In this article we will discuss about the green ear disease of bajra caused by fungi.
Introduction to the Green Ear Disease of Bajra:
The green ear disease of Bajra is a common disease and has been reported from several countries including India, Iran, Israel, China, Fiji, Japan and the countries wherever Bajra crop is grown.
In India, the disease was first reported and studied by Butler (1907) who considered the disease to be sporadic in nature not causing much damage to the crop. Mitter and Tandon (1930) reported the disease from Allahabad, Uttar Pradesh and confirmed the observations of Butler (1907).
Since then, the disease on Bajra has been reported from all the states wherever Bajra is cultivated as one of the crops of ‘Kharif’ season.
Effect of Green Ear Disease:
Initially the disease was regarded as sporadic in nature causing’ not much damage to the crop except in low-lying fields where the loss could be quite significant. However, Rai and Sinha (1965), Mathur and Dalela (1971) and Nene and Singh (1976) have estimated the loss to be as high as 27-30 percent.
The disease appeared in an epidemic form in Karnataka and Maharashtra during 1975 causing almost total loss of the crop.
Symptoms of Green Ear Disease:
Two stages of the symptoms of the disease have been recorded: the downy mildew stage prominent on the leaves and the green ear stage affecting the inflorescence (ears). The latter is more prominent than the former symptom since it has been reported that the strain of the pathogen occurring in India produces more oospores than the sporangia.
The growth of the plants affected is checked and the plants appear stunted and sick, pale yellow in colour. Even young plants show this symptom. Soon, the leaves begin to show chlorosis in streaks on the upper surface while the lower surface shows downy growth of the fungus.
After some time chlorotic areas turn brown and in advanced stages shredding of the leaves has also been observed. Since the plant is unbranched, the disease causes stimulation of nodal bud’s and lateral shoots develop which is an abnormal character.
Associated with it, the leaves also show additional symptoms. The usually green colour of the leaves may change wholly or partly, to whitish or brown colour. Whitening of the younger leaves is evident along the streaks while in older leaves, the colour changes to brown.
In older plants, this occurs especially in those leaves from the axil of which the inflorescence develops. The change of the colour of leaves is associated with twisting, folding and shredding towards the tip.
In older plants where green ears have been formed the upper leaves are mostly brown and split. A large number of leaf buds develop into a large mass of white or twisted brown leaves. The axil of these buds produce green leafy human ear like structures.
The disease becomes prominent when the inflorescence gets converted into green leafy ears.
This is due to transformation of floral parts into twisted leafy structures, giving the ear an appearance of green leafy mass. Hence, the common name of the disease-‘Green ear’.
Generally the following types of green ears have been observed:
(i) Entire ear (inflorescence) is transformed into green leafy mass.
(ii) The lower part of the inflorescence is converted to green leafy mass but the upper part bears seeds.
(iii) The development of inflorescence is completely suppressed and in its place is formed a small bunch of leafy structures.
The disease causes changes in the florets as well as floral parts. The bristles of spikelet’s become contorted and hypertrophied. The number of spikelet’s may change from one to two in the same pedicel. A very common feature is the increase in the number of florets in each spikelet.
The fertile parts especially the stamens and carpels usually become sterile, leaf like and suppressed to rudimentary peg like structures. Sometimes the stamens appear as brown leathery, pointed bodies without any differentiation into filament and anther.
In severely attacked plants,’ the carpels rarely develop and is replaced by small, leafy shoots or horn like outgrowths. This may be attributed to hypertrophy and hyperplasia of the affected tissues.
The causal organism is Sclerospora graminicola (Sacc.) Schroet. It is an obligate parasite.
The primary infection occurs through oospores or mycelium present in the seeds produced on diseased ears. After the return of favourable conditions, the oospores present in the soil, germinate and enter the young seedlings of host through the underground parts and cause primary infection.
When seeds containing mycelium are sown in the fields, these germinate and grow and along with it the mycelium also grows and causes primary infection as well. The infection spreads systemically along with the growth and development of seedlings into mature plants.
In early stages, symptoms appear on leaves as downy growth of the fungus on the lower surface of leaves. After some times the characteristic green ears appear on the diseased plants.
The secondary infection takes place through sporangiophores and sporangia produced on the host as a result of primary infection. These sporangia are disseminated by wind, water and insects, land on the susceptible parts of the host, and germinate producing zoospores.
These zoospores germinate by germ tube and cause secondary infection. Since the sporangia are reported to germinate only in the presence of enough dew on leaf surface, the chances of secondary infection are remote.
Towards the end of the growing season of the crop, the pathogen produces oospores through sexual reproduction. The oospores are thick walled and serve as resting spores, keeping the pathogen alive during the unfavourable conditions.
During harvesting of the crop, the oospores along with plant debris are left in the soil of the fields where the oospores perennate waiting for the favourable conditions to return back so that these can serve as the source of primary inoculum.
Control Measures of Green Ear Disease:
Green ear disease is primarily soil borne and the following control measures have been suggested:
(i) Rotation of crop, with non-host types may check the disease.
(ii) Removal of diseased plants and their burning within a month of the disease detection checks the disease to a large extent.
(iii) Spraying with Dithane M-45 also helps in controlling the disease.
(iv) Seed treatment with 0.1 percent Agrosan GN and 0.4 percent thiram has been reported to control the disease to 50 percent.
(v) Use of disease resistant varieties like HB-15, PHB-10 and PHB-14 has been recommended.