Tropical maize: improvement and production. Maize diseases. R.L. Paliwal

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2 Tropical maize: improvement and production ~ Maize diseases R.L. Paliwal 83 Maize in tropical environments is attacked by a wide array of pathogens causing significant and economic damage to maize production. Wellman's (1972) monograph Tropical American plant diseases reported that 130 diseases affect the maize crop in the tropics compared to only 85 maize diseases in temperate environments. The hot, humid climate under which most maize is grown in, the tropics is more conducive to the growth and spread of disease pathogens. However, maize is grown under a wider diversity of environments in the tropics. In the highlands, maize is grown in small niches where various races ofpathogens have coexisted with maize for centuries. Good progress has been made in the development of stable genetic resistance for most of the maize diseases. However, large areas in tropics are still planted with landraces, farmers' own varieties and unimproved seeds. This is one reason the disease situation in tropical maize environments appears to be more severe than the situation in temperate environments where largely improved disease resistant cultivars are planted. Detailed information on maize diseases is provided by Wellman (1972), Ullstrup (1976, 1977, 1978), Renfro (1985) and Smith and White (1988). The University of Illinois and the United States Department ofagriculture (USDA) (Anonymous, 1973) published a Compendium ofcorn di.~ea~es, an illustrated account of pathogenic and non-pathogenic problems affecting maize. De Leon (1984) published an illustrated field guide for the identification of important maize diseases. He lists 44 diseases caused by fungi, three by bacteria and ten caused by viruses and mollicutes. Some diseases are of a global nature and occur in most of the maizegrowing environments. These include leaf blights, leaf rusts, leaf spots, stalk rots and ear rots. There are some diseases that are of regional importance but can cause severe economic loss. These include downy mildews in Asia, which are also spreading to some parts of Africa and the Americas, maize streak in sub-saharan Africa and maize stunt and tar spot in Mexico and Central and South America. A parasitic weed, Striga, also causes serious loss to maize production in sub-saharan Africa In this chapter, important diseases affecting the maize crop at various stages of plant growth are described. The symptoms and epidemiology of the diseases is based on descriptions given in Anonymous (1973) and De Leon (1984). The diseases found throughout tropical maize environments are described first, followed by diseases of regional occurrence. Breeding for resistance to various diseases is discussed in chapter "Breeding for disease resistance". WIDESPREAD DISEASES Seed rots and seedling blights Germinating maize seeds may be attacked by some seed-borne pathogens or soil-borne fungi that can cause the seed to rot before germination or cause the young seedling to rot, which is sometimes called damping-off. This is not a serious problem in most lowland tropical maize plantings where the temperature is high and germination is quite rapid. Seed rots and seedling blights can be a matter of concern where temperature at the time of planting is low and/or the soils are wet. Such conditions do not normally occur in the lowland tropical maize crop in the

3 64 summer season. However, in the winter maize crop and in subtropical environments, seed and seedling rots are encountered. Floury maize cultivated in the highlands and also sweet grain maize are more vulnerable and are often affected by seed rot. Wellman (1972) believes that tropical farmers generally do not give much attention to the problem of poor plant stands resulting from seed rots and seedling blights. Replanting of the plot or planting in the gaps is the normal practice in the tropics. As tropical agriculture becomes more intensive and competitive, these diseases and their control will have to be given more careful attention. Seed rots and seedling blights are generally caused by the Pythium species. which is a saprophyte and is quite at home in tropical soils. A healthy and fast growing seedling escapes the attack of this fungus. The problem can be successfully handled by planting healthy seeds treated with a seed fungicide (for example, Thiram or Captan) in a properly prepared seedbed that is not too wet and when the soil temperature is not too low (below 10 C). Resistance to seedling disease organisms could be a good trait in germplasm for winter maize environments and for highland areas. Genetic resistance has been studied and appears to be complex, involving several genes. Strong non-cytoplasmic maternal effects have been reported (Renfro, 1985). The rolled towel cold tolerant test for germinating seeds can be used to screen germplasm for resistance to seedling blights (Poehlman, 1987). Root rots Root rot is also found in conditions and environments similar to seed rots and seedling blights. Root rots are generally caused by fungal pathogens of the Fusarium and Pythium species. The root becomes weak, water-soaked and brown and starts rotting. The water and food supply to the plant is retarded. The plant can suffer from root lodging. The rot may advance into the main Maize diseases roots, seedling and crown tissue. Two other fungi, Diplodia maydis and Gibberella zeae, may enter the plant through damaged or injured roots and cause stalk rots. Krueger (1991) reported a positive association of the incidence of root rot with stalk rots. Root rot can be controlled with the same precautions used for seed rot and seedling blight. Any damage to roots during cultivation should be avoided. Genetic resistance is available and in the case of Fusarium, it appears to show additive gene action and with dominant maternal effects. Stalk rots Stalk rots are of global importance and affect maize in almost all environments. The disease appears after the elongation phase of the plant has started and the internodes have begun expanding. Both bacteria and fungi are involved as stalk rotting pathogens, and quite often a combination of more than one pathogen is present. Stalk rots may attack the plant early in the active stages of plant growth before tasselling or may also attack in the post-flowering stage. Stalk rots cause premature drying, stalk breakage and death of the plant. Stalk rots occur in all maize environments: from cool to warm to hot; in the lowlands, mid-altitude and highlands; and in dry to wet climates. They are more prevalent in warm climates with temperatures above 30 C, high humidity, high fertility levels and good plant growth with high plant density. These conditions create a very favourable atmosphere for the growth of bacteria and fungi. Early bacterial stalk rots are caused by Erwinia and Pseudomonas spp. These bacteria attack maize during mid-season and spread rapidly and quickly in the plant, which suddenly falls over. Stalks become dark brown, water-soaked, soft and slimy and may easily collapse. The bacterial decomposition produces an unpleasant odour. One or two dominant genes, with some epistatic effects, are reported to be

4 !!5!-ical maize: improvement and production involved in resistance to Erwinin stalk rot. Stewart's wilt is caused by the bacterium Xanthomonas stewartii. The pathogen is transmitted by seed and infection occurs in the early stages of plant development. Water-soaked oval lesions develop on the leaves where the pathogen enters through wounds made by insect vectors. The lesions grow and the leaf may show complete necrosis. The pathogen may spread into the stem and cause a general wilting of the plant. The plant shows abnormal weak growth and dies at or shortly after tasselling. The use of disease-free seed and resistant varieties can completely control this disease. Resistance is dominant and governed by two major complementary genes and one minor gene. Ul1strup (1977) reported that red cob colour was linked with resistance genes and white colour with susceptibility. Early stage fungal stalk rot is caused by the Pythium species (Plate 12). Symptoms are similar to early bacterial stalk rot. The single internode just above the soil surface is affected. The stalk twists and the plant normally falls over, remaining green for quite some time as the vascular system is not cut off. Most damage from Pythium stalk rot appears just before and at tasselling time. Resistance to Pythium stalk rot seems to be quantitative with additive effects (Diwakar and Payak, 1975). Use of resistant germplasm with clean cultivation is the best solution for the control of early stalk rots. Post-flowering stalk rots These stalk rots appear in the later stages of plant development and cause serious damage from grain development to physiological maturity. Three major fungi are involved in causing late stalk rots: the Diplodia, Fusarium and Gibberella species. In addition, there are three other significant stalk rot diseases: late wilt caused by the Cephalosporium species, black bundle disease caused by Cephalosporium acremonium and charcoal rot caused by Mocrophomina phoseoli. Diplodin stalk rot is caused by Dlplodin maydis (Plate 13, Plate 14). It generally appears a few weeks after silking. The leaves wilt and become greyish-green. The lower internodes turn brown to straw-coloured and become spongy. The pith disintegrates, becomes discoloured and only the vascular bundles are left intact. The weakened stalks break very easily. This stalk rot is more prevalent in cool and humid areas. Gibberella stalk rot is caused by Gibberella zeae. The leaves turn dull greyish-brown. while the lower internodes become soft and tan to brown in coiow'. The pith becomes shredded and is reddish in the affected area. Fusarium stalk rots are caused by Fusarium moniliforme (Gibberella fujikutoi) and Fusarium graminearum (Gibberella zeae). The rot starts soon after pollination and affects the roots, base of the plant and lower intemodes. The rotting gets worse as the plant matures. Stem breakage and premature ripening occurs as in other stalk rots. Plants may remain standing even when dry but will fall over when knocked. As in Gibberella stalk rot, the pith shreds and surrounding tissues become discoloured. Late wilt is caused by Cephalosporium maydis. The disease symptoms appear at flowering time. The leaves start wilting quite rapidly, generally beginning with the top leaves, which tum a dull green and soon wilt completely and dry up. The vascular bundles are discoloured and the basal part ofthe stem becomes dry, shrunken and hollow. Other fungi are also usually involved, and stalk rot symptoms become modified and variable. The disease develops in hot climates, in heavy and dry soils and also in very light sandy soils. The pathogen is seed- and soilborne, and infection starts through entries in the roots or mc5ocotyi. Late wilt is serious only in the Middle East and South Asia. It is the most serious disease affecting maize in Egypt. Local varieties have shown good resistance to late wilt and have now been successfully used to develop resistant hybrids

5 66 and new improved varieties. Black bundle disease is caused by Cephalosporium acremonium. It is more widespread than late wilt. Infection appears when the ear is well-developed and grains are at the dough to hard starch stage. The vascular bundles become black and this blackening extends throughout several internodes. The plants only develop nubbins or ears with shrunken, poorly developed kernels. The fungus is seed- and soil-borne. The infection normally occurs through wounds in rind and stalk tissues. Charcoal rot is caused by Macrophomina phaseoli. The fungus enters through the roots at the seedling stage and sometimes causes seedling blights. Mostly, the fungus grows through the outer layers of the stalk and reaches the lower internodes. Symptoms appear as the plant nears maturity. The plant shows premature ripening. The stalk tissues show black discoloration and shredding of the vascular bundles and the stalk appears to be charred. Charcoal rot occurs in hot dry environments, particularly under water stress and high temperatures. Some other fungi that infect the leaves of the maize plant may also cause stalk rots. One example is anthracnose stalk rot caused by Col/efofrichum graminicolum, which also causes leaf anthracnose. In addition to the nine types ofstalk rots mentioned here, there are some very minor stalk rots occasionally reported on the maize plant in the tropics. Only two stalk rots, Fusarium stalk rot and Diplodia (= Sfenocarpella) stalk rot, are of major economic significance. These two stalk rots cause economic losses on about onethird of the area planted to maize in the tropics. The use of resistant germplasm is the best prevention and control ofstalk rots. De Leon and Pandey (1989) have reported improvement in tropical germplasm by 'ecurrent selection for resistance to F moni/(forme ear and stalk rots. Balanced soil fertility with not too high levels of nitrogen and an increased dose of potassium helps. Maize diseases Any stress during the growth period renders plants more susceptible to stalk rots (Dodd, 1980). Avoiding damage to the roots, rind and stalk reduces the chances offungus entry into the plants. Stay-green plants with thick rinds and strong stalks are reported to show less infection and loss due to stalk rots (Zuber ef al ). Genetic resistance to various stalk rots has been reported. A number of genes are involved in resistance and inheritance appears to be quantitative. Resistance to Diplodia stalk rot involves additive and dominance gene action and occasionally epistasis (Renfro, 1985). Draganic and Boric ( 1991 ) reported that resistance to rot pathogens is polygenic and, though the development ofresistant hybrids is difficult, it has been possible to breed high yielding hybrids with horizontal (general) resistance. In late wilt, resistance is reported to be partially dominant and largely controlled by additive-type gene action, non-additive gene action being of minor importance (Khan and Paliwal. 1979, 1980). Shehata (1976) reported that dominance and epistatic effects played a major role in the inheritance of disease reaction to late wilt. EI-Itriby ef al. (1984) reported that a minimum of three major genes are involved in conditioning resistance to late wilt and epistatic gene action was more important. Inheritance and gene action for resistance to charcoal rot and black bundle disease is not a~ well-known. Foliar diseases Foliar diseases are the most visible diseases on a maize plant and, therefore, appear to be more alarming at first sight. Most foliar diseases progress from the lower leaves upward as sugar is translocated from the leaves to the ear. The diseases of global importance found throughout the tropics are leaf blights, leaf spots and leaf rusts. All of these diseases kill a sizeable leaf area and thus reduce photosynthetic leaf surface. Generally, these are not life-threatening diseases and the plant does not die. It continues photosynthetic

6 Tropical maize: improvement and production -activity with the parts of the leaf that remain green and unaffected by the disease. However, the productivity of the plant is greatly reduced. In the case of forage maize, total dry matter is reduced and forage quality decreases. Foliar diseases fall into three major classes: leaf blights, leaf spots and leafrusts. Leafblights Northern or turcicum leaf blight is caused by Exserohilum turcicum (syn. Helminthosporium turcicum) (Plate 15). This blight commonly occurs in cooler, subtropical winter maize and highland maize environments. It is particularly severe in subtropical cultivars where temperate germplasm has been introgressed. It does not affect tropical germplasm too severely. The first symptoms of the disease appear as oval water-soaked small spots on the lower leaves that progress to the upper leaves. These spots join or coalesce with each other to grow into elongated, spindle-shaped necrotic lesions. Under heavy infection, leaves may dry completely and die prematurely as in a drought-affected plant. Host specific races and physiologic races of the fungus are known to exist. Both monogenic and polygenic sources of resistance have been found and used to develop resistant germplasm (Hooker, 1977; Ullstrup, 1977). Stable polygenic resistance to turcicum leaf blight has been developed in most improved germplasm and appears to be effective against all races. Many genes are involved, some with major and other with minor effects. Genes for resistance show partial dominance. Additive gene action appears more important than dominance or epistatic effects. Turcicum leaf blight is now seen as a problem only in unadapted, exotic, introduced and temperate germplasm when grown in the tropics. Southern or maydis leaf blight is caused by Bipolaris maydis (syn. Helrninthosporium maydis) (Plate 16). It affects maize, teosinte and also sorghum. It is prevalent in hot and humid environments and it affects the main 67 maize crop in the summer season in lowland tropical and highland environments. It also affects winter maize later in the season when temperature starts to rise. Both turcicum and maydis leaf blights can be found affecting the maize crop at different times in the same season. Three races of maydis leaf blight are known to cause serious damage to the maize crop. One is the "0" race, which is more prevalent and widespread in the tropics. Its lesions are small and diamond-shaped in early stages. They elongate, but growth is limited by the veins of the leaf and the lesions remain small and rectangular. Later these lesions may coalesce to produce large dry or "bumt out" patches on the leaf. The lesions of the 0 race are found only on the leaves. Another race is the "T" race (Plate 17), which is associated with T cytoplasm involved in cytoplasmic-genic male T cm sterile lines (Texas cytoplasmic male sterility). The lesions are bigger, spindle-shaped or elliptical with yellow-green or chlorotic haloes. The third race is the "C" race, which was identified in 1987 in China. It is closely related to race T. In addition to the leaves, the lesions of races T and C also appear on leaf sheaths, ear husks and sometimes on stalks and cobs. It is difficult to distinguish races 0, T and C from leaf symptoms alone when this blight is present on normal (N) cytoplasm plants. Race T is particularly virulent on maize with Texas male sterile cytoplasm, where it attacks leaves, stem and ear. Race T became a matter of great worldwide concern in 1970 when the maydis leaf blight epidemic devastated the maize crop with Texas-type cytoplasm in the United States. Mercado and Lantican (1961) had earlier reported the extreme susceptibility of male sterile maize with Texas cytoplasm grown in the Philippines. Resistance to maydis leaf blight is controlled by the cytoplasm as well as the nuclear genes and is known to be both monogenic and polygenic in inhentance. Use ofresistant germplasm and resistant cytoplasm has considerably reduced the extent of

7 68 damage earlier caused by maydis leaf blight. Both monogenic and polygenic resistance has been used for the development of resistant germplasm. Relatively few genes are reported to be involved in polygenic resistance with both additive and dominant genetic effects (Ullstrup, 1977, 1978). The polygenic resistance system reduces both lesion size and number. The monogenic system with the mm gene in a homozygous state results in small chlorotic lesions with reduced sporulation and is effective up to the time the maize plant flowers (Thompson and Bergquist, 1984). Hooker (1978) has described the cytoplasmic sources and genes that impart resistance to the T race ofmaydis leaf blight. Yellow leaf blight is caused by Phyllosticta maydis. It occurs in cooler and humid environments. The fimgus shows differential pathogenicity in Nand T cytoplasm backgrounds and particularly affects maize plants with T cytoplasm. It is found at all stages of plant development from seedling stage to mature plant. Yellow to cream or tan coloured lesions appear on the outer surface of the leaf. In later stages, lesions may appear on leaf sheaths and outer husks and the upper part of the leaf may appear blighted. Symptoms resemble maize plants suffering from nitrogen deficiency. The use of resistant germplasm gives the best control. With the shift away from the use oft cytoplasm, this disease is of no major significance (Smith and White, 1988). Crop rotation and clean cultivation can also minimize early stage infection. Banded leaf and sheath blight is caused by Hypochnl/s sasakii (Corticium sasakii = Rizoctonia solani). It produces large discoloured areas on the leaf, separated by concentric dark bands. The symptoms may appear on leaves and husks. The disease results in the brownish rotting of the ears with brown cottony mould. This disease causes economic loss in some parts ofasia. Lea/spots Helminthosporium leaf spot is caused by Maize diseases Helminthosporium carbonum, also called Bipolaris zeicola. It is found in cooler areas and is prevalent in temperate regions. It is not of much significance in the tropics. Three races of the fimgus have been identified. Genetic resistance is well-known. It is controlled by two recessive genes for race 1. Polygenes with additive genetic effects are involved in resistance for race 3 (Halseth, Pardee and Viands, 1991). Resistant germplasm has been developed. The disease can be easily controlled with use of resistant germplasm and crop rotation with conventional tillage practices (Smith and White, 1988). Curvularia leaf spot is caused by Curvularia lunata and C. pallescens (Plate 18). The disease produces small necrotic or chlorotic circular to oval spots with a light coloured halo and reddish-brown to dark brown margins. It is prevalent in hot, humid maize environments. Economic losses caused by this disease may not be very significant. Polygenic resistance is known with both additive and epistatic effects. Leaf anthracnose is caused by Colletotrichum graminicolum. It has two phases, a leaf blight phase that is less important than a stalk rot phase. It is not a major maize disease in the tropics. The pathogen spores enter the leaves first and cause leaf spots. Small round to irregular water-soaked, semi-transparent spots appear on the leaves early in the growing season. The spots later enlarge, coalesce and turn brown with reddish-brown borders. The fimgus may cause seedling blight and also stalk rot. Polygenic resistance with additive gene effects and some partial dominance have been reported (Carson and Hooker, 1981). Brown spot is caused by Physoderma maydis (Plate 19) and occurs in hot and humid environments of the tropics. It affects both maize and teosinte. The symptoms first appear on the leaf blade as small yellow chlorotic spots. In the mid-ribs, leaf sheaths, stems and sometimes ear husks lesions develop as small brown spots. Genetic resistance is known and involves at least four

8 !!!!E!.cal maize: improvement andproduction genes with additive effects. Dominance and epistatic gene effects have also been reported. Lal and Chakravarti (1977) recommend the use of systemic fungicides for post-infection control of brown spot disease. Eye spot (called brown spot in Japan) of maize is caused by Kabatiella zeae (Plate 20). It occurs in cool and moist environments and, in addition to maize, it affects several species of teosinte. The disease causes translucent circular to oval lesions in the early stages. Initially, the lesions are water-soaked with a cream to tan coloured point in the centre surrounded by a brown or purple ring with a narrow yellow halo. This gives the appearance of an eye spot, and thus gives the disease this name. The symptoms of eye spot disease are similar to those of Curvularia leaf spot or non-pathogenic physiological and genetic spots found on the maize plant in some tropical environments. Genetic resistance is partially dominant and only a few genes are involved (Reifschneider and Amy, 1983). The use of resistant varieties, crop rotation and clean cultivation control the disease quite effectively. Phaeosphaeria leaf spot is caused by Phaeosphaeria maydis (Plate 2\). This is not a very widespread disease and is reported in South Asia, Mexico and other countries in South America in cool and high rainfall maize environments. The disease initially produces small pale green or chlorotic lesions that later become bleached, dried and develop brownish margins. The spots are elongate to oblong and appear all over the leaf. The fungus persists in diseased plant parts in the field. Under favourable conditions the spores germinate and infect the leaves of the next crop. Crop rotation can reduce infection of this disease. Cereospora or grey leaf spot is caused by Cereospora zeae-maydis. It occurs in cool humid environments. It is reported that the incidence of this disease is increasing where a continuous crop ofmaize is grown without rotation and with the continued use of minimum tillage practices (Latterell and 69 Rossi, 1983; Donahue, Stromberg and Myers, 1991). The disease produces pale brown streaks, which are delimited by the veins ofthe leaf, or spots that are grey to tan and yellow to purple on the leaves of the mature plant. The disease is found throughout the tropics, but it does not cause significant economic loss. Genetic resistance has been identified and is governed by additive genetic effects (Bergquist, 1985; Donahue, Stromberg and Myers, 1991; Bubeck et ai., 1993). The use of resistant germplasm, crop rotation and conventional tillage has been recommended to minimize the incidence ofthe disease. Zonate leaf spot is caused by Gloeocercospora sorghi. The disease is more prevalent on sorghum but also infects the maize crop in dry and hot environments. Initially, lesions are reddish-brown and watersoaked. Later, these enlarge and produce characteristic large concentric necrotic rings. Larger lesions may be 5 cm in diameter on older maturing leaves. Leptosphaeria leaf spot is caused by Leptosphaeria michora. It occurs in the humid areas ofhighland maize environments. The disease causes smal1 lesions that become large, concentric and cover the leaf. Usual1y it is confined to the lower leaves and appears at flowering time. Septoria leaf blotch is caused by Septoria maydis. It occurs in cool humid environments. The leaves of infected plants first show small light green to yellow spots. These grow and coalesce to produce severe blotching and necrosis. The last five leaf spot diseases are found occasionally and at present do not cause any significant damage in tropical maize-growing environments. Anyone of these could become a disease of concern if it increases and a large percentage ofplants are affected. Lea/rusts Three types of rust found in maize are of major economic importance. These are:

9 70 common rust, southern rust and tropical rust. Common rust is more prevalent in cool environments in the highlands. Southern rust, on the other hand, is the disease of low elevations and warm environments. These two rusts sometimes exhibit a seasonal distribution. Common rust occurs early in the maize season, while southern rust usually occurs later in the season when rain intensity decreases and the rains are about to finish. Tropical rust is more irregular in its distribution. Landraces of maize where these rusts are endemic have developed a good level of tolerance to the disease. Exotic and introduced gerrnplasm are more severely affected by these rusts. Common rust is caused by Puccinia sorghi (Plate 22) and is widespread. [t attacks maize and teosinte, but is not generally seen on sorghum plants. Its alternate host is Oxa/is (Plate 23). Common rust is most conspicuous on susceptible maize varieties at the time of tasselling, when small brown powdery pustules can be seen on both sides of the leaves. The pustules tum brownish-black as the plant matures. Cool temperature and high humidity favour rust development and spread. Several physiological races of P. sorghi have been identified and separated by their reaction to different lines of maize. Pathogen race specific resistance has been identified and is controlled individually by five different gene loci located on three chromosomes (Saxena and Hooker, 1974). Such specific resistance results in restricted pustule development. General resistance is also known, which results in a reduction of pustule number and size and reduced leaf necrosis. Few genes are involved in general resistance, which is highly inheritable (Kim and Brewbaker, 1977). Gerrnplasm with polygenic and stable resistance to common rust can be developed. The use ofresistant gerrnplasm and control of the Oxalis weed can eliminate the problem of common rust very effectively. Southern rust is caused by Puccinia po/ysora (Plate 24). It attacks maize, teosinte and also Tripsacum and is more prevalent in Maize diseases warm and humid environments. Earlier, this rust was called American maize rust as it was found only on the American continent. In the late 1940s, it was introduced in Africa (Wellman, 1972; Renfro, 1985) and in the next ten years it spread to all tropical maizegrowing environments of Africa, Asia and the Pacific Islands. The symptoms are similar to that of common rust described above. The pustules are smaller, lighter in colour and densely scattered on both surfaces ofthe leaf. They tum dark brown as the plant reaches maturity. Later the leaves become chlorotic and dry. Southern rust does not have an alternate host coexisting with it as does common rust with Oxa/is. Several physiologic races of this rust have been identified. Specific resistance to various races has also been identified. Eleven loci are reported to influence resistance (Scott, King and Armour, 1984). General resistance also probably exists and could be used (Smith and White, 1988). Lu et al. (1990) reported from China that resistance to common rust was significantly correlated with resistance to southern rust. Tropical rust is caused by Physopel/a zeae. It is still limited to the warm, humid tropical maize environments of Mexico, Central America, South America and the Caribbean. Small cream to pale yellow pustules develop beneath the epidermis, with a small pore or slit opening. The pustules later become purplish, circular to oblong blotches with the central part remaining creamy in colour. It does not have and alternate host. The use of resistant gerrnplasm is recommended. It is suggested that in addition to breeding resistance against a specific rust, a generalized resistance or tolerance to all three rusts and their races would provide a better solution to rust problems in maize (Wellman, 1972). Diseases of the Inflorescence Five diseases affect the inflorescence parts, which include the flowers, young developing ovaries and grains. These are: crazy top,

10 ,!!!!!!ica/ maize: improvement and production which affects the tassel (and also the plant) and is a regional disease; head smut, which affects the tassel and ear; false head smut, which affects only the tassel; common smut, which affects mostly the ear; and ergot. Crazy top is discussed in the section "Regional diseases". Head smut is caused by Sphocelotheca reiliana. It occurs in dry and hot maizegrowing environments. Infection is systemic, the fungus penetrates the seedling and grows throughout the plant without showing any symptoms until flowering time. The tassel shows prominent disease symptoms and becomes malformed and excessively overgrown. Tassel infection may be confined to individual spikelets causing shoot-like growth or phyllody. In other cases, the entire tassel may proliferate forming bizarre leafy structures. Ears of infected plants are also normally smutted and ears are replaced by a black mass of spores. Teosinte and teosintemaize hybrids are also affected by this disease. Genetic resistance has been identified and there is considerable variability in the reaction to the fungus (Frederiksen, 1977). In a recent study, Bernardo, Boumer and Oliver (1992) reported that additive effects are very strong in conditioning resistance to the disease, while dominance and epistatic effects play only a minor role. Resistant germplasm has been selected and the use of such germplasm is the best control measure against head smut disease. False smut is caused by Ustilaginoitfea virens. It occurs in hot environments in many parts of the world, but generally is not a serious economic disease except in some isolated pockets. False smut infests only a few male spikelets on the tassel and develops ergot-like galls, which produce dark green masses of spores. False smut does not result in yield reduction and therefore is of no economic significance. Common smut, also known as Boil smut, is caused by Ustilago maydis (= U. zeae). It OCCurs worldwide in moderately dry to humid areas, but is not a very severe disease. Any aboveground part ofthe plant can be affected, particularly actively growing meristems and other young tissues. More damage occurs when the apical meristem in seedlings becomes infected. lypical symptoms are the boil-like galls that appear on the stem and leaves. The disease, if it comes early, can stunt growth or result in the death of the plant On the ears, the fungus finds entry through the silks and conspicuous white galls, which are formed instead of kernels. When the galls rupture, the black mass of spores is released, which can infect the next crop. Several races are present and generalized resistance against the disease is required as it affects almost all plant parts. Genetic resistance is available (Bojanowski, 1969). It is polygenic and quantitative in action involving both additive and non-additive gene actions. Planting of resistant germplasm, avoiding mechanical injury to plants and removing and burning galls before spores are released can reduce the disease to insignificant levels. Ergot or Horse's tooth is caused by Claviceps giganlea. The disease is limited to the humid highland valleys of Central Mexico. White to cream coloured, sticky and hollow sclerotia replace kernels on the ear. One too many sclerotia may develop on one ear and produce toxic alkaloids. Ear rots Several fungi (and some bacteria) infect ears and kernels causing them to rot. Most of the pathogens involved in stalk rots are also involved in ear rots. Some of the ear rots are widespread and most cause significant damage between the silk stage and harvest in humid areas with high rainfall. When germplasm with loose husk cover is used, when husk cover is damaged by birds or when store grain insects damage ears and kernels in the field, the crop suffers more damage from ear and kernel rotting fungi. Ear and kernel rots reduce yield very significantly in high rainfall environments during the drydown period and in the highlands. In 71

11 72 addition, the quality ofthe grain and seed is adversely affected. In environments where the incidence ofear rots is high, seed production and maintaining good gennination is difficult. The development of gennplasm with high levels of resistance to ear and kernel rots remains a priority in several maize-growing environments in the tropics. Ear rots are named after the pathogen causing the disease. Major ear rots and their symptoms are described below. Diplodia ear rots are caused by Diplodia maydis and D. macrospora (Plate 25, Plate 26). The husks of the infected ears appear bleached and straw coloured. ]f infection occurs early, the entire husk cover turns greyish-brown and appears dry while the plant is fully green. When opened, the ear appears chatty and bleached with a white cottony growth on the ear and between the kernels. The ears infected late in the season may not show such extreme symptoms. The ears are very light in weight. The ear bends rather than breaking sharply and mould can be seen between the kernels, whose tips are discoloured. In environments with high rainfall between the silk stage and harvest, problems of ear rot can be avoided by harvesting the crop for green ears. In some areas fanners avoid the accumulation of water inside the husk cover by bending the stalk at the internode just below the ear. The use of gennplasm with tight husk cover and appropriate maturity can minimize losses from ear rot. Gennplasm having good levels oftolerance to ear rots has been developed. Fusarium ear and kernel rots are caused by Fusarium moniliforme and its related variety suhg/utinans. The pathogen enters through the silks and usually at the tip of the ear. Infection remains limited to some kernels or to a small section of the ear. A powdery or cottony whitish-pink mould develops on the kernels. Maize borers and ear wonns assist in the establishment ofthe pathogen on the kernels and mould can be seen growing along the tunnels made by the Maize diseases insect. Kernels infected late in the season may not show much mould and may only show some streaks on the pericarp. This rot is very widespread throughout tropical maize environments. Some kernels infected with Fusarium can be found even in a very clean lot of maize ears. Control of borers and ear wonns - thus avoiding damage to the ears and the use of resistant gennplasm provides good preventive mechanisms. Tropical maize gennplasm has considerable variability for susceptibility and resistance. Opaque-2 maize and other maize types with soft starch show much greater susceptibility to ear rot than nonnal maize. ]t is possible to screen and develop gennplasm having high levels of tolerance to Fusarium ear rot (De Leon and Pandey, 1989). Gibberella ear rot is caused by Gibberella zeae (Plate 27). It occurs after silking in cooler environments with heavy rainfall. It causes the ear to become a reddish colour, with the development of a reddish mould on the infected kernels. Infection starts at the ear tip and moves downwards. Unlike Fusarium ear and kernel rot, where only a few scattered kernels are infected, Gibberella ear rot produces large sections that are infected and rot. If the infection starts early, the whole ear may develop mould with pinkish to reddish colour mould growing between the husk and the ear. In such cases, the husk also develops mould and glues itself to the ear. Quite often the infected and mouldy kernels start germinating on the ear. The fungus produces several mycotoxins. Variability for resistance to the fungus has been reported (Gendloff et al., 1986; Hart, Gendloff and Rossman, 1984). Gennplasm for tropical environments with some level of resistance has been developed. Grey ear rot is caused by Physa/ospora zeae. It occurs in warm wet weather and persists for several weeks following silking. The symptoms in the early stages are similar to Diplodia ear rot. A greyish-white mould develops on and between the kernels.

12 !!!!picot maize: improvement and production The husk leaves become bleached and are tightly glued together. At maturity the diseased ears are slate-grey to black in colour (instead of greyish-brown as in Diplodia ear rot) and remain upright. Hot and wet weather for several weeks after flowering is conducive to the development of grey rot. Control measures are the same as those for Diplodia ear rot. Penicillium ear rot is caused by Penicillium oxalicum, which is the most prominent causal organism involved, though some other species ofpenicillium may also be involved. This disease develops on ears that are damaged mechanically or by insects. The characteristic symptom is the powdery green or blue-green mould growing on and between the kernels starting at the ear tip. The mould appears on the cob surface as well. Aspergillus ear rot is caused by several species of Aspergillus (plate 28). The rots caused by Aspergillus jlavus are the most serious because they are involved in the production of at least two mycotoxins (called aflatoxins) in maize. The fungus Aspergillus niger is the most widespread and causes a black powdery mass of spores. Other species produce a greenish-yellow or tan growth on and between the kernels. Usually, kernels at the tip ofthe ear are infected first. The attack of Aspergillus species can be activated or augmented by the attack of storage grain weevils in the field. Some other factors, such as high temperature and plant stresses particularly moisture stress before harvest are associated with an increased incidence of Aspergillus infection (Widstrom, McWilliams and Wilson, 1984). The problem of the toxic organic compound aflatoxin and other mycotoxins produced by Aspergillus fungi becomes serious when humidity is high at harvest time, when grain is not well-dried to between 15 and 18 percent moisture and when the infected grain is stored with a high moisture content in a humid and hot environment. Aflatoxins are extremely toxic to human beings and animals because oftheir 73 carcinogenic and other toxic effects. Genetic resistance to Aspergillus is reported (Wallin, Widstrom and Fortnum, 1991). Barry, Widstrom and Darrah (1992) reported that two cultivars (M020W x Teosinte and Ibadan B) produced less aflatoxin in pre-harvest grain. Gorman, Kang and Cleveland (1992) concluded from an extensive study that germplasm experiencing a drought environment showed the highest concentration of four aflatoxins B-1, B-2, G 1 and G-2. Additive genetic correlations based on GCA (General Combining Activities) effects among the four aflatoxins were significant, indicating that in general increasing resistance to one toxin may lead to resistance to the other three toxins. The incidence of aflatoxins can be reduced with the use of resistant germplasm and appropriate cultivation and storage conditions (Zuber, Lillehoj and Renfro, 1987). Cob rot is caused by Nigrospora oryzae. The plant does not show any symptoms until the ears are harvested. The ears are very light and chaffy, with the lower end shredded. Ifthe ear is pressed the kernels are pressed into the cob. Maize plants grown in soils with low fertility or plants weakened due to other diseases or injuries - are more susceptible to this fimgus. This disease is quite widespread, but rarely causes economically significant damage. Cladosporium kernel and ear rot is caused by Cladosporium herbarum. This fungus attacks the kernels near the base of the ear, particularly if the kernel tip is injured. The characteristic symptoms are dark, greenishblack, blotched or streaked kernels scattered over the ear. After harvest, infected grains further rot during storage. This disease does not cause economic damages. Rhizoctonia ear rot is caused by Rhizoctonia zeae. It occurs when warm and wet weather persists for long periods. The fungus produces salmon-pink mould growth on the ear. At maturity, infected ears become dull grey with numerous white to salmon coloured to dark brown or black sclerotia that develop on the outer husks.

13 74 Storage moulds Some species of fungi, particularly Penicillium oxa/icum, Aspergillus jlavus and A. niger. that cause kernel rot in the field are also store grain fungi and can cause damage to maize grain during storage. In the field, these fungi attack and damage the kernel when moisture in the grain is quite high, usually above 18 percent. During storage, the fungi attack and damage the grain when moisture is below 18 percent (Smith and White, 1988) but higher than 14 percent. These storage fungi are a problem when maize is harvested by combine and when it is quite wet and not dried properly before storage or transport. In the tropics, most maize is harvested on the ears, which are dried before shelling. The moisture in the grain is low, usually below 14 percent. Under these conditions storage fungi are not a problem. This subject is discussed further in chapter "Post-harvest management". REGIONAL DISEASES These diseases are limited to specific regions, but are of great economic significance in the region where they occur. Two of these are fungal diseases, downy mildews and tar spot. The other two are maize streak and maize stunt, caused by a virus and spiroplasma respectively. Downy mildew disease was first reported in the Philippines and is an important disease in South and Southeast Asia. It is one of the few old world diseases of maize. Now it is found in the tropical maize environments of other continents. It is reported in Mexico, South America, West Africa and also in Egypt. Downy mildews are caused by fungi included in three genera and nine species. These are Peronosclerospora species, syn. Sclerospora species and related fungi Sclerophthora species. Only four of the nine species are important in maize. The most common downy mildews in Asia are Philippine downy mildew caused by Peronosclerospora philippinensis, sorghum downy mildew Maize diseases caused by P. sorghi and sugarcane downy mildew caused by P. sacchari. The fourth type is called brown stripe downy mildew and is caused by Sclerophthora rayssiae var. zeae. The other less important downy mildews are: Java downy mildew caused by Peronosclerospora maydis; leaf splitting downy mildew caused by Peronosclerospora mi~canthi; spontaneum downy mildew caused by Peronosclerospora spontana; crazy top caused by Sclerophthora macrospora; and graminicola downy mildew caused by Sclerospora graminicola. Renfro and Bhat (1981) have listed several alternate hosts harbouring various downy mildews and their role in the spread of the disease. Williams (1984) has made an extensive review of downy mildews in tropical cereals. Until some time ago, the downy mildews were a dreaded disease and caused very heavy damage to the maize crop. The systematics and classification of downy mildew diseases, the fungi causing these diseases and their epidemiology and symptoms have been described by Frederiksen and Renfro (1977). Downy mildews are systemic diseases and the initial infection of plants is usually by oospores, and the fungus grows along with the plant. The first external symptoms are seen when the plant appears to be unhealthy and the young leaves are not dark green (Plate 29). A white downy growth appears on the leaf surfaces and can be easily seen on the lower surface in the morning (plate 30). The plant is stunted and the leaves show white stripes (plate 31, Plate 32). The ear is replaced by leafy structures or nubbins only (more than 95 percent barren) are produced (plate 33). If a normal ear develops, it has only a few scattered kernels. These kernels may be internally infected by the fungus mycelium, which is short lived. The transmission of downy mildew disease in maize by seed has not been conclusively demonstrated (as it has been in sorghum and pearl millet). Substantial work has been done on the genetics of resistance to various downy mildews. Landraces of maize as well as

14 ,!!!!!,!caf maize: improvement andproduction agronomically superior sources of resistance have been identified. Renfro (1985) has provided a brief summary ofwork on genetic resistance to various downy mildew species. polygenic resistance has been reported for all species of downy mildew. Only in the case of sugarcane downy mildew in Taiwan, Province of China, has monogenic resistance been reported (Chang, 1972). Kaneko and Aday (1980) concluded from a series of studies that resistance to P. philippinensis is governed by a polygenic system. Recently, De Leon et af. (1993) also confioned from studies under artificial inoculation that resistance is polygenic and controlled mainly by additive effects. Susceptibility is largely governed by dominance and epistatic effects. Quantitative inheritance showed a strong threshold effect to changes in disease severity. Resistance showed a dominant expression under low disease pressure. Under moderate disease pressure resistance showed partial dominance, while under heavy disease pressure susceptibility became dominant. A completely resistant variety for heavy disease pressure is not yet available. Best varieties show about an 80 percent level ofresistance under heavy downy mildew disease pressure. In sorghum, a downy mildew polygenic system, with both dominance and additive genetic variance, has been reported that controls resistance to the disease (Singburaudom and Renfro, 1982). Resistance to brown stripe downy mildew is also controlled by a polygenic system with additive effects being prominent' and with some partial dominance component (Renfro, 1985). Resistant varieties and hybrids are available for all types of downy mildews and the problem of this disease has been very well contained. Resistance to downy mildew developed in Asia against Philippine and sugarcane downy mildews also shows resistance to sorghum downy mildew. In addition, seed treatments are very effective against downy mildews (Frederiksen and Odvody, 1979). The disease has also been 75 avoided or kept under control with crop rotation and by avoiding plantings with a host crop (Siradhana et al., 1978). Since the varieties and hybrids do not show complete resistance under heavy disease pressure, it is advisable to use resistant germplasm with appropriate cultural practices to avoid the build-up ofdisease pressure. Crazy top is caused by Sclerophthora macrospora. Although crazy top is a widespread disease, it is considered a minor disease and only in occasional localized spots where there is severe infection it causes some economic damage. It affects maize, teosinte and maize x teosinte hybrids and is found on 140 grass species. The disease causes excessive tillering of the infected plant, with rolling and twisting of the new leaves. The most obvious symptom is on the tassel, which becomes excessively branched and shows renewed vegetative growth or phyllody. Hence, the name ofthe disease crazy top. The pathogen is carried by seed, but is readily killed during the grain drying process and also during storage (Smith and White, 1988). A waterlogged situation favours crazy top. Improved field drainage provides a good control measure. Genetic resistance to the fungus is also known. The tar spot disease complex is caused by Phyllachora maydis (Plate 34) and the associated fungi Monographella maydis and Coniothyrium phyllachorae. The disease occurs in the mid-altitude areas of Mexico and also in cool lowland tropical environments in Mexico and some other countries of Central America. The symptoms appear as very small black spots on the upper surface of the lower leaves that progress successively to the upper leaves. The epidemiology has only recently been worked out (Dittrich, Hock and Kranz, 1991; Hock et al., 1992). The disease can be controlled with a foliar spray of fungicides when the first spots appear. Monogenic resistance against tar spot has also been found and resistant germplasm has been

15 _. developed (Gonzalez et al., 1992; Vasal, Gonzalez and Srinivasan, 1992). Maize stunt disease is found in the southern United States, Mexico and Central America (Plate 35, Plate 36). It is caused by a Spiroplasma lamkelii, which is transmitted by the Dalbulus species of leafhoppers. In addition to maize, the disease also infects various species of teosinte. The disease is transmitted in the very early stages of seedling growth. The first symptoms are visible as chlorosis ofthe leaf margins ofthe whorl leaf. The lower older leaves then become reddened as in the case of plants suffering from phosphorus deficiency in cold weather conditions. New leaves show chlorotic spots that develop into chlorotic stripes extending up to the tip of the leaf. Plants are stunted and produce several small ear shoots in the leaf axil instead of one single well-developed ear. Genetic resistance has been screened and resistant varieties and hybrids are available that have minimized the losses caused earlier by maize stunt disease (De Leon, 1983). Maize streak disease is important in sub Saharan Africa and so far is confined to this area (Plate 37, Plate 38). It is caused by a virus that is transmitted through the Cicadlliina species ofleafhoppers. The disease is reported to cause economically significant damages in the lowland tropical to midaltitude environments of sub-saharan Africa, particularly when the crop suffers from drought. In favourable conditions, when moisture is not a limiting factor, the plant is able to outgrow the virus infection without appreciable reduction in yield. The infected plant shows white streaks running along the leaf, and the plant is stunted. Under heavy infection, plants do not produce ears and death of the plant may occur. The disease can be effectively controlled with the application ofa systemic insecticide, which' reduces the population of leafhoppers and the spread of the virus. Good sources of resistance have been identified. Resistance was reported to be controlled by a single gene with modifiers Maize disease (Storey and Howland, 1967) and by three major genes with modifiers (Bjamason, 1986). Kim et al. (1989) reported that resistance is controlled by two to three genes and can be easily transferred to superior germplasm. Varieties and hybrids with good levels of resistance are available for various maizegrowing environments of sub-saharan Africa (Reynaud, Guinet and Marchand, 1988). OTHER VIRAL DISEASES Other viral diseases have been reported on maize, only a few of which are widespread. Maize dwarf mosaic virus (MDMV) is included in the same group as sugarcane mosaic virus (SCMV), Johnson grass mosaic virus (JGMV) and other less important polyviruses. MDMV and SCMV are widespread in the tropics. These viruses are transmitted mechanically through plant sap by a vector aphid (Rhopalosiphum maidis). They affect several cereal crops including sugarcane. The first symptoms are the presence of a mosaic pattern of green and chlorotic tissues on the young leaves. Later, leaves may develop general chlorotic streaks, and plants may show a purple colour and become stunted. Maize stripe virus is also reported to be widespread in the tropics. It is transmitted by leafhopper Peregrinus spp. Chlorotic bands running from the base to the tip of the young leaves are typical symptoms. Other virus diseases are reported that are not widespread and are generally limited to the Americas. These are: maize bushy stunt disease, maize chlorotic dwarf virus, maize chlorotic mottle virus, maize lethal necrosis, maize mosaic virus 1 and maize fine stripe virus (Plate 39) (De Leon, 1984). Maize chlorotic mosaic virus is reported to be transmitted by thrips (Jiang, Meinke and Wright, 1992). Genetic resistance is available for several of the viral diseases and is controlled by a few major genes, usually one to two, for example, in maize dwarf mosaic virus, maize mosaic virus and maize stripe mosaic virus (Renfro, 1985).

16 Tropical maize: improvement and production ~ STRIGA Striga (also called witchweed), Striga asiatica and S. hermonthica, are two parasitic weeds that infect the maize crop in Africa and also in Asia (Hassan, Ransom and Ojiem, 1995). Striga attaches itself to the roots of the maize plant shortly after germination and is parasitic on maize for its water and nutrient requirements. The parasite further exerts a potent phytotoxic effect on the maize plant thus causing a reduction in yield, which is in excess of what would be expected from competition for nutrients and water (Ransom, Eplee and Palmer, 1990). Striga is a poor maize environment disease and occurs when a crop is grown under low fertility and low moisture conditions. Improving soil fertility, incorporating maize stover in the soil to add organic matter and hand pulling Striga plants are effective in controlling the weed (Odhiambo and Ransom, 1995). Kim (1994) reported that there is evidence for quantitative inheritance with polygenic control oftolerance to Striga hermonthica. Screening of maize genotypes for resistance/tolerance to Striga and the possibility of developing tolerant germplasm is being investigated (Kim and Adetimirin, 1995). REFERENCES Anonymous, A compendium of com diseases. Urbana, IL, USA, University of Illinois and Extension Service, United States Department of Agriculture Publication. Barry, D" Widstrom, N.W. & Darrah, L.L Maize ear damage by insects in relation to genotype and aflatoxin contamination in preharvested maize grain. J. Con. Entomol., 85: BergqUist, RR Inheritance estimates ofresistance in maize (Zea mays) to gray leaf spot (Cereospora zeae-maydis). Abstr. Phytopath., 75: Bernardo, R, Bourrier, M. & OUvier, J.L. T Generation means analysis of resistance to head smut in maize. Agronomie, 12: Bjarnason, M Progress in breeding for resistance to the maize streak virus disease. In B. Gelaw, ed. To Feed Ourselves. Proc. 1st Eastem. Central and Southern Africa Reg. Maize Workshop, Lusaka, zambia, p Mexico, DF, CIMMYT. Bojanowski. J Studies of inheritance of reaction to common smut in com. Theor. Appl. Genet., 39: Bubeck, D.M., Goodman, M.M., Beavis, W.D. & Grant, D Quantitative trait loci controlling resistance to gray leaf spot in maize. Crop Sci., 33: Carson, M.L. & Hooker, A.L Inheritance of resistance to anthracnose leaf blight in five inbred lines of com. Phytopathology. 71: Chang, S.C Breeding for sugarcane downy mildew resistance in com in Taiwan. In Proc. 8th Inter-Asian Com lmprov. Workshop. p New Delhi, The Rockefeller Foundation. De Leon, C Conceptos fitopatol6gicos en el mejoramiento de poblaciones de maiz. In Proc. 10th Reunion de Especialistas en Maiz de la Zona Andina, Santa Cruz, Bolivia. Cali, Colombia, CIMMYT. De Leon, C Maize diseases, a guide for field identification. Mexico, DF, CIMMYT. De Leon, C., Ahuja, v.p., Capio, E.R. & Mukerjee, B.K Genetics of resistance to Philippine downy mildew in three maize populations. Indian J. Genet. Pl. Breed.. 53: De Leon, C. & Pandey, S Improvement of resistance to ear and stalk rots and agronomic traits in tropical maize gene pools. Crop Sci., 29: Dittrich, U., Hock, J. & Kranz, J Germination of Phyllachora maydis ascospores and conidia of Monographella maydis. Cryptogamic Bot., 2/3:

17 78 Diwakar, M.e. & Payak, M.M Gennplasm reaction to Pythium stalk rot of maize. Indian Phytopath., 28: Dodd, J.L The role ofplant stresses in development of com stalk rots. Plant Dis., 64: Donahue, P.J., Stromberg, E.L. & Myers, S.L Inheritance ofreaction to gray leaf spot in a diallel cross of 14 maize inbreds. Crop Sci., 31: Draganic, M. & Boric, B Survey of studies on maize resistance to stalk and ear rot pathogens in Yugoslavia. zartita Bilja. 42: EI-Itriby, H.A., Khamis, M.N.,.EI Demerdash, RM. & EI-Shafey, H.A Inheritance of resistance to latewilt (Cephalosporium maydis) in maize. In Proc. 2nd Medit. Con! Genet.. Cairo, Egypt, p Cairo, Mediterranean Congress ofgenetics. Frederiksen, RA Head smuts ofcom and sorghum. In RD. Loden & D. Wilkinson, eds. Proc. 32nd Ann. Com and Sorghum Ind Res. Con!, Chicago, Illinois, p Washington, DC, ASTA. Frederiksen, R.A. & Odvody, G Chemical control of sorghum downy mildew. Sorghum Newsl., 22: 129. Frederiksen, RA. & Renfro, B.L Global status of maize downy mildew. Ann. Rev. Phytopath.. 15: GendlofT, E.H., Rossman, E.e., Casale, W.L., Isleib, T.G. & Hart, L.P Components of resistance to Fusarium ear rot in field com. Phytopathology, 76: Gonzalez, Re., Vasal, S.K., Srinivasan, G. & Eaton, D.L Progress from selection for Tarspot resistance in four CIMMYT populations. Abstract, Int. Crop Sci. Congo I, Ames, la, USA. Gorman, D.P., Kang, M.S. & Cleveland, T Combining ability for resistance to field aflatoxin accumulation in maize grain. Plant Breed.. 109: Maize diseases Halseth, D.E., Pardee, W.D. & Viands, D.R Inheritance of resistance to Helminthosporium carbonum race 3 in maize. Crop Sci.. 31: Hart, L.P., GendlofT, E.H. & Rossman, E.e Effect of com genotype on ear rot infection by Gibberella zeae. Plant Dis., 68: Hassan, R, Ransom, J.K. & Ojlem, J The spatial distribution and farmers strategies to control Striga in maize: survey results from Kenya. In D.C. Jewell, S.R. Waddington, J.K. Ransom & K. V. Pixley, eds. Maize Research for Stress Environments. Proc. 4th Eastern and Southern Africa Reg. Maize Con!, Harare, Zimbabwe, p Mexico, DF, CIMMYT. Hock, J" Dittrich, U., Renfro, B.L. & Kranz, J Sequential development ofpathogens in the maize tarspot disease complex. Mycopathologia, 117: Hooker, A.L A second major gene locus in corn for chlorotic lesion resistance to Helminthosporium turcicum. Crop Sci., 17: Hooker, A.L Genetics of disease resistance in maize. In D.B. Walden, ed. Maize breeding andgenetics, p New York, NY, USA, 1. Wiley & Sons. Jiang, X.Q., Meinke, L.J. & Wright, RJ Maize chlorotic mottle virus in Hawaiian-grown maize: vector relations, host range and associated viruses. Crop Prot.. II: Kaneko, K. & Aday, B.A Inheritance of resistance to Philippine downy mildew of maize, Peronosclerospora philippinensis. Crop Sci., 20: Khan, A.Q. & Paliwal, R.L Inheritance of stalk rot resistance in maize. Indian J. Genet. Pl. Breed, 39: Khan, A.Q. & Paliwal, R.L Combining ability for stalk rot resistance in maize. Indian J. Genet. Pl. Breed, 40: Kim, S.K Genetics ofmaize tolerance

18 Tropical maize: improvement andproduction - of Striga hermonthica. Crop &i., 34: Kim, S.K. & Adedmirln, V.O OveIView of tolerance and resistance of maize to Striga hermonthica and S. asiatica. In D.C. Jewell, S.R. Waddington, J.K. Ransom & K,y. Pixley, eds. Maize Research for Stress Environments. Proc. 4th Eastern and Southern Africa Reg. Maize Coni, Harare, Zimbabwe, 1994, p Mexico, DF, CIMMYT. Kim, S.K. & Brewbaker, J.L Inheritance ofgeneral resistance in maize to Puccinia sorghi Schw. Crop Sci., 17: Kim, S.K., Efron, Y., Fajemisin, J.M. & Buddenhagen,I.W Mode ofgene action for resistance in maize to maize streak virus. Crop Sci., 29: Kroeger, W Investigations into the relationship between root and stalk rot of maize. Zeitschrift juer Pj1anzenk. und PjIanzens., 98: LaI, B.B. & Chakravarti, B.P Root and collar inoculation and control of brown spot of maize by post-infection spray and soil application of systemic fimgicides. Plant Dis. Rep., 61: LattereII, F.M. & Rossi, A.E Gray leaf spot of com: a disease on the move. Plant Dis. Rep., 67: Lu, n.s., Tsai, w.n., Shieh, G.J. & no, C.L Agric. Res. China, 39: Mercado, A.C. & Lantican, R.M The susceptibility of cytoplasmic male sterile lines ofcom to Helminthosporium maydis Nisikado & Miv. Philipp. Agric., 45: Odhiambo, G.D. & Ransom, J.K Long term strategies for Striga control. In D.e. Jewell, S.R. Waddington, J.K. Ransom & K.V. Pixley, eds. Maize Research for Stress Environments. Proc. 4th Eaftern and Southern Africa Reg. Maize Coni, Harare, Zimbabwe, 1994, p Mexico, DF, CIMMYT. Poehlman,.I.M Breeding field crops, 79 3rd ed. Westport, CT, USA, AVI Publishing. Ransom, J.K., Eplee, R.E. & Paimer, A.F.E Estimates of the competitive and phytotoxic effects of Striga on maize. Agron. Abstr., p.61. Reifschneider, F.J.B. & Amy, D.C Yield loss ofmaize caused by Kabatiella zeae. Phytopathology. 73: Renfro, B.L Breeding for disease resistance in tropical maize and its genetic control. In A. Brandolini & F. Salamini, eds. Breeding strategies for maize production improvement in the tropics, p Rome, FAO, Florence, Italy, Istituto Agronomico per L'Oltremare. Renfro, B.L. & Bhat, S Role of wild hosts in downy mildew diseases. In D.M. Spencer, ed. Downy mildew diseases, p New York, NY, USA, Academic Press. Reynaud, B., Guinet, I. & Marchand, J.L IRAT/CIRAD breeding programme for virus resistance. In Towards Self Sufficiency. Proc. 2nd Eastern, Central and Southern Africa Reg. Maize Workshop, p Harare, CIMMYT. Saxena, K.M.S. & nooker, A.L A study on the structure of gene Rp3 for rust resistance in Zea mays. Can. 1. Genet. Cytol., 16: Scott, G.E., King, S.B. & Armour, J.W., Jr Inheritance of resistance to southern com rust in maize populations. Crop Sci., 24: Shehata, A.n Gene action involved in the manifestation of late-wilt (Cephalosporium maydis) of maize. Egypt. 1. Genet. Cytol., 5: Singburaudom, N. & Renfro, B.L Heritability of resistance in maize to sorghum downy mildew (Peronosclerospora sorghi (Weston and Uppal) e.g. Shaw). Crop Prot., 1: Siradhana, B.S., Dange, S.R.S., Rathore,

19 80._ =.::.=.::..-=:..:::-=::. Maize diseases R.S. & Singh, S.D Ontogenic predisposition of Zea mays to sorghum downy mildew. Plant Dis. Rep., 62: Smith, D.R. & White, D.G Diseases of corn. In G.F. Sprague & J.W. Dudley, eds. Com and com improvement, 3rd ed., p Madison, WI, USA, American Society ofagronomy. Storey, H.H. & Howland, A.K Transfer of resistance to the streak virus into east African maize. East Africa Agric. Forest. J., 33: Thompson, D.L. & Bergquist, R.R Inheritance of mature plant resistance to Helminthosporium maydis race a in maize. Crop Sci., 24: Ullstrup, A.J Highlights in com pathology during the past half-century. 9th Ann. Brazilian Phytopath. Soc. Meeting Proc., p Brasilia, Brazilian Phytopath. Society. UUstrup, A.J Diseases of corn. In G.F. Sprague, ed. Corn and corn improvement. p Madison, WI, USA, American Society ofagronomy. UUstrup, A.J Evolution and dynamics of com diseases and insect problems since the advent of hybrid corn. In D.B. Walden, ed. Maize breeding and genetics, p New York, NY, USA, J. Wiley & Sons. Vasal, S.K., Gonzalez, F. & Srinivasan, G Genetic variation and inheritance of resistance to the "Tar Spot" disease complex. Maize Genet. Coop. Newsl., 66: 74. WaUin, J.R., Widstrom, N.W. & Fortnum, W.A Maize population with resistance to field contamination by aflatoxin B-1. J. Sci. Food Agric., 54: Wellman, F.L Tropical American plant disease (neotropical phytopathology problems). NJ, USA, The Scarecrow Press. Widstrom, N.W., McWilliams, W.W. & WUson, D.M Contamination of preharvest com by Aflatoxin. In H.D. Loden & D. Wilkinson, eds. Proc. 39th Ann. Com and Sorghum Ind. Res. Coni, Chicago, Illinois, p Washington, DC, ASTA. Williams, R.J Downy mildews of tropical cereals. Adv. Plant Pathol., 2: Zuber, M.S., Anisworth, T.C., Blanco, M.H. & Darrah, L Effect of anthracnose leaf blight on stalk rind strength and yield in FI crosses in maize. Plant Dis., 65: Zuber, M.S., LiUehoj, E.B. & Renfro, B.L., eds Aflatoxin in Maize. A Proc. of the Workshop. Mexico, DF, CIMMYT.