Powdery mildew, caused by the fungus Blumeria graminis (DC) E.O. Speer f. sp. tritici Em. Marchal (syn. Erysiphe graminis DC f. sp. tritici Marchal), is one of the most important foliar diseases of wheat worldwide. It is an obligate parasite, growing only on living tissue. Spores of the fungus germinate on the leaf surface and invade the plant. The fungus then colonizes the epidermis of the leaf by obtaining nutrients from the plant cells without killing them. A vast literature exists on powdery mildew of wheat and other cereals. This chapter presents an overview of the disease and its management, with emphasis on recent literature.
Symptoms and signs
Powdery mildew produces white to grey, cottony fungal growth mostly on the upper leaf surface, although some pustules may develop on the underside of the leaf (Daamen, 1989; Wiese, 1987). Pustules begin as small white circular patches of fungal mycelium often surrounded by chlorosis, most visible on the underside of the leaf. 'Green islands' appear near infected areas as the plant transports nutrients to non-diseased cells (Schafer, 1987). Pustules often join together to form large masses of fungal growth on the upper surface of leaves when conditions are favourable (Plate 46, Plate 47). As the diseased area expands, tissue around older pustules dies and turns brown. Severely diseased leaves collapse and die. Powdery mildew is most prevalent on lower leaves but can cause blighting of the upper leaves, heads and awns of susceptible cultivars. Within a few days after they appear, the white powdery pustules produce large quantities of small asexually produced conidia (also called oidia) in long chains, which are easily dislodged by wind or rain. These spores are single-celled, oval (8 to 35 µm) and colourless. As lesions age, the mycelium becomes more dense and turns grey (Wiese, 1987). Dark round cleistothecia (135 to 280 µm in diameter) develop in the fungal mass as the pustules get older. Ascospores develop in the cleistothecia and serve as the long-term survival structures. Cleistothecia may be empty if examined when wheat is harvested because ascospores often do not mature for several months.
Powdery mildew occurs almost everywhere wheat is grown. It is important economically under humid rainfed conditions and in dryland areas when irrigation is used for production of improved cultivars with high yield potential. Powdery mildew has increased in importance in some regions because of increased application of nitrogen fertilizer, which favours the disease. The disease is important in regions where rain occurs early in the season and where temperatures are relatively cool, such as regions with maritime climates, and in cooler regions with a humid continental climate (Bennett, 1984). Powdery mildew is important in the cooler regions of China, Japan and other areas in Asia, in North and East Africa, in northern Europe and eastern North America (Roelfs, 1977; Saari and Wilcoxson, 1974). It is also important in warmer, humid regions with mild winters where wheat is planted in the autumn, such as parts of the Southern Cone of South America and the southeastern United States. In regions or seasons in which rain is frequent and heavy, the occurrence of powdery mildew may be very low because spores are washed from the leaves or they burst in water (Merchan and Kranz, 1986).
Powdery mildew typically begins rapid growth on the lower leaves and sheaths when plants begin to joint. It is usually the first leaf disease of the season because it is favoured by temperatures between 10 and 22°C. Infection and disease development decline after flowering when temperatures increase above 25°C. Conidia are the primary inoculum source for dissemination of the fungus. They are easily dislodged from lesions by wind and rain. Production of conidia is optimal at 20°C and declines rapidly above and below that temperature (Ward and Manners, 1974). Although conidia only survive for several days, they are capable of disseminating the fungus long distances. New pustules with conidia are produced every seven to ten days at optimal conditions and provide repeating cycles of spores. Conidia germinate most rapidly at 97 to 100 percent relative humidity, but their high water content allows them to germinate when humidity declines below 50 percent. However, germ tube growth and appressorium production are greatly reduced below 92 percent relative humidity (Friedrich and Boyle, 1993). Frequent light rain removes conidia from leaves and thus reduces the number of new colonies that form. Periods of heavy rain slow the development of established pustules (Merchan and Kranz, 1986). Conidia do not germinate in free moisture, which can cause them to burst. After crop maturity, ascospores in cleistothecia serve as survival structures, but their role in initiating disease is much less important than that of the conidia in most environments. Conidia produced on grasses and volunteer wheat also maintain inoculum until wheat is planted. In autumn-sown wheat, infections that do not result in visible symptoms can maintain the fungus in leaves through the winter (Frank and Ayers, 1986).
Early season powdery mildew stimulates production of tillers, which later in the season fail to produce seed. These non-productive tillers reduce food reserves and grain yield. Therefore, a low level of disease in susceptible cultivars can still reduce yield (Bowen et al., 1991; Everts and Leath, 1992). Reduction in yield was best related to disease severity at Feekes stage 10 (boot stage) (Large, 1954). At Feekes 9 (flag leaf expanded), ratings of the F-1 to F-3 leaves were most useful for prediction of yield. Because powdery mildew infects plants early in the season, application of a fungicide at Feekes 9 or earlier is important if disease is increasing rapidly (Royse et al., 1980). Yield reduction may be as high as 40 percent. Yield reduction is related to reduction of grain size and number per unit area, although which components are affected may be influenced by the wheat genotype (Bowen et al., 1991; Dickson, 1956; Royse et al., 1980). Powdery mildew decreased flour protein but did not affect milling and baking quality of soft red wheat used for general purpose and pastry flour (Johnson et al., 1979).
Assessment scales are used for two distinct purposes: to assess resistance of a wheat genotype and to predict disease severity and potential yield reduction. Moseman et al. (1984) described a 0 to 9 scale to categorize resistant and susceptible infection types. This scale was modified by Niewoehner and Leath (1998). Several methods are available to estimate powdery mildew severity in the greenhouse and field. These methods can be used for assessment of susceptibility or to predict disease severity. The rating system used depends upon the objectives of the user. Powdery mildew was rated using a 0 to 9 scale in which 0 = no disease and 9 = more than 90 percent of plant tissue diseased (Bennett and Westcott, 1982). Ratings on this scale can be made using standard area diagrams to assess disease severity (James, 1971a, 1971b). Ratings can be made on whole plots, whole plants, or on individual leaves of single tillers depending on the stage of plant growth (Daamen, 1989; Shaner and Finney, 1977). Counts of the number of mildew pustules on individual leaves can be made for accurate assessment, but this method is laborious (Daamen, 1986). Lipps and Madden (1989a) found that several methods of rating two or three leaves on individual tillers for percent disease severity or using a 0 to 10 rating scale were highly correlated with grain yield depending on growth stage. The most consistent correlations with yield were when assessments were made at Feekes 10.3 (50 percent heading). In field experiments, at least ten tillers per plot need to be evaluated for reliable estimates. Assessments to make decisions about application of a foliar fungicide need to be made prior to heading.
Cropping practices can have a significant effect on development and severity of powdery mildew. High seeding rate, high nitrogen fertility and semidwarf growth habit can increase severity of powdery mildew (Last, 1954; Tompkins et al., 1992). High nitrogen increases plant height and tillering, which reduces culm strength. This leads to increased lodging and prolonged leaf wetness favourable for infection (Shaner and Finney, 1977). Residual nitrogen from a previous crop to which high rates of nitrogen were applied and legume crops, which produce nitrogen, resulted in higher severity of powdery mildew in a following wheat crop (Parmentier and Rixhon, 1973). Variation in row spacing has been reported both to increase and decrease disease. Prolonged survival of debris-borne inoculum in reduced tillage systems has little effect on powdery mildew because most inoculum is windborne. However, volunteer wheat in reduced tillage systems can serve as an inoculum source.
Powdery mildew can develop at any growth stage. In areas where winter wheat is grown, early planting and above-average autumn temperatures favour infection although symptoms may not be readily visible. These autumn infections can contribute to yield reduction (Frank et al., 1988). Planting toward the latter part of the recommended planting period for the region can reduce early infection.
The use of cultivar mixtures to slow an epidemic of powdery mildew has been studied most intensely in winter barley (Wolfe, 1984). The anticipated benefits are to slow the rate of the epidemic to reduce or eliminate the need for foliar fungicide and thereby reduce the development of fungicide resistance in the pathogen. Deployment of a larger number of resistance genes also aims to diversify the population of B. Graminis f. sp. tritici. Mixtures of cultivars that carry several different resistance genes slowed the progress of a powdery mildew epidemic in both spring and winter wheat and improved yield by about 5 percent (Stuke and Fehrmann, 1988). Although shown to be beneficial in several wheat-pathogen systems, cultivar mixtures have been used only on a limited scale. Cultivar maturities in the mixture must be similar and the end use must be considered, especially if the crop is to be sold through typical grain marketing channels.
Genetic resistance has been the primary means to manage powdery mildew. Only a brief summary of mechanisms of resistance and the genes that are used will be presented here. Bennett (1984) and Ecker and Lein (1994) have reviewed the use of several important resistance genes and their deployment in Western Europe and North America. Genes for resistance have been identified in at least 30 loci in wheat (Järve et al., 2000; Liu et al., 2001; McIntosh et al., 1998, 2000, 2001; Peusha et al., 2000; Shi et al., 1998; Rong et al., 2000). These genes often act only against specific races of the pathogen causing a hypersensitive resistance reaction in the wheat plant. A major concern is that only a few genes have been used widely in cultivar development. Resistance may be lost when new strains of the fungus develop. For example, Persaud et al. (1994) found increased virulence toward Pm17, a widely used gene from Amigo wheat (Heun et al., 1990; Lowry et al., 1984). However, the genetics of B. Graminis f. sp. tritici is complex. Higher frequencies of virulence were also found in the powdery mildew population due to Pm genes not known to be widely deployed (Niewoehner and Leath, 1998).
Resistance to powdery mildew is also accomplished by a combination of factors that slow the rate of disease progress so that plants mature before significant damage occurs. This is known as slow-mildewing or partial resistance and is race-nonspecific. Plants are susceptible as seedlings but are less susceptible in the adult stage so that this is a form of adult plant resistance. Several genes usually control partial resistance. Griffey and Das (1994) found that as few as two or three genes provided long-lasting adult plant resistance in two wheat cultivars. The factors that contribute to partial resistance include an increase in the time from infection until new spores are produced (latent period), reduced size of pustules and reduced production of spores. The infection frequency, the number of spores that successfully infect the plant, may also be reduced (Shaner, 1973). The slow rate of disease development can be quantified by calculating the area under the disease progress curve (AUDPC) based on three or more disease severity ratings during the season. AUDPC is useful to compare cultivars for differences in powdery mildew resistance (Shaner and Finney, 1977; Hautea et al., 1987). Recently, it has become possible to use molecular techniques to find quantitative trait loci (QTL) for powdery mildew resistance on gene maps to identify quantitative disease resistance (Chantret et al., 2000; Keller et al., 1999). The ability to use molecular markers associated with QTL holds promise for more rapid development of cultivars with partial resistance to powdery mildew.
Genes for avirulence in the fungus may be expressed differently depending on the host genotype. An isolate of B. Graminis f. sp. tritici may grow rapidly on one genotype but much more slowly on another genotype, so that the response of the host-parasite interaction is a partial resistance (Martin and Ellingboe, 1976).
Wild relatives of wheat have been exploited as sources of new resistance genes (Bennett, 1984). Wild emmer, Triticum turgidum var. dicoccoides, is a source of genes, some of which are expressed in both seedling and adult plants and some of which are expressed only in adult plants. Some wild emmers also possess genes for partial resistance (Silfhout and Gerechter-Amitai, 1988; Moseman et al., 1984). Triticum timopheevii var. araraticum collected in the Middle East has a gene for resistance that differs from Pm6 from cultivated T. timopheevii (Brown-Guedira et al., 1996). Genes from rye (Secale cereale), including Pm8 and Pm17, have been used widely in wheat cultivars. New genes from rye can be transferred to wheat the by use of wheat-rye translocation lines (Heun and Friebe, 1990; Merker and Forsstrom, 2000).
Regional surveys are needed to determine which virulences are present so that breeding strategies can be planned to use the most effective genes. The cultivar Chancellor and its isogenic lines containing individual Pm genes are useful to determine virulence in B. Graminis f. sp. tritici (Briggle, 1969). Recent surveys for virulence genes and identification of resistance genes in soft red wheat in the United States include procedures for inoculation and evaluation of disease reactions (Niewoehner and Leath, 1998; Persaud et al., 1994; Persaud and Lipps, 1995).
Application of foliar fungicides has traditionally been the only means of chemical control for powdery mildew. Seed-applied systemic fungicides are now available that control early season development of the disease. These are especially effective for winter wheat. Triadimenol seed treatment prevented excess tillering caused by mildew infection early in the season and contributed to a higher grain yield, especially when high temperatures during grainfilling reduced the amount of disease later in the season (Everts and Leath, 1992; Frank and Ayers, 1986; Leath and Bowen, 1989). Difenoconazole also has systemic activity against powdery mildew. These fungicides have a wide spectrum of activity and may be economical seed treatments when they also contribute to reduction of smuts and other foliar pathogens.
Foliar fungicides are effective but should only be applied if the cultivar is susceptible and an economic return is likely (Leath and Bowen, 1989). Pustules may develop on lower leaves early in the season on resistant cultivars but not on upper leaves later in the season. Avoid applying fungicides too early to be effective during the grainfilling period. When powdery mildew was moderate prior to flowering, early season applications of the systemic fungicide triadimefon at Feekes 6 to 8, maintained yield at 8 to 17 percent above the control (Lipps and Madden, 1989b). Comparisons must be made over several years to determine whether or not the cost of fungicide application is economical.
Fungicide insensitivity is a concern where fungicides are used intensively, such as in Western Europe. Reduced effectiveness of the triazole fungicides triadimefon and propiconazole was found in the Netherlands following intensive use (De Waard et al., 1986). More than 570 isolates of B. graminis f. sp. tritici collected throughout the eastern and southern United States, where fungicide use is much less, were sensitive to triadimenol (Niewoehner and Leath, 1998). Fungicides in the strobilurin group, such as azoxystrobin, with modes of action different from the triazoles, are currently being deployed for use against powdery mildew.
An integrated disease management system should be used with genetic resistance as the cornerstone of the programme. Cultural management, including proper management of nitrogen fertilization, is essential to minimize risk of crop damage from powdery mildew. Fungicides should be used in conjunction with a disease monitoring system employed from planting through the flowering stage of growth to estimate economic return.
Bennett, F.G.A. 1984. Resistance to powdery mildew in wheat: a review of its use in agriculture and breeding programmes. Plant Pathol., 33: 279-300.
Bennett, F.G.A. & Westcott, B. 1982. Field assessment of resistance to powdery mildew in mature wheat plants. Plant Pathol., 31: 261-268.
Bowen, K.L., Everts, K.L. & Leath, S. 1991. Reduction in yield of winter wheat in North Carolina due to powdery mildew and leaf rust. Phytopathology, 81: 503-511.
Briggle, L.W. 1969. Near-isogenic lines of wheat with genes for resistance to Erysiphe graminis f. sp. tritici. Crop Sci., 9: 70-72.
Brown-Guedira, G.L., Gill, B.S., Bockus, W.W., Cox, T.S., Hatchett, J.H., Leath, S., Peterson, C.J., Thomas, J.B. & Zwer, P.K. 1996. Evaluation of a collection of wild timopheevii wheat for resistance to disease and arthropod pests. Plant Dis., 80: 928-933.
Chantret, N., Sourdille, P., Roder, M., Tavaud, M., Bernard, M. & Doussinault, G. 2000. Location and mapping of the powdery mildew resistance gene MIRE and detection of a resistance QTL by bulked segregant analysis (BSA) with microsatellites in wheat. Theor. Appl. Genet., 100: 1217-1224.
Daamen, R.A. 1986. Measures of disease intensity in powdery mildew (Erysiphe graminis) of winter wheat. 1. Errors in estimating pustule number. Neth. J. Pl. Pathol., 92: 197-206.
Daamen, R.A. 1989. Assessment of the profile of powdery mildew and its damage function at low disease intensities in field experiments with winter wheat. Neth. J. Pl. Pathol., 95: 85-105.
De Waard, M.A., Kipp, E.M.C., Horn, N.M. & van Nistelrooy, J.G.M. 1986. Variation in sensitivity to fungicides which inhibit ergosterol biosynthesis in wheat powdery mildew. Neth. J. Plant Pathol., 92: 21-32.
Dickson, J.G. 1956. Diseases of field crops, 2nd ed. New York, NY, USA, McGraw Hill Book Company.
Ecker, U. & Lein, K.A. 1994. Use and significance of resistance genes against powdery mildew (Erysiphe graminis) in German wheat varieties in the years 1980 to 1993. Pflanzenschutz-Nach., 47: 91-128.
Everts, K.L. & Leath, S. 1992. Effect of early season powdery mildew on development, survival, and yield contribution of tillers of winter wheat. Phytopathology, 82: 1273-1278.
Frank, J.A. & Ayers, J.E. 1986. Effect of triadimenol seed treatment on powdery mildew epidemics on winter wheat. Phytopathology, 76: 254-257.
Frank, J.A., Cole, H., Jr. & Hatley, O.E. 1988. The effect of planting date on fall infections and epidemics of powdery mildew on winter wheat. Plant Dis., 72: 661-664.
Friedrich, S. & Boyle, C. 1993. Wirkung unterschiedlicher Luftfeuchten auf die Production und Keimung der Konidien von Erysiphe graminis f. sp. tritici in vitro. J. Plant Dis. Prot., 100: 180-188.
Griffey, C.A. & Das, M.K. 1994. Inheritance of adult-plant resistance to powdery mildew in Knox 62 and Massey winter wheats. Crop Sci., 34: 641-646.
Hautea, R.A., Coffman, W.R., Sorrels, M.E. & Bergstrom, G.C. 1987. Inheritance of partial resistance to powdery mildew in spring wheat. Theor. Appl. Genet., 73: 609-615.
Heun, M. & Friebe, B. 1990. Introgression of powdery mildew resistance from rye to wheat. Phytopathology, 80: 242-245.
Heun, M., Friebe, B. & Bushuk, W. 1990. Chromosomal location of the powdery mildew resistance gene of Amigo wheat. Phytopathology, 80: 1129-1133.
James, W.C. 1971a. An illustrated series of assessment keys for plant diseases, their preparation and usage. Can. Plant Dis. Surv., 51: 39-65.
James, W.C. 1971b. A manual of assessment keys for plant diseases. St Paul, MN, USA, APS Press.
Järve, K., Peusha, H.O., Tsymbalova, J., Tamm, S., Devos, K.M. & Enno, T.M. 2000. Chromosome location of a T. timopheevii-derived powdery mildew resistance gene transformed to common wheat. Genome, 43: 377-381.
Johnson, J.W., Bäenziger, P.S., Yamazaki, W.T. & Smith, R.T. 1979. Effects of powdery mildew on yield and quality of isogenic lines of 'Chancellor' wheat. Crop Sci., 19: 349-352.
Keller, M., Keller, B., Schachermayr, G., Winzeler, M., Schmid, J.E., Stamp, P. & Messmer, M.M. 1999. Quantitative trait loci for resistance against powdery mildew in a segregating wheat x spelt population. Theor. Appl. Genet., 98: 903-912.
Large, E.C. 1954. Growth stages in cereals: illustration of the Feekes scale. Plant Pathol., 3: 128-129.
Last, F.T. 1954. The effect of time of application of nitrogenous fertiliser on powdery mildew on winter wheat. Ann. Appl. Biol., 41: 381-392.
Leath, S. & Bowen, K.L. 1989. Effects of powdery mildew, triadimenol seed treatment, and triadimefon foliar sprays on yield of winter wheat in North Carolina. Phytopathology, 79: 152-155.
Lipps, P.E. & Madden, L.V. 1989a. Assessment of methods of determining powdery mildew severity in relation to grain yield of winter wheat cultivars in Ohio. Phytopathology, 79: 462-470.
Lipps, P.E. & Madden, L.V. 1989b. Effect of fungicide application timing on control of powdery mildew and grain yield of winter wheat. Plant Dis., 73: 991-994.
Liu, Z.Y., Sun, Q.X., Ni, Z.F., Nevo, E. & Yang, T.M. 2001. Molecular characterization of a novel powdery mildew resistance gene Pm30 in wheat originating from wild emmer. Euphytica, 121: (In press).
Lowry, J.R., Sammons, D.J., Bäenziger, P.S. & Moseman, J.G. 1984. Identification and characterisation of the gene conditioning powdery mildew resistance in 'Amigo' wheat. Crop Sci., 24: 129-132.
Martin, T.J. & Ellingboe, A. H. 1976. Differences between compatible parasite/host genotypes involving the Pm4 locus of wheat and the corresponding genes in Erysiphe graminis f.sp. tritici. Phytopathology, 66: 1435-1438.
McIntosh, R.A., Hart, G.C., Demos, K.L., Gale, M.D. & Rogers, W.W. 1998. Catalogue of gene symbols for wheat. In A.E. Slinkard, ed. Proc. 9th Int. Wheat Genetics Symp., Saskatoon, Saskatchewan, Canada, 2-7 Aug., vol. 5, p. 123-127. Saskatoon, Canada, University of Saskatchewan Extension Press. 235 pp.
McIntosh, R.A., Devos, K.M., Dubcovsky, J. & Rogers, W.J. 2000. Catalogue of gene symbols for wheat: 2000 supplement. p. 25-27. http:// wheat.pw.usda.gov/ggpages/wgc/2000Supplement/2000upd.html.
McIntosh, R.A., Devos, K.M., Dubcovsky, J. & Rogers, W.J. 2001. Catalogue of gene symbols for wheat: 2001 supplement. p. 15. http:// wheat.pw.usda.gov/ggpages/wgc/2001upd.html.
Merchan, V.M. & Kranz, J. 1986. Die Wirkung des Regens auf die Entwicklung des Weizenmehltaus (Erysiphe graminis DC. f. sp. tritici Marchal). J. Plant Dis. Prot., 93: 262-270.
Merker, A. & Forsstrom, P. 2000. Isolation of mildew resistant wheat-rye translocation lines from a double substitution line. Euphytica, 115: 167-172.
Moseman, J.G., Nevo, E., El Morshidy, M.A. & Zohary, D. 1984. Resistance of Triticum dicoccoides to infection with Erysiphe graminis tritici. Euphytica, 33: 41-47.
Niewoehner, A.S. & Leath, S. 1998. Virulence of Blumeria graminis f. sp. tritici on winter wheat in the eastern United States. Plant Dis., 82: 64-68.
Parmentier, G. & Rixhon, L. 1973. Influence des précédents culturaux sur l'infection öidienne du froment d'hiver. Parasitica, 29: 129-133.
Persaud, R.R. & Lipps, P.E. 1995. Virulence genes and virulence gene frequencies of Blumeria graminis f. sp. tritici in Ohio. Plant Dis., 79: 494-499.
Persaud, R.R., Lipps, P.E. & Campbell, K.G. 1994. Identification of powdery mildew resistance genes in soft red winter wheat cultivars and Ohio breeding lines. Plant Dis., 78: 1072-1075.
Peusha, H., Enno, T. & Prüliin, O. 2000. Chromosomal location of powdery mildew resistance genes and cytogenetic analysis of meiosis in common wheat cultivar Meri. Hereditas, 132: 29-34.
Roelfs, A.P. 1977. Foliar fungal diseases of wheat in the People's Republic of China. Plant Dis. Rep., 61: 836-841.
Rong, J.K., Millet, E., Manisterski, J. & Feldman, M. 2000. A new powdery mildew resistance gene: Introgression from wild emmer into common wheat and RFLP-based mapping. Euphytica, 115: 121-126.
Royse, D.J., Gregory, L.V., Ayers, J.E. & Cole, H., Jr. 1980. Powdery mildew of wheat: Relation of yield components to disease severity. Can. J. Pl. Pathol., 2: 131-136.
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.
Schafer, J.F. 1987. Rusts, smuts, and powdery mildew. In E.G. Heyne, ed. Wheat and wheat improvement, 2nd ed., p. 542-584. Madison, WI, USA, ASA, CSSA, SSSA.
Shaner, G. 1973. Reduced infectability and inoculum production as factors of slow mildewing in Knox wheat. Phytopathology, 63: 1307-1311.
Shaner, G. & Finney, R.E. 1977. The effect of nitrogen fertilization on the expression of slow-mildewing resistance in Knox wheat. Phytopathology, 67: 1051-1056.
Shi, A.N., Leath, S. & Murphy, J.P. 1998. A major gene for powdery mildew resistance transferred to common wheat from wild einkorn wheat. Phytopathology, 88: 144-147.
Silfhout, C.H. van & Gerechter-Amitai, Z.K. 1988. A comparative study of resistance to powdery mildew in wild emmer wheat in the seedling and adult plant stage. Neth. J. Pl. Pathol., 94: 177-184.
Stuke, F. & Fehrmann, H. 1988. Pflanzenpathologische Aspekte bei Sortenmischung im Weizenbau. J. Plant Dis. Prot., 95: 531-543.
Tompkins, D.K., Wright, A.T. & Fowler, D.B. 1992. Foliar disease development in no-till wheat: Influence of agronomic practices on powdery mildew development. Can. J. Plant Sci., 72: 965-972.
Ward, S.V. & Manners, J.G. 1974. Environmental effects on the quantity and viability of conidia produced by Erysiphe graminis. Trans. Brit. Mycol. Soc., 62: 119-128.
Wiese, M.V., ed. 1987. Compendium of wheat diseases, 2nd ed. St Paul, MN, USA, APS Press.
Wolfe, M.S. 1984. Trying to understand and control powdery mildew. Plant Pathol., 33: 451-466.