The ergot of Bajra (pearl millet) was first reported from south India. The first report of its occurrence in epidemic form was made in 1956 from south ‘Satara’ area of Maharashtra. Severe epidemics of the disease are known to occur in Delhi, U.R, Rajasthan, Maharashtra, Karnataka, Tamil Nadu, A.R, and Haryana. Natarajan et al. (1974) estimated the average incidence to be about 62.4% with grain loss of about 58%.
The damage caused by the disease depends upon the weather at the time of ear formation. Presence of toxic alkaloids in the ergot adds to the importance of the disease. The sclerotia contain ‘ergo-toxin’ which, when consumed in excessive quantities, proves to be toxic to life. But, when taken in prescribed quantities it proves to be beneficial as it has some medicinal value too.
Symptoms of Ergot Disease:
The disease occurs only at the time of flowering. Small droplets of a light, honey coloured dew-like substance exudes from infected spikelets. A few too many spikelets may be found in a group which darkens with age and small, greyish or dark brown sclerotia are formed. These sclerotia replace the ovary or grain and are about 0.5-1.0 cm in length. They are hard and woody.
Causal Organism of Ergot Disease:
The fungus attacks the ovary and grows profusely producing masses of hyphae. These hyphae produce, firstly, small conidiophores which, later on, give rise to conidia. One can see honey dew-like droplets oozing out of infected ovary of the affected ears which are full of conidia.
However, after sometimes, the masses of hyphae filling in the ovary harden in addition with the honey dew-like substance and give rise to sclerotia. The sclerotia become somewhat elongated and project out the surface of the ear. These are the sclerotia which borne sex-organs therein at maturity.
Ergot Disease Cycle:
(i) Perennation:
These are the sclerotial bodies which help pathogen perennate from season to season. They remain in the soil or with plant debris, overcome the unfavourable circumstances, and germinate in favourable conditions during the next season producing ascospores to cause primary infection.
The fungus infects various collateral hosts like other species of Pennisetum, Cenchrus ciliaris, and C. setigerus producing ergot. The role of these collateral hosts in the perennation of the pathogen may also be significant.
(ii) Primary Infection:
Primary infection on healthy crop plants is brought into being after the sclerotia germinate in about a month’s time. The sclerotia germinate producing stripes, which bear perithecial heads that contain many perithecia embedded in them. Perithecia represent the fruiting bodies of the fungus and produce many asci inside. No paraphyses have been reported.
Asci, however, contain filiform, hyaline, septate, thin walled, ascospores (eight in number in each ascus) which get disseminated when the wall of the asci are burst-open. The disseminated ascospores, then fall on spike and under suitable conditions, germinate, enter inside the ovary, and cause primary infection. After the primary infection is established, the hyphae fill in the ovaries, mature, and lead to conidial stage. The hyphae give out small conidiophores, which produce conidia on them.
(iii) Secondary Infection:
These are the conidia produced during primary infection which represent the secondary inoculum (source of secondary infection) for the current season. The conidia are contained within the honey dew-like exudate. The latter are taken away by insects which, when they sit on other plants, spread the conidia on them. The conidia germinate there and cause secondary infection. In this way the secondary infection is insect-borne.
After sometimes, the hyphal masses filling in the ovaries as a result of primary as well as secondary infections harden giving rise to sclerotia. The latter are the structures which perennate and work as the source of primary infection during next growing season.
Predisposing Factors:
High humidity in and around the field at the time of infection is considered the most suitable condition for the severity of the disease. It is because the disease spreads very rapidly through secondary inoculum (conidia) during such environmental condition.
Management of Ergot Disease:
(i) Long crop rotation programme essentially helps avoid the disease incidence as this makes the pathogen inocula present in soil wait the proper host for a long length of time. In the mean-time many of the soil-borne inocula (mainly the sclerotia) become unviable.
(ii) The most commonly used method to control this disease is using clean seeds. For this, the seeds are soaked in 20-30% salt solution. The sclerotia come on to the surface of the salt solution and float. Floating sclerotia can be collected by hand and destroyed.
(iii) Repeated ploughing may reduce the viability of deep buried sclerotia in soil.
(iv) Resistant varieties should preferably be grown.
(v) Growth of a fungus, namely, Fusarium roseum on Claviceps fusiformis (= microcephala) as a mycoparasite has been commonly seen in the ‘teria’ area of Uttar Pradesh. The former can be used as highly potential biological control agent against the latter and the incidence of the disease can be effectively reduced employing this method.
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