parents was greater than that of the cytoplasm (Rai and Thakur, 1995). See also Thakur (1990) and Willingale and Mantle (1985).

Resistant varieties: Although it has been difficult and time consuming to find true genetic resistance to C. fusiformis in germplasm accessions of P. glaucum, significant advances have been made by pedigree breeding for improved resistance (Thakur et al., 1982, 1993; Kumar and Andrews, 1984; Andrews et al., 1985; Hash et al., 1999). Several of these lines have been utilized in breeding hybrid parental lines and varieties. Pearl millet male sterile line ICMA92666 and its maintainer line ICMA92666, released in 1996 for use as seed parents in hybrid breeding programmes, are resistant to C. fusiformis, Tolyposporium penicillariae and Sclerospora graminicola (Rai et al., 1998).

The grain yields of hybrids based on A2, A3 and violaceum sources of cytoplasm were comparable or better than yields of A1 source hybrids, and there was better resistance to downy mildew, ergot and smut than in the control (Mangat et al., 1996). Pearl millet lines PIB 189-2-5-2 and PIB 1108-2-2 had stable resistance to C. fusiformis (Virk et al., 1989).Inbred lines ICML1 and ICML2, which were selected for stable resistance to C. fusiformis, also had resistance to S. graminicola and T. penicillariae (Thakur and King, 1988a). Four pearl millet populations (ICMP1, ICMP2, ICMP3 and ICMP 4) and several inbred lines (ICMPES 1, 2, 23, 27, 28, and 32)) developed as sib-bulks of several selected lines with combined resistance to the three pathogens, have been recommended for use in breeding disease-resistant synthetics (Thakur et al., 1985, 1988). Resistance to ergot was identified in ICMPES lines developed at ICRISAT including ICMPES28, ICMPES29 and ICMPES45 but yields in these lines were lower than in local African cultivars (Mbwaga et al., 1995).In Zimbabwe, Mushonga (1983) reported that infection in inbreds 10 days after inoculation ranged from 0 (ICMPE13-6-13) to 10.9%, but was 95% in the hybrid BJ104. In fact, under disease pressure varieties with functional field resistance may produce higher yields than those of hybrid lines (Thakur & Rai, 2003).See also Williams and Andrews (1984), Andrews et al. (1985) and Hash et al. (1999).

Inheritance of resistance: Screening millet germplasm under artificial epiphytotic conditions revealed a lack of major gene resistance to C. fusiformis. Chahal et al. (1981) have developed and pursued a new strategy involving recurrent selection to concentrate minor genes controlling polygenic resistance for intra-population improvement. The inheritance of resistance to ergot was complex, and both parents needed to be resistant in order to obtain a resistant hybrid (Mehta and Dang, 1987). The effect of cytoplasm on ergot susceptibility was significant. The higher ergot susceptibility of A lines and A × R hybrids, compared with B lines and B × R hybrids, could be attributed to the cytoplasmic, nuclear, and cytoplasmic × nuclear factors affecting the flowering events that influence ergot susceptibility (Thakur et al., 1989b).

Cultural Practices

The use of clean seed, the adjustment of sowing dates, deep ploughing, the judicious application of fertilizers, and intercropping have all been reported to reduce infection by C. fusiformis in pearl millet.

Delayed sowing, so that flowering occurred in rainy periods (Randhawa et al., 1992). or during cooler weather (Sharma et al., 1987), increased the incidence of ergot Bajra sown before 20 July under rainfed conditions in Karnataka, India, gave higher grain and fodder yields and lower incidence of ergot than later-sown crops (Desai et al., 1988). Deep ploughing soon after the crop harvest helps to bury the sclerotia deep in the soil which prevents their germination and thus reduces the primary inoculum. A high level of N increases susceptibility to ergot whereas a high level of potash reduces infection (Thakur, 1984). The germination of sclerotia was completely inhibited in soil amended with urea, diammonium phosphate and NPK (Mahadevamurthy et al., 1990). Intercropping pearl millet with mungbean has also been reported to reduce ergot infection (Thakur, 1983).

Chemical Control

A number of chemical fungicides have been tested against C. fusiformis, but these have either failed or only partially controlled the disease (Roy and Kumar, 1988b; Sharma et al., 1984). Chemical control is not currently considered an effective or economical control measure for the disease. Ziram and carbendazim were effective, both as protective and curative sprays, in controlling ergot in research studies (Pawar et al., 1986; Kumar and Thakur, 1996). Crude neem (Azadirachta indica) leaf extract and the neem products Achook and Neemark were effective against C. fusiformis on pearl millet, increasing yield. Sprays applied before or after inoculation were on a par with carbendazim and superior to mancozeb or carboxin (Kumar et al., 1995).

Biological Control

Although several antagonists to C. fusiformis have been isolated from infected panicles, no effective biocontrol method is currently available for pearl millet ergot. Fusarium sambucinumGibberella pulicaris (Fr.:Fr.( Sacc.] and Dactylium (= Fusarium) fusarioides were isolated from C. fusiformis and the nature of their antagonism tested (Tripathi et al., 1981).

Studies with antagonistic organisms have continued to show promise. Fusarium semitectum var. majus was effective in controlling ergot by reducing infection and the formation of sclerotia in infected florets and by disintegrating the sclerotia (Rao and Thakur, 1988). Fusarium chlamydosporum colonizes sclerotia in the field, and a culture filtrate of this fungus inhibited C. fusiformis growth in vitro, causing cell discoloration and the formation of chlamydospores instead of normal mycelial growth and conidial formation (Gill and Chahal, 1988). Three antagonists, Trichoderma harzianum, T. viride and Gliocladium virens, significantly reduced sclerotial germination (Mohan and Jeyarajan, 1990). Treatment with Aspergillus niger or T. viride completely inhibited the germination of sclerotia (Mahadevamurthy et al., 1990). Under field conditions, spore suspensions and culture filtrates of a number of fungi and bacteria (F. chlamydosporum, F. heterosporum, T. harzianum, T. viride, A. niger, Epicoccum andropogonis, Bacillus subtilis) reduced the incidence of ergot when applied to flowering heads (Mahadevamurthy et al., 2006).

Pollen-based Control

Increased pollen availability in hybrids during the early stages of flowering protects them from ergot infection. Significant reductions in infection and considerable increases in grain yield occurred in pearl millet hybrids grown with the pollen donor line (Thakur et al., 1983). The pollination of inflorescences before or at the same time as inoculation with conidia of C. fusiformis greatly reduced ergot intensity (Kumar et al., 1997b).A field experiment was conducted in Hisar, Haryana, India during the kharif seasons of 1993-94 to determine the efficacy of controlling pearl millet ergot by pollen management. The treatments comprised: no pollination-no inoculation, inoculation-no pollination, pollination-no inoculation, pollination followed by inoculation the next day, simultaneous inoculation and pollination, and inoculation followed by pollination the next day. The lowest disease incidence was recorded for pollination (3.72%) followed by bagging and the no pollination-no inoculation treatment (5.50%) (Kumar R et al.,2002).

Integrated Disease Management

The use of clean, sclerotia-free seeds, disease resistant/tolerant pearl millet varieties (particularly open-pollinated varieties), early sowing and the judicious use of fertilizers (NPK) can help to reduce the incidence of ergot considerably (Sharma et al., 1984; Thakur and King 1992; Chahal et al., 1994; Thakur, 1998).

References

Nomenclature

Specimens in BPI

Additional distribution data

 

Suggested citation: Chalkley, D. Systematic Mycology and Microbiology Laboratory, ARS, USDA. . Invasive Fungi. Ergot of pearl millet - Claviceps fusiformis. Retrieved April 24, 2014, from /sbmlweb/fungi/index.cfm .



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Claviceps fusiformis
Claviceps fusiformis
Claviceps fusiformis
Claviceps fusiformis
Claviceps fusiformis
Claviceps fusiformis
Claviceps fusiformis
Claviceps fusiformis