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Septoria diseases of wheat
L. Gilchrist, H.J. Dubin


There are two major Septoria diseases in wheat. These are Septoria tritici blotch, incited by the fungus Septoria tritici (teleomorph: Mycophaerella graminicola), and Septoria nodorum blotch, caused by the fungus Septoria nodorum (teleomorph: Leptosphaeria nodorum). Both diseases cause serious yield losses reported to range from 31 to 53 percent (Eyal, 1981; Babadoost and Herbert, 1984; Polley and Thomas, 1991). Worldwide, more than 50 million ha of wheat, mainly growing in the high-rainfall areas, are affected. During the past 25 years, these diseases have been increasing and have become a major limiting factor to wheat production in certain areas. Under severe epidemics, the kernels of susceptible wheat cultivars are shrivelled and are not fit for milling. Epidemics of Septoria tritici blotch and Septoria nodorum blotch of wheat are associated with favourable weather conditions (frequent rains and moderate temperatures), specific cultural practices, availability of inoculum and the presence of susceptible wheat cultivars (Eyal et al., 1987).

The primary inoculum may arise from wind-blown infested crop debris, airborne ascospores, volunteer wheat, other susceptible grass species and seed in the case of S. nodorum. Infection may occur in crops grown in areas where wheat has not been cultivated for a number of years if infected seed is used. This clearly demonstrates the role of seed as one of the potential sources of primary inoculum in Septoria nodorum blotch.

First symptoms from S. tritici in susceptible wheat are expressed on leaves as irregular rectangular chlorotic lesions that usually appear five to six days after pycnidiospore penetration. The necrotic lesions appear sunken and greyish-green at first. Pycnidium formation can often be seen in a line following the stomatal pattern, usually after 15 days.

Septoria tritici pycnidiospores germinate on a suitable substrate when the plants are wet (Plate 33). Spores begin to germinate within 12 hours, and leaf penetration occurs after 24 hours. Moisture is required for all stages of infection: germination, penetration, development of the mycelium within the plant tissue and subsequent pycnidium formation (Browning, 1979; Hooker, 1957; Shaner and Finney, 1982). The pycnidia range in colour from light to dark brown. Pycnidiospore production may be related to cultivar response, with lower pycnidiospore production occurring on resistant cultivars (Plate 34, Plate 35) (Gough, 1978).

The splash dispersal mechanism, influenced by rain, limits distances to which pycnid-iospores can be spread. The usual vertical progress of Septorias from lower to upper leaves is affected by the distance between consecutive leaves. As a result, pycnidia often appear earlier on upper plant parts of dwarf cultivars than they do on leaves of taller cultivars (Eyal et al., 1987). Thus both resistance and plant architecture influence disease spread and resulting severity. Under severe epidemics, the differences in plant architecture and stature of susceptible cultivars are of no importance with respect to disease spread (Plate 36). In moderate to light epidemics, however, upper plant parts of dwarf cultivars are more infected than in taller wheats since they are nearer to inoculum sources (Eyal, 1971).

Septoria nodorum blotch lesions are often lens-shaped with a yellow-green border surrounding the dead tissue area (Plate 37). Pycnidia may or may not appear within the centre of the lesion, but are more common on nodes and stems, leaf sheaths and glumes (Plate 38). Pycnidium distribution is random and does not follow the stomatal pattern distribution in line as does Septoria tritici blotch. Whenever nodes are infected, it may cause distortion and bending of the straw with a possibility of lodging and breakage of the straw at the node with subsequent losses in yield.

The mycelium of S. nodorum can also be seed-borne and can cause seedling infection. Brown lesions occur on coleoptiles of wheat seedlings grown from infected seed (Machacek, 1945).

Pycnidiospore germination and penetration are greatest between 15° and 25°C, with a minimum of six hours of wetness necessary for good infection (Plate 39) (Sharen and Krupinsky, 1970). The period from penetration to the production of mature pycnidia is as short as six days when the temperature is 22°C and in a water-saturated atmosphere (Tomerlin, 1985). The pycnidiospores are spread by splashing or wind-blown rain (Plate 40). Septoria nodorum pycnidiospores are mostly dispersed over short distances within crops causing localized disease spread. Wind greatly increases the dispersal of smaller droplets and spores in the downwind direction (Brennan et al., 1985a, 1985b).

Tall cultivars often show lower levels of infection with S. nodorum than short ones. The dispersal of S. nodorum from the base to the top of the plant is less when the distance to be travelled is greater (Scott et al., 1985).

Septorias have been controlled as part of an integrated crop management system using resistant cultivars, cultural practices and chemical control. Wheat cultivars reported to be resistant in one country may sometimes succumb to attack by Septoria populations in another country. The composition of virulence within a population may be affected by the presence of the sexual state, gene flow, selection pressure exerted by the host (cultivar, species), the interaction between isolates, cultural practices and the environment (Eyal, 1995).

The variation in virulence among S. tritici isolates from diverse geographic sources as elucidated by Eyal et al. (1985) and Silfhout et al. (1989) suggests a broad spectrum of virulence with a certain association with geography and wheat management practices, durum versus bread wheat and germplasm that can serve as wheat differentials or as sources for breeding resistance (Eyal, 1995).

In many countries, durum wheats and triticales have a higher resistance to S. tritici than spring bread wheats. However, in Tunisia several bread wheat lines and cultivars were highly resistant to S. tritici whereas very few durum wheat cultivars showed good resistance (Djerbi et al., 1976).

Resistances to S. tritici and S. nodorum appear to be more widely distributed among bread wheat cultivars with winter growth habit than among those with spring growth habit. Resistance has also been reported in several wild relatives of wheat (Brokenshire, 1975; William and Jones, 1973; Wilson, 1985).

Dominant, partially dominant, recessive and additive gene actions were found to condition resistance to both S. tritici and S. nodorum (Nelson, 1980; Nelson and Gates, 1982; Saari and Wilcoxson, 1974; Rosielle and Brown, 1979; Rufty et al., 1981; Wilson 1985). Polygenically inherited resistance and additive gene action seem to be of greater importance (Camacho-Casas, 1989).

Strong efforts to identify and incorporate sources of resistance to develop resistant cultivars have been pursued (Rajaram and Dubin, 1977; Mann et al., 1985; Eyal et al., 1985). New sources of resistance have been identified and incorporated in adapted wheat cultivars (van Ginkel and Rajaram, 1989; Gilchrist, 1994).

Wild relatives of wheat may also provide resistance genes against these diseases. Alien species have further provided valuable diversity, and many resistance genes found in wheat cultivars have been transferred from other wheatBread wheat: improvement and production275275 species and genera of the Triticeae (Sharma and Gill, 1983; Cox et al., 1992) and through intergeneric and/or interspecific hybridization (Mujeeb-Kazi et al., 1996; Gilchrist and Mujeeb-Kazi, 1996).

Soil management practices that leave large amounts of wheat stubble and debris on the soil surface increase the chance of Septoria epidemics under favourable climatic conditions. Cultural practices that reduce wheat residue through ploughing, removal for feeding and crop rotation help remove the major source of primary inoculum. A combination of these practices and seed chemical treatment need to be considered, especially for S. nodorum.

Chemical control has been used to obtain high yields with susceptible cultivars. Prior to applying chemicals, wheat growers and/or researchers must decide whether to resort to chemical control of a specific wheat field. The considerations are as follows (Eyal et al., 1987):

The most important group of systemic fungicides for controlling S. tritici are: benomyl, prochloraz, propiconazole and triadimefon (Diaz de Ackermann, 1995). Triticonazole can be applied as a seed dressing to give protection in areas where seedling stage is affected (Mugnier et al., 1993).

REFERENCES

Babadoost, M. & Herbert, T.T. 1984. Factors affecting infection of wheat seedlings by Septoria nodorum. Phytopathology, 74: 592-595.

Brennan, R.M., Fitt, B.D.L., Taylor, G.S. & Colhoun, J. 1985a. Dispersal of Septoria nodorum pycnidiospores by simulated rain and wind. Phytopathol. Z., 112: 291-297.

Brennan, R.M., Fitt, B.D.L., Taylor, G.S. & Colhoun, J. 1985b. Dispersal of Septoria nodorum pycnidiospores by simulated raindrop in still air. Phytopathol. Z., 112: 281-290.

Brokenshire, T. 1975. The role of graminaceus species in the epidemiology of Septoria tritici on wheat. Plant Pathol., 24: 33-38.

Browning, J.A. 1979. Genetic protective mechanism of plant pathogen populations: their coevolution and use in breeding for resistance. In M.K. Harris, ed. Biology and breeding for resistance. Texas Publ. MP-1451, p. 52-57. Texas, USA, Texas A&M University Press, College Station. 605 pp.

Camacho-Casas, M.A. 1989. Inheritance of Septoria Leaf Blotch and the possible influence of heading date and plant height on the disease expression in a winter wheat cross. Ph.D. thesis. Oregon, USA, Oregon State University.

Cox, T.S., Raupp, W.J., Wilson, D.L., Gill, B.S., Leath, S., Bockus, W.W. & Browder, L.E. 1992. Resistance to foliar diseases in a collection of Tritici tauschii germplasm. Plant Dis., 76: 1061-1064.

Diaz de Ackermann, M. 1995. Chemical control of Septoria tritici on spring wheat. In L. Gilchrist, M. van Ginkel, A. McNab & G.H.J. Kema, eds. Proc. Septoria tritici Workshop. Mexico, DF, CIMMYT.

Djerbi, A., Ghodbane, A. Daaloul, A. & Varughese, G. 1976. Studies on the Septoria leaf blotch disease of wheat: search for resistant germplasm to Septoria tritici. Rob. and Desm. Poljopr. Znan. Smotra, 39: 137-142.

Eyal, Z. 1971. The kinetics of pycnidiospore liberation in Septoria tritici. Can. J. Bot., 49: 1095-1099.

Eyal, Z.E. 1981. Integrated control of Septoria diseases of wheat. Plant Dis., 65: 763-768.

Eyal, Z. 1995. Virulence in Septoria tritici, causal agent of Septoria tritici blotch of wheat. In L. Gilchrist, M. van Ginkel, A. McNab & G.H.J. Kema, eds. Proc. Septoria tritici Workshop. Mexico, DF, CIMMYT.

Eyal, Z.E., Sharen, A.L., Huffman, M.D. & Prescott, J.M. 1985. Global insight into virulence frequencies of Mycosphaerella graminicola. Phytopathology, 75: 1456-1462.

Eyal, Z., Sharen, A.L., Prescott, J.M. & van Ginkel, M. 1987. The Septoria diseases of wheat: concepts and methods of disease management. Mexico, DF, CIMMYT.

Gilchrist, L.I. 1994. New Septoria tritici resistance sources in CIMMYT germplasm and its incorporation in the Septoria Monitoring Nursery. In Proc. 4th Int. Workshop on: Septoria of Cereals. 4-7 July. Radzikov, Poland, IHAR.

Gilchrist, L.I. & Mujeeb-Kazi. 1996. Septoria tritici leaf blotch resistant germplasm derived from bread wheat/D genome synthetic hexaploids. In ASA Conference, Indianapolis, IN, USA.

Gough, F.G. 1978. Effect of wheat host cultivars on pycnidiospore production by Septoria tritici. Phytopathology, 68: 1343-1345.

Hooker, A.L. 1957. Methods of inoculation and determining varietal reactions in the Septoria disease of oats. Plant Dis. Rep., 41: 592-597.

Machacek, J.E. 1945. The prevalence of Septoria on cereal seed in Canada. Phytopathology, 35: 51-53.

Mann, C.E., Rajaram, S. & Villareal, R.L. 1985. Progress in breeding for Septoria tritici resistance in semidwarf wheat at CIMMYT. In A.L. Scharen, ed. Septoria of Cereals. Proc. Workshop, Bozeman, MT, USA, 2-4 Aug. 1983, p. 22-26. USDA-ARS Pub. No. 12. 116 pp.

Mugnier, J., Klittich, C., Glouot, J.M., Vea, E., Hutt, J. & Greiner, A. 1993. Triticonazole a new seed treatment fungicide for cereals. Rhone-Poulec Agro, Lyon, France and Rhone-Poulenc Ag. Co., Research Triangle Park, NC, USA, Abstract (089): 3.7.1993. In 6th Int. Cong. Plant Pathology, Montreal, Canada, p. 92.

Mujeeb-Kazi, Rosas, A.V. & Roldan, S. 1996. Conservation of the genetic variation of Triticum tauschii (Coss)Schmalh (Aegilop squarrosa auct. non L.) in synthetic hexaploid wheats (T. turgidum L.s.lat. x T. Tauschii; 2n=6x=42, AABB-DD) and its potential utilisation for wheat improvement. Genet. Res. Crop Evol., 43: 129-134.

Nelson, L.R. 1980. Inheritance of resistance to Septoria nodorum in wheat. Crop Sci., 20: 447-449.

Nelson, L.R. & Gates, C.E. 1982. Genetics of host plants resistance of wheat to Septoria nodorum. Crop Sci., 27: 771-773.

Polley, R.W. & Thomas, M.R. 1991. Surveys of disease of wheat in England and Wales, 1976-1988. Ann. Appl. Biol., 119: 1-20.

Rajaram, S. & Dubin, H.J. 1977. Avoiding genetic vulnerability in semi-dwarf wheats. Ann. N.Y. Acad. Sci., 287: 243-254.

Rosielle, A.A. & Brown, A.G.P. 1979. Inheritance, heritability and breeding behaviour of resistance to Septoria tritici in wheat. Euphytica, 21: 152-161.

Rufty, R.C., Herbert, T.S. & Murphy, C.F. 1981. Evaluation of resistance to Septoria nodorum in wheat. Plant Dis., 65: 406-409.

Saari, E.E. & Wilcoxson, R.D. 1974. Plant disease situation of high-yielding dwarf wheats in Asia and Africa. Ann. Rev. Phytopath., 12: 49-68.

Scott, P.R., Benedikz, P.W., Jones, H.G. & Ford, M.A. 1985. Some effects of canopy structure and microclimate on infection of tall and short wheat by Septoria nodorum. Plant Pathol., 34: 578-593.

Shaner, A.L. & Krupinsky, J.M. 1970. Cultural and inoculation studies of Septoria nodorum, caused of glume blotch of wheat. Phytopathology, 60: 1480-1485.

Sharen, A.L. & Krupinsky, J.M. 1970. Cultural and inoculation studies of Septoria nodorum, cause of glume blotch of wheat. Phytopathology, 60: 1480-1485.

Sharma, H.C. & Gill, B.S. 1983. Current status of wide hybridization in wheat. Euphytica, 32: 17-31.

Silfhout, C.H., van Arama, P.F. & Kema, G.H.J. 1989. International survey of factors of virulence of Septoria tritici. In P.M. Fried, ed. Septoria of Cereals. Proc. 3rd Int. Workshop, p. 36-38. Zurich, Switzerland.

Tomerlin, J.R. 1985. Preliminary studies on the effect of interrupted wet periods on infection of wheat by Septoria nodorum. In A.L. Scharen, ed. Septoria of Cereals. Proc. Workshop, Bozeman, MT, USA, 2-4 Aug. 1983, p. 68-69. USDA-ARS Pub. No. 12. 116 pp.

van Ginkel, M. & Rajaram, S. 1989. Breeding for global resistance to Septoria tritici in wheat. In P.M. Fried ed. Septoria of Cereals, p. 174-176. Zurich, Switzerland.

William, J.R. & Jones, D.G. 1973. Infection of grasses by Septoria nodorum and S. Tritici. Trans. Br. Mycol. Soc., 60: 355-358.

Wilson, R.E. 1985. Inheritance of resistance to Septoria tritici in wheat. In A.L. Scharen, ed. Septoria of Cereals. Proc. Workshop, Bozeman, MT, USA, 2-4 Aug. 1983, p. 33-35. USDA-ARS Pub. No. 12. 116 pp.


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