| Systematic spread of Karnal bunt (Neovossia indica
(Mitra) Mundkur) disease of wheat H.S. DHALIWAL, K.S. GILL, A.S. RANDHAWA and S.K. SHARMA Punjab Agricultural University, Regional Research Station, Gurdaspur, Punjab, India. Karnal bunt (Neovossia indica (Mitra) Mundkur) disease of wheat, identified as early as 1930 at Karnal in India, was mainly confined to northern India until 1960's. But now, it has spread to all the wheat growing states of India and a few other countries. The disease is not internally seed-borne. Its infection is reported to occur at the time of anthesis from the sickle-shaped primary sporidia produced from the soil borne chlamydospores. Low temperature and high humidity at the time of anthesis favour maximum disease development (BEDI et al., 1949). The infected grains are damaged to varying extent ranging from only a small black spot on the embryonic end to the entire grain being transformed into a bunt-ball. As a result of Karnal bunt disease the grain yield is reduced and the quality of wheat products is deteriorated. Inspite of its early identification and frequent epidemics in India, the mode of primary infection and further development of Karnal bunt has not been established on the firm footing. Infection has been reported to occur at the time of anthesis whereas maximum infection was obtained on artificial inoculation at the boot stage when there is no anthesis in the spike. It has been reported that the distribution of Karnal bunt infected grains in a spike is random and each floret gets infected by separate air borne sporidia at the time of its anthesis. The distribution of the Karnal bunt affected florets in the intact spikelets and spike under natural incidence has not been investigated so far. The distribution of Karnal bunt infected florets (grains) under natural incidence of disease in intact spikelets and spikes was studied in wheat variety WL 711 (highly susceptible to Karnal bunt) in 1981 and 1982. In each year 10 spikes with naturally infected grains were selected from the seed multiplication plots. In each spike the row with the lower most fertile spikelet was designated as I and the opposite row as II. The data on number of spikelets per spike, number of infected/total grains per spikelet in each row from botton to the tip of spike, number of primary infection sites and the percentage of spikelets infected per spike in 1981 and 1982 is given in Table 1 and 2 respectively. In each spike, the spikelets with maximum grain damage were assumed to be the primary infection sites (parenthesis). The natural incidence of Karnal bunt was higher in 1981 than in 1982. Similarly the number of primary infection sites per spike in 1981 varied from 1-3 whereas in 1982 all the spikes analysed had only one primary infection site. In both years upper half of spikes had higher incidence of Kamal bunt than the lower half. The primary infection sites also appeared to be slightly more frequent in the upper half than in the lower half. The primary infection appears to be more or less random as it can occur any where in the spike. Its higher frequency in the upper half of spike may be attributed to the higher number of florets and early anthesis in the upper half of spike. The upper half is also probably more exposed to air borne sporidia than the lower half. It is, however, not established at what stage the primary infection occurs as it has also been possible to get very high incidence of the disease on artificial inoculation at the boot stage (Aujla, pers. comm.). |
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