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African Crop Science Journal
African Crop Science Society
ISSN: 1021-9730 EISSN: 2072-6589
Vol. 3, Num. 2, 1995, pp. 185-189

African Crop Science Journal, Vol. 3. No.2, pp. 185-189, 1995

Foliar and head diseases of sorghum


Serere Agricultural and Animal Production Research Institute. P.O. Soroti. Uganda

Code Number: CS95025
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The major foliar and head diseases of sorghum are discussed in this paper. Some, especially anthracnose, leaf blight and grain moulds cause considerable economic losses. Host plant resistance is certainly the most cost-effective means of controlling these diseases. With the advent of biotechnology, opportunities now exist for more accurate diagnosis of disease etiology, and most likely will facilitate breeding for resistance to these diseases.

Key Words: Anthracnose, biotechnology, breeding, grain moulds, leaf blight


Le papier passe en revue les maladies foliaires et celles de tete de sorgho. Certaines comme l'anthracnose, la rouille et la moisissure de graines causent des pertes economiques considerables. La resistance est certainement le moyen de controle le plus economique. Avec l'avenement de la biotechnologie, des perspectives existent maintenant pour u n diagnostic plus sur de l'etiologie de maladies et plus probablement cela facilitera l'amelioration pour la resistance a ces maladies.

Mols Cles: Anthracnose, biotechnologie, amelioration, moisissures de graines, rouille


Among the cereals, sorghum (Sorghum bicolor (L.) Moench) is known to have the greatest number of diseases. This is partly because it is cultivated under a wide range of environmental conditions. Sorghum diseases are caused by fungi, bacteria, viruses and mycoplasma-like organisms. The crop suffers from both systemic and local lesion infections. Diagnosis is often complicated by variations inplant characteristics such as height, head shape, pigment, vigour and maturity.


Foliar infections are, sometimes difficult to diagnose because of the response of plant pigments to the infections. Depending on the pathogen, the lesion may appear tan, purple or red to straw-coloured, brown, dark-red or black. Most infections result in senescence. Some of the most common and important foliar infections are listed below.

Anthracnose. Anthracnose is caused by Colletotrichum graminicola (Ces.) Wilson. This is the conidial state of Glomerella graminicola Politis. The fungus, or related species, attacks maize, sugarcane and other grasses.

The disease occurs wherever sorghum is grown, especially in areas of warm, and humid conditions. The leaf blight phase of the disease is the most serious. In severe cases, yield losses can be as high as 50% or more, especially under alternating wet and dry cycles and high temperatures. Disease symptoms are typically circular lesions with straw coloured centres. On these centres appear numerous small black areas which constitute the fruiting bodies (acervuli) of the fungus (Warren. 1986).

The most effective control measure is through the use of resistant cultivars. The disease can be managed by cultural practices such as crop rotation, field sanitation or removal of plant debris at the end of the season.

Leaf blight. Leaf blight is caused by Exserohilum turcicum (Pass.) Leonard & Suggs (teleomorph of Trichometasphaeria turcica Luttrell). The perfect state rarely occurs in nature. In the laboratory, it may occur as black, globose pseudothecia. The disease occurs wherever sorghum and maize are grown. It is favoured by mild temperatures and humid weather conditions with heavy dew (Bergquist, 1986). Sudangrass. johnsongrass. teosinte and other grass species are also attacked by E. turcicum. The disease occurs as long elliptic tan lesions that develop first on the lower leaves and progress upward.

Resistance offers the best method of control. Two types of resistance are known: polygenic resistance, characterized by few and small lesions; and monogenic resistance, characterized by a hypersensitive fleck and little or no lesion development (Bergquist, 1986).

Downy mildew. Sorghum is attacked by two different downy mildew pathogens namely; Sclerophthora macrospora (Sacc.) Thirum et al., causing crazy top, and Peronosclerospora sorghi (Weston and Uppal) Shaw which causes sorghum downy mildew.

Sorghum downy mildew is a devastating disease on both sorghum and maize, both in the tropics and sub-tropics (Frederiksen et al. 1969). Peronosclerospora sorghi produces two forms of inoculum, oospores and conidia. Oospores are the sexual resting structure of the fungus. They reside in the soil and allow the pathogen to survive from one season to another in the absence of a host. Oospores germinate by a germ tube in response to host root exudate (Pratt, 1978), which then infects the sorghum seedling to give rise to systemic infection. Conidia disseminated from systemically-infected plants infect leaves and produce local lesions. Conidial infections of very young seedlings may induce systemic infection (Yeh and Frederiksen, 1980). Systemically infected seedlings are chlorotic, stunted and may die prematurely. In cool, humid weather. the abaxial surfaces of chlorotic leaves become covered with a white, downy growth consisting of the conidiophores and conidia of the fungus. Later stages of the disease result in death of interveinal tissue of the leaves which eventually shred. Diseased plants are usually barren or partially barren. Localized infections appear as brown necrotic lesions on leaf blades. Three pathotypes (physiological races) of P. sorghi (P1 . P-2 and P-3), have been identified in Texas (Craig, 1986).

Other foliar diseases. There are foliar diseases which frequently occur on sorghum but of relatively minor importance. These include bacterial leaf stripe (Pseudomonas andropogonis (Smith) Stapp), gray leaf spot (Cercospora sorghi Eli. & Ev.), zonate leaf spot (Gloeocercospora sorghi Bain & Edg.), sooty stripe (Ramulispora sorghi (Ell. & Ev.) Olive & Lefebvre, and rust (Puccinia purpurea Cooke).


Sorghum panicle disease occur in two forms: pathogens may colonize the grain (grain moulds) or they may infect the inflorescence, thereby replacing grain with fungal masses (smuts and ergot). They are invariably caused by fungi.

Grain moulds. Sorghum grain mould is probably the most important biotic constraint to grain sorghum production (Williams and Rao, 1981). Grain mould is a condition of sorghum grain resulting from the infection of the developing floret by one or more parasitic fungal species.

Forty or more fungal genera have been associated with grain mould. Most of these are unspecialized or facultative parasites and the predominant species vary with location, year and season. However, Fusarium moniliforme Sheld. and Curvularia lunata (Wakker) Boed. are the most important (Williams and Rao, 1981; Bandyopadhyay and Mughogho, 1988).

The most obvious sign of grain mould is the appearance of pink, orange, gray, white or blackish mycelium on the grain surface. For example, F. moniliforme produces pinkish white mycelium which is powdery in appearance, whereas C. lunata infected grain appear as shiny, velvety black growths. Severely moulded grain are generally lighter in weight than clean grain and disintegrate easily when pressed.

Alternate wetting and drying coupled with prolonged rainfall, high humidity and high temperature favour grain deterioration. Damage caused by grain mould is both quantitative and qualitative (Williams and Rao, 1981). Quantitatively grain mould causes actual yield losses. Qualitatively, the disease results in loss in market value, processing and nutritive values. Mycotoxin contamination, resulting from grain mould infection, has received some attention (McMillian et al., 1983). Mycotoxins decrease growth rates of livestock on feed, predispose animals to toxicity and may be carcinogenic.

Avoidance and the use of resistant cultivars are the only two methods recommended for controlling sorghum grain mould.

Ergot. Ergot, sometimes also known as "sugary disease" is caused by Sphacelia sorghi McRae, which is a conidial state of Claviceps spp. (Bandyopadhyay, 1992). It occurs in many sorghum growing areas of the semi-arid tropics. The disease is largely a problem in cool, moist weather, mostly in highland sorghums and offseason plantings. Ergot is particularly important on male sterile lines. Hence, it is a factor in hybrid seed production.

Symptoms appear as turbid drops of honey dew dropping from infected spikelets. Individual spikelets scattered in the ear or in groups are infected. The honey dew droplets are sweet to taste and attract flies and ants. In the affected spikelets, the grains are replaced by soft masses of mycelia. In severe infections, yield losses are considerable. In advanced stages, sclerotia can be found in the spikelets. Often the infected spikelets are overgrown by a hyperparasitic fungus, Cerebella sp., affecting grain quality. The sclerotia of the fungus also contain alkaloid mycotoxins.

Several strategies for the control of sorghum ergot have been advocated. Quarantine has been effective in excluding the pathogen especially in USA and Australia. Cultural practices such as early planting or the use of early maturing cultivars or pathogen free seed have also been used successfully.

Smuts. There are four distinct sorghum smuts, which are widely distributed. These are covered kernel smut (Sporisorium sorghi Ehrenberg (Link)), loose smut (Sphacelotheca cruenta (Kuhn) Potter), head smut (Sporisorium reilianum (Kuhn) Langdon & Fullerton) and long smut (Tolyposporium ehrenbergii (Kuhn) Patouillard). Of these, covered kernel smut is the most economically important in Africa.

Covered kernel smut replaces ovules as a smut sorus, which is covered by a persistent peridium. The sori are conical or oval and resemble an elongated sorghum seed. They may occupy all the florets in the head or only a portion of them. In many cases, the infected plants are not affected in height or other agronomic characters.

The teliospores of S. sorghi are seedborne and germinate with the seed. Infection occurs at seedling stage, and the fungal mycelium grows with the plant, eventually occupying the florets. Mature sori rupture, releasing teliospores, which contaminate seed. Only seedborne spores cause infection (Frederiksen, 1986). The disease can be controlled by seed fungicides used as dressings.

Loose kernel smut is less important than covered kernel smut. Usually, all spikelets are affected, although sometimes the unaffected ones may be hypertrophied. Affected plants are often shorter, have thinner stems and tend to tiller. Sphacelotheca cruenta is primarily seedborne and the disease is controlled by fungicide seed dressings. Head smut is widely distributed geographically. The intensity of the disease appears to increase as sorghum is more intensively cultivated. The disease affects

the whole inflorescence. Long smut commonly develops in the drier regions of the Sahel. This floral infecting smut rarely causes extensive loss, but occasionally plants in some fields are severely damaged. While there are some genetic differences

in reaction, little has been done to control long smut.


Molecular biotechnology can be used for sorghum pathology in two main areas: Diagnosis and utilization of resistance sources.

Diagnosis. Biotechnology permits accurate diagnosis of plant disease. ELISA and PCR techniques are used in the identification of viral and bacterial diseases. Biotechnical procedures can also be used to determine the type and extent of variability existing in the pathogen. An understanding of pathogen variability leads to identification of more durable sources of host resistance.

Variability enables a pathogen to overcome cultivar resistance. The pathogen continuously produces a variety of pathotypes (virulence forms). For sorghum, variability of C. graminicola makes it difficult to control anthracnose by conventional breeding strategies. Molecular genetic markers, such as RAPDs (Random Amplified polymorphic DNA) and RFLPs (Restriction Fragment Length polymorphisms), can help identify variation among pathogen isolates. RAPDs have been successfully used to define the genetic lineage of C. graminicola isolates from USA and Brazil (Casela, 1992).

Use in disease resistance breeding. An important use of biotechnology in crop improvement will be to facilitate resistance breeding. Gene technology is an essential element in modern plant breeding. The genetic code is universal. Therefore, it is theoretically possible to express virtually any genetic trait of an organism in plants. The development of recombinant DNA technology makes it possible to isolate individual genes and

incorporate resistance genes into otherwise agronomically acceptable cultivars. Gene pyramiding is made easier with molecular markers. Since plant genetic engineering is based on transfer of defined genes, the risks are predictable


Bandyopadhyay, R. 1992. Sorghum Ergot. In: Sorghum and Millets Diseases:A Second World Review. de Milano, W.A.J.,Frederiksen R.A. and Bengtson, G .D. (Eds .), pp.235-244. ICRISAT, Patancheru, 502324, A.P., India.

Bandyopadhyay, R. and Mughogho, L. 1988. Evaluation of field screening techniques for resistance to grain molds. Plant Disease 72: 500-503.

Bergquist, R. 1986. Leaf blight. In: Compendium of Sorghum Diseases. Frederiksen, R.A. (Ed.), pp. 9 - 10. American phytopathological Society, St. Paul, MN, USA.

Casela, C.R. 1992. Investigations on the Variability of the Sorghum Anthracnose Fungus Colletotrichum graminicola. Ph.D. Dissertation, Texas A&M University, College Station, TX, USA.

Craig, J. 1986. Downy mildews. In: Compendium of Sorghum Diseases. Frederiksen, R.A. (Ed.), pp. 24-27. American phytopathological Society, St. Paul, MN, USA

Frederiksen, R.A. 1986. Head smut. In: Compendium of Sorghum Diseases. Frederikesen, R.A. (Ed.), pp. 17-18. American Phytopathological Society, St. Paul, MN, USA Frederiksen, R.A-, Amador, J., Jones, B.L. and Reyes, L. 1969. Distribution, symptoms and economic loss from downy mildew caused by Sclerospora sorghi in grain sorghum in Texas

Plant Disease Reporter 53: 995-998.

McMillian, W.W., Wilson, D.M., Mirocha, C.J. and Windstrom, N.W. 1983. Mycotoxm contamination in grain sorghum from fields in Georgia and Mississippi. Cereal Chemistry 60: 226-227.

Pratt, R.C. 1978. Germination of oospores of Sclerospora sorghi in the presence of growing roots of host and non-host plants.

phytopathology 68:1606-1613.

Yeh, Y. and Frederiksen, R.A. 1980. Sorghum downy mildew: Biology of systemic infection by conidia and of a resistant response in sorghum. Phytopathology 70: 372-376.

Warren, H.L. 1986. Leaf anthracnose. In: Compendium of Sorghum Diseases. Frederiksen, R.A. (Ed.), pp. 1O- 11. American Phytopathological Society, St Paul, MN., USA.

Williams, R.J. and Rao, K.N. 1981. A review of sorghum grain moulds. Tropical Pest Management 27:200-211.

Copyright 1995 African Crop Science Society

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