Karnal bunt of wheat also known as “new bunt” or “partial bunt” and was first reported by Mitra (1931) from botanical station, IARI, Karnal (Haryana). This disease was reported occurring in isolated pockets of north-western region of our country till 1974 and its intensity in most of the cases was low, but the disease incidence gradually increased after 1975 and presently it has become a major constraint for wheat production as well as quality of grain.
The disease now occurs generally in the states of Jammu-Kashmir, Punjab, Haryana, H.P., U.P., and parts of Bihar, M.P., Rajasthan, West Bengal, and Gujarat. In Punjab alone, however, the disease intensity has increased from 39.5 to 93% during the period 1975-81. The disease shortens the length of ears as well as number of spikelets in the infected heads. Also, the viability of infected seeds is impaired and the quality is degraded.
Symptoms of Karnal Bunt Disease:
Symptoms appear only when the grains develop. The pathogen affects grains partially and the infected portion of the grain is converted into black shooty mass of spores. In badly infected spikelets, the glumes spread apart and quite often fall off on to the ground.
Freshly infected grains, however, emit foul smell like a rotten fish due to a chemical called trimethylamine. Due to the presence of foul smell, the disease has been mentioned as “stinking smut” by early workers. However, not all the ears standing become diseased and even in a diseased ear only few grains are bunted.
Causal Organism of Karnal Bunt Disease:
Mitra (1931) first reported that the causal organism of Karnal bunt of wheat is Tilletia tritici. In 1940, Mundkur changed the name of the pathogen as Neovossia indica (Mitra) Mundkur. Fischer (1953) limiting the species of Neovossia again transferred N. indica to Tilletia indica. Though, however, the taxonomy of the pathogen is still controversial in the light of morphological characters, most of the Indian workers still adhere to the name N. indica.
The teleutospores of the pathogen are spherical to oval with reticulations looking as curved spines on the epispore, darker brown in colour, and measure 22 to 49 microns in diameter. The electron microscopic studies have revealed that a teleutospore wall consists of three layers; perisporium (or sheath), episporium, and endosporium.
The perisporium, which is a thin hyaline membrane, surrounds the reticulations. The reticulations consist of two double strands cemented together by two cross bands at or near the apex. Teleutospores, however, are mixed with yellowish sterile cells.
On germination, a teleutospore gives rise to a pro-mycelium that bears long, sickle-shaped sporidia in a cluster at its tip; each cluster or whorl generally consists of 60-185 sporidia. These sporidia are called primary sporidia and are unicellular. They detach from the pro-mycelium (or basidium) in groups.
The primary sporidia are incompatible with each other, i.e., they do not fuse with each other. Instead, they mostly produce another crop of sporidia called secondary sporidia. The compatible primary sporidia and secondary sporidia fuse and develop into the dikaryotic hyphae and/or sporidia. The infection is caused by these dikaryotic hyphae or sporidia.
Karnal Bunt Disease Cycle:
(i) Perennation:
The consensus favours the view that the disease is soil-borne. The pathogen perennates through teleutospores, which reach the soil either directly falling on the ground or through sticking on the surface of infected seeds and survive until flowering time of the next wheat crop. Dhiman (1982) has reported that the teleutospores also survive in wheat straw. It has been reported, however, that the maximum survival period for teleutospores at soil depths of zero, three, and six inches is 45, 39, and 27 months, respectively.
(ii) Infection:
When favourable conditions become available at the time of flowering of the wheat crop, the perennating teleutospores germinate producing short, stout pro-mycelia. Each pro-mycelium gives rise to primary sporidia in whorl. The primary sporidia produce secondary sporidia.
The sporidia are wind/or water-splash disseminated to the flowers whereupon the compatible primary and secondary sporidia fuse producing dikaryotic hyphae and/or sporidia. These are the dikaryotic hyphae and/or sporidia which cause primary infection of individual florets.
Bedi and Dhiman (1984) have studied that during extremely favourable weather conditions the secondary and tertiary spread of the pathogen within and between spikelets takes place through secondary sporidia and dikaryotic mycelia produced on the primarily infected spikelets.
Predisposing Factors:
It has been found that disease incidence is influenced by the climatic conditions prevailing at the time of flowering. If at the time of flowering, the temperature ranges between 19-23°C and 8-10°C coupled with slight shower providing high atmospheric humidity, the disease occurs very well.
Aujla et. at. (1981) found that those varieties get severely infected which come into flowering from the fourth week of February to first week of March when the temperature usually ranges from 18-22°C and relative humidity (RH) above 70%. However, fields provided with excess irrigation and nitrogenous fertilizers also experience heavy incidence of the disease.
Management of Karnal Bunt Disease:
(i) Since the pathogen perennates in soil, crop rotation is considered as the possible means of control of this disease.
(ii) Seed treatment with either Brestanol 45W or Duter 20W at the rate of 0.25% before storage reduces pathogen inoculum by more than 95% and 85%, respectively, without any injury to treated seeds.
(iii) Munjal (1970, 71, 74) has advocated the use of Ceresan, New Improved Ceresan, Aureofungin or Vitavax sprays to find good control of disease.
(iv) It has been found in the mid-1980s that infection of wheat flowers can be prevented by a spray of either Mancozeb (0.2%) or Carbendazim (0.1%) at the early heading stage before flowering of the crop.
(v) Use of resistant varieties may prove most effective method for disease control. For instance, sonalika variety of wheat has not permitted any significant build-up of inoculum and proves resistant to this disease wherever it is grown. In varietal trials at IARI (New Delhi) varieties HD 1907, HP 743, HI 358, L 176, L 191, M 137-A, MW 59-4X 6A have shown resistance against the pathogen. UP 270, UP 368, HD 2222, 2227, 2235 have remained free from the disease under natural conditions of infection at Pantnagar.
Varieties which prove to be susceptible to N. indica should not be preferred. Some of such varieties are HD 2099, 1982, Arjun, WG 357, WG 377, WL 711, UP 319, and UP 362.
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