Ramakrishnan (1942) reported this leaf spot disease for the first time in Godavari and Malabar regions of India. Later on, the disease was reported from Sarawak (Anonymous, 1972). Sohi et al. (1964) have reported the disease in Himachal Pradesh, and it also occurs widely in Kerala state (Anonymous, 1974). Singh et al. (2000a) reported the disease from Chhatisgarh. This disease is now widespread in most ginger-growing countries.
Small, oval to elongated spots, measuring 1 to 10 mm X 0.5 to 4 mm appear on younger leaves. The spots have white papery centers and dark brown margins surrounded by yellowish halos (Ramakrishnan, 1942). The spots later increase in size and coalesce to form larger lesions (Figure 8.7A, B). The affected leaves become shredded and disfigured and may suffer extensive desiccation. As the plants put forth fresh leaves, they subsequently become infected. The crop attains a gray disheveled look as a result of infection (Sohi et al., 1964; Shukla and Haware, 1972).
Figure 8.7 (B) Leaf spots, enlarged view. The Pathogen
Leaf spot disease is caused by the fungus Phyllosticta zingiberi T.S. Ramakr. The fungus forms amphigenus, subglobose, dark brown, ostiolate pycnidia measuring 78 to 150 fxm in diameter on the host. On standard media, the fungus forms pycnidia with 100 to 270 ^m diameter bearing hyaline, unicellular, oblong, biguttulate spores measuring 3.7 to 7.4 X 1.2 to 2.5 (4.3 to 1.6) ^m (Ramakrishnan, 1942).
The disease begins to appear toward the end of June when the plants are at the most susceptible stage (three- to four-leaf stage) and have received high cumulative rainfall that is conducive for the disease spread. During this period, the temperature varies between 23.4 and 29.6°C and relative humidity is between 80 and 90 percent. Later in July, when the number of rainy days and total rainfall increase, the disease aggravates and spreads fast. As the number of rainy days decrease, disease spread also decreases (Brahma and Nambiar, 1984). Ginger plants up to the age of 6 to 7 months are susceptible to the disease and 2-week-old leaves are most susceptible.
The diseased leaves present in the debris of an infected field serve as a primary inoculum in the next season. In leaves, pycnidiospores and mycelia remain viable for 14 months under laboratory conditions (Brahma and Nambiar, 1982). Pycnidia survive in the leaf debris at the temperature range of 30 to 35°C. The pycnidiospores remain viable in soil even at 25 cm depth for 6 months. The optimum temperature range for mycelial growth of Phyllosticta is 25.0 to 27.5°C, with maximum and minimum being 32.5 and 10.0°C, respectively. At 5 and 35°C, complete inhibition of mycelial growth was observed (Cerezine et al., 1995).
The extent of dispersal of the causal fungus depends upon the intensity of precipitation. A higher intensity of rain accompanied by wind seems to exert a greater impact on leaves, as a result pycnidia are splashed on more leaves and to greater distances, resulting in liberation of a greater amount of spores and spreading the disease incidence (Brahma and Nambiar, 1984).
Sanitation and Shade: The destruction of diseased crop debris by burning is an important practice to reduce the primary inoculum of the disease. The disease incidence is much less under shade. At the Indian Institute of Spices Research, Calicut, India, the germplasm collection maintained under open conditions became infected, whereas when grown under shade net, the incidence of the disease was significantly less and the yield also increased significantly.
Chemical Control: The disease is controlled by one or two applications of Bordeaux mixture (Ramkrishnan, 1942). In Himachal Pradesh, Sohi et al. (1973) managed the disease by spraying Dithane Z-78 (0.2 percent ) six times at 2-week intervals. They have also recommended other fungicides: Flit 406(0.3 percent), Dithane M-22 (0.2 percent), or Bordeaux mixture (1 percent). Grech and Frean (1988) compared five fungicidal treatments and found that Benomyl (0.1 percent) + mancozeb (0.2 percent) + soluble boron (0.1 percent) and iprodione (0.2 percent) reduced the average number of lesions per leaf and increased the yield. In Brazil, Cerezine et al. (1995) found the highest reduction in the disease progress with the use of chlorothalonil. With dithionan, copper oxychloride, folpet, mancozeb, and captan, the area under disease progress curve (AUDPC) was on an average 15 to 19 lesions/leaf. One spray of Bavistin (0.15 percent) and two sprays of Dithane M-45 (0.25 percent) gave good protection against the disease and resulted in higher yield under a pot culture experiment (Verma and Vyas, 1981). Bavistin was observed to persist for a longer period on the ginger leaves. Captan and mancozeb at 1,000 mg/ml and triadimenol at 100 mg/ml inhibited mycelial growth of the fungus completely whereas; iprodione, thiophanate-methyl and chlorothalonil at 1,000 mg/ml inhibited the mycelial growth partially (Cerezine et al., 1995). Das and Senapati (1998) reported that captan (0.3 percent) gave the best control of disease followed by mancozeb (0.3 percent) + thiophanate methyl (0.01 percent).
Resistant Cultivars: Setty et al. (1995b) studied the reaction of 18 cultivars of ginger to P. zingiberi for 6 months under the coastal climate of Karnataka state (India). None of the cultivars tested was resistant to the disease. However, the cultivars Narasapatom, Tura, Nadia, Tetraploid, and Thingpuri were classed as moderately resistant with a disease index less than 5 percent. Other cultivars, namely, Rio de Janeiro, Kunduli Local, Waynad Local, Kurupampady, Suravi, and Karakal, were susceptible with a disease index of more than 10 percent. In Himachal Pradesh, none of the tested material of ginger was rated resistant to P. zingiberi; however, eight lines showed moderate resistance (Dohroo et al., 1986b). Germplasm collections SG 554, VIS 18, and RGS-5 were reported to be resistant to Phyllosticta leaf spot (Singh et al., 2000a).
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