Green ear disease occurs commonly and is very serious one in almost all bajra growing areas of our country. It has also been reported from many other countries of the world but from South America and Australia.
However, Butler (1907) first reported this disease in India in a sporadic form. Mathur and Dalela (1971) and Nene and Singh (1976) have estimated the loss as much as 27-30%. An outbreak of the disease on an unprecedented scale has been evidenced in Karnataka and Maharashtra during the ‘Kharif’ season of 1975 and a loss of almost 100% has been recorded.
Symptoms of Green Ear Disease:
Two stages of symptoms are recorded. One, the downy mildew stage which is predominant on the leaves and the other, the green ear stage affecting the inflorescence. However, the downy mildew stage on leaves is not as conspicuous as the green ear stage on inflorescence.
In downy mildew stage, the infected leaves start showing chlorotic streaks on their upper surface and, just opposite to the streaks on the lower surface, one can see a fine downy growth of the pathogen. After sometime, the chlorotic streaks turn brown and, in advance stages, the infected leaves become distorted, wrinkled, and tend to split along the veins.
In green ear stage, the symptoms of which are more pronounced and considered the principal one, the whole or part of the ear (inflorescence) is transformed into twisted leafy structures. This imparts the ear an appearance of green leafy mass and hence the name “green ear”. The transformation of floral parts into leafy structures is due to over-development (hypertrophy and hyperplasia) of the concerned tissue.
Causal Organism of Green Ear Disease:
The pathogen is an obligate parasite. The hyphae are coenocytic, intercellular and send small bulbous haustoria inside the host cells to obtain nutrients. Though hyphae are reported almost in all parts of affected plants due to systemic nature of infection, they collect in the form of tufts in the air spaces beneath the stomata and produce sporangiophores which emerge in clusters through stomata. The important point to note is that the sporangiophores are produced only on infected normal leaves, never on the inflorescence.
Each sporangiophore is a long, stout hypha, with many upright branches near the tip region which are slightly swollen and bear sterigmata. These are the sterigmata on which hyaline, broadly elliptical (sometimes broadly cylindric) sporangia are produced, which are slightly pointed or papillate at the free-end. Since the sporangiophore is of determinate growth, the sporangia are produced nearly at one time and also fall off simultaneously leaving the sporangiophore free of sporangia. Sporangia soon germinate producing bi-flagellate, reniform zoospores (3-13).
The sexual stage, the oosporic stage, of the pathogen is the most common and predominant stage in India. Unlike sporangiophores, the sex organs (antheridia and oogonia) are produced in both the infected leaves and the leafy structures formed as a result of transformation of floral parts of the inflorescence.
After fertilization through fertilization tube, oospores containing thick and warty wall are formed inside oogonia. The oospores remain scattered in the intercellular spaces of the infected host tissue. They do not germinate readily and are reported to have a prolonged resting period.
Green Ear Disease Cycle in Bajra:
(i) Perennation:
The disease is mainly soil-borne but some believe that it is seed-borne too. In the first case, the oospores fall down on the ground along with infected plant debris wherein they enjoy prolonged resting period and overcome the unfavourable environmental conditions. In the second case, however, the pathologists claim traces of mycelium present in the embryo of bajra seeds collected from partially transformed ears and advocate their role in perennation.
(ii) Primary Infection:
After the favourable conditions return, the oospores present in soil germinate and cause primary infection of the underground parts of the host plant. The infection spreads upwards systemically therefrom along with growing plant and the symptoms manifest on the leaves and on the inflorescence.
However, the susceptibility of the underground part decreases with the advancing age of the host plant. The primary infection results in the production of sporangiophores and sporangia on the infected leaves, which serve as the source of secondary infection during the same growing season.
(iii) Secondary Infection:
Secondary infection in the growing season occurs through zoospores produced by germination of sporangia formed during primary infection. These sporangia are disseminated by wind, water and insects, and reach susceptible parts of the host whereupon they germinate producing zoospores.
The zoospores germinate by germ tube and cause secondary infection. Since the sporangia are considered to germinate early in the morning when there is enough dew present on leaf surface and, their germination ceases when dew dries (after about 7.30 a.m.), the chances of considerable secondary spread of disease look very poor.
Towards the end of the growing season the pathogen enjoys sexual course of reproduction and produces oospores within all infected parts. The oospores represent resting structures of the pathogen and serve as source of primary infection during the next growing season.
Predisposing Factors:
Abundant air supply heavily charged with oxygen, low percentage of moisture in soil and a temperature range between 20 – 25°C are considered most favourable conditions for the germination of oospores in the soil. If the soil enjoys high moisture content, the seedlings emerge before the oospores germinate and thus escape the primary infection.
Management of Green Ear Disease:
1. Cultural practices play important role. Early planting, avoidance of ratooning, rouging and gap filling, deep ploughing, sun-exposure to ploughed soil, removal of infected crop debris, avoidance of monoculture, crop rotation, and avoidance of water-logging reduce the incidence of the disease.
2. HB-5, NHB-10 and NHB-14 are the commonly cultivated varieties, which are resistant in Indian conditions. Open pollinated varieties WC-C 75 and ICPT 8203 have shown durable resistance in our country. ICMH 451 and Pusa 23 are the varieties that have remained free from the disease for seven years hence recommended. Hybrid ICMH 88088 produced by ICRISAT shows high level of resistance to downy mildew and yields better than all other available cultivars.
3. Since the seeds are considered to carry part of infection, their treatment with 0.1% Agrosan-GN + 0.4% Thiram has resulted in about 50% reduction in disease incidence.
Ceresan and Captafol are also recommended for seed treatment. Seed treatment with Ridomil (8 g/kg of seed) followed by one spray of 0.1% Ridomil 20 days after plantation is recommended. Some pathologists report that seed treatment with crude extracts of Vinca rosea, Ocimum sanctum, Allium sativum, Datura stramonium, Azadirachta indica, Thuja sinensis, and Parthenium hysterophorus reduces disease incidence and increases crop yield.
4. Rouging of disease bearing plants within a month of sowing followed by Dithane M-45 spraying also helps controlling the disease.
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