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moniliforme occurs mainly on individual kernels or on limited areas of the ear (Photos 61, 62). Infected kernels develop a cottony growth or may develop white streaks on the pericarp and germinate on the cob. Ears infested by earworms are usually infected with F. moniliforme. The fungus produces mycotoxins known as fumonisins, which are harmful to several animal species.
67Ergot, horse’s toothClaviceps gigantea
This disease (anamorph Sphacelia sp.) is endemic to certain high, cool, humid areas of the central plateau of Mexico. Infected kernels grow into large fungal structures known as sclerotia along with normal healthy kernels (Photo 63). In early stages of infection, sclerotia are pale colored, soft and slimy, finally hardening toward harvest time. These sclerotia do not produce the black powder characteristic of common smut. When sclerotia are dropped on the ground, they germinate and develop many head-like structures (stromata) that release new spores when the maize plants silk the following season (Photo 64).
The pathogen is closely related to the fungus that causes ergot of rye, and also produces toxic alkaloids.
68 63 64 69 65 66 67 70 Charcoal ear rot Macrophomina phaseolina Like charcoal stalk rot (see page 57), the disease can be found in hot, humid areas with dry periods, mainly during flowering time. At harvest kernels are pale yellow with black streaking below the pericarp, and the ear is loose and chaffy.
Kernels are easily removed from the cob, and they show small, round, black, pinhead-like sclerotia on the surface (Photos 65-67).
Plants affected by charcoal stalk rot do not necessarily develop ear rot from the same pathogen.
The disease is widely distributed, and the causal fungus normally overwinters on plant residues.
Infected ears are chaffy and lightweight. Kernels are discolored and easily removed from the cob. Under close examination, cob tissues and kernel tips show small black masses of spores (Photos 68, 69).
72 68 69 73 70 74 Gray ear rot Physalospora zeae (syn. Botryosphaeria zeae) (Anamorph: Macrophoma zeae) Hot, humid weather for several weeks after flowering favors development of this ear rot. Early symptoms are very similar to those caused by stenocarpella ear rot, where a white-gray mycelium develops between kernels and husks, which become bleached and glued together. In the later stages of infection, the two fungi
can be readily identified:
(a) Gray ear rot. Ears have a distinct black color; the mycelium is also dark and develops small sclerotia (specks) scattered throughout the cob (Photo 70, courtesy Dr. A. J. Ullstrup).
(b) Stenocarpella ear rot (see page 83). The ear is gray-brown and the mycelium is white, with small black pycnidia on the cob and kernels.
Common smut occurs throughout most maize growing regions, but can be more severe in humid, temperate environments than in hot, humid, tropical lowlands.
The fungus attacks ears, stalks, leaves, and tassels (Photos 71-73). Conspicuous closed white galls replace individual kernels. In time the galls break down and release black masses of spores that will infect maize plants the following season. The disease is most severe in young, actively growing plants and may stunt or kill them.
This is easily distinguished from head smut by the lack of host vascular bundles that appear as fibers in smut-infected ears.
76 71 73 72 77 74 75 78 Botryodiplodia or black kernel rot Botryodiplodia theobromae The disease has been reported in India, Nigeria, Pakistan, and Thailand, and to a lesser extent in the Americas. The same fungus can produce stalk rot with a conspicuous black discoloration in moist, hot environments (see page 58).
Affected ears develop deep black, shiny kernels (Photos 74, 75), and husk leaves can also turn black and be shredded.
There are no reports of economic losses from this disease.
This disease is common in hot, lowland tropical and subtropical areas. Infected kernels show white streaks in the pericarp (Photo 76). The symptoms are similar to those of kernels infected by Fusarium moniliforme.
Hormodendrum ear rot Hormodendrum cladosporoides (syn. Cladosporium cladosporoides), C. herbarum There are no reports of economic losses from this disease.
Dark brown-green streaks on kernels start at the kernel and cob bases. When damage is complete, ears look dark and lightweight (Photo 77). In some instances, fungal penetration results from physical injury to kernel tips.
80 76 77 81 78 79 82 Stenocarpella ear rot Stenocarpella maydis, syn. Diplodia maydis, S.
macrospora, syn. D. macrospora Stenocarpella ear rots are commonly found in hot, humid maize-growing areas.
Maize ears show characteristic development of irregular bleached areas on husks. These areas enlarge until the husks become completely dried, although the plant is still green. If husks are removed, ears appear chaffy and bleached, with a white, cottony growth between the kernels (Photo 78). Late in the season, many small, black pycnidia form on kernels and cob tissues (Photo 79). These pycnidia serve as sources of inoculum for the following season’s crop. Microscopic observation of the spores is the only way to identify which pathogen is present.
Severely infected ears are very light. Infection more frequently occurs through the shank and moves from the cob to the kernels. Stem borer injury in the ear often increases incidence of this disease.
Stenocarpella maydis produces the mycotoxin diplodiatoxin and S. macrospora produces diplodiol, both harmful to birds.
This pathogen appears in areas with high temperatures and high relative humidity. It spreads rapidly in the host plant and quickly kills it.
Infected plants show a dark color and water soaking at the base of the stalk (Photos 80, 81) and lodge, dying shortly after tasseling.
The bacterial decomposition produces a characteristic, unpleasant odor.
84 80 81 85 82 83 86 Stewart’s wilt Erwinia stewartii, syn. Pantoea stewartii The pathogen is reportedly transmitted by maize flea beetles (Chaetocnema pulicaria) and also at very low frequency through infected seed. With early infection, lesions are first water-soaked, turning long and pale yellow with irregular margins running the length of the leaves (Photo 82). Infection may move into the stem, causing a general stunting, wilting, and plant death. Severely infected plants that set seed develop small nubbins with few kernels. Late infection can cause severe leaf necrosis but does not lead to wilting (Photo 83).
Feeding wounds from the insect vector serve as points of entry for the pathogen, which is carried from one season to the next by the flea beetle.
No substantial crop damage has been reported from this disease, although it may be of concern where susceptible germplasm is being utilized in certain hot and humid areas.
Bacterial stripe affects susceptible maize plants from seedling to post-flowering stages. Leaves develop several small, pale-green lesions. Under optimum weather conditions, lesions expand along veins producing a conspicuous striping, mainly in the youngest leaves; stripes later dry and brown (Photo 84), often with shredding of the infected leaf tissue. Severe damage of the top leaves results in tassel rotting, when dead leaves enclose the tassel (Photo 85).
88 84 85 89 86 90 Maize chlorotic dwarf virus (MCDV) Infected plants initially show small chlorotic spots developing later into a general chlorosis in the whorl leaves (Photo 86). Plants become stunted due to shortening of internodes, and leaves may become reddish late in the season, resembling the reddening symptoms caused by corn stunt and maize bushy stunt.
MCDV is transmitted by the leafhoppers Graminella nigrifrons and G. sonora for an extended period of time after they have fed on infected plants. Johnsongrass serves as a reservoir host for the virus and the vector when maize is not being grown. So far this disease has been found only in the continental United States, but probably has a wider distribution.
91Maize chlorotic mottle virus (MCMV)
In early stages, the youngest leaves show fine chlotoric spots that coalesce and develop into broad chlorotic stripes along the veins. These chlorotic stripes contrast with dark green tissue when observed against the light (Photos 87, 88). Leaves showing chlorosis finally die.
Plants are stunted because of shortened internodes.
Infected plants produce fewer and smaller ears. In most cases, the male inflorescence is malformed.
The virus is transmitted mainly by several chrysomelid leaf beetles such as Chaetocnema pulicaria and Diabrotica spp., over a short period of time. Reports indicate that it is transmitted at very low rates via infected seed.
When MCMV occurs in combination with maize dwarf mosaic virus (MDMV) or wheat streak mosaic (WSMV), it produces a severe reaction known as maize lethal necrosis (MLN; see page 96).
92 87 88 93 89 91 90 94 Maize dwarf mosaic virus (MDMV) Sugarcane mosaic virus (SCMV) These viruses are transmitted by several genera and species of aphids, including Rhopalosiphum maidis (Fitch) and also by seed at low rates (Photo 89). After feeding on an infected plant, the aphid can immediately transmit the virus. These pathogens can infect other grass and cereal hosts, such as sorghum, Johnsongrass, and sugarcane. No infection occurs in broad-leaf plants.
Infected plants develop a distinct mosaic— irregularities in the distribution of normal green color—on the youngest leaf bases (Photo 90). Sometimes the mosaic appearance is enhanced by narrow chlorotic streaks extending parallel to the veins. Later on, the youngest leaves show a general chlorosis, and streaks are larger and more abundant (Photo 91). As plants approach maturity, the foliage can turn purple or purple-red.
Depending on time of infection, there may be severe stunting of the plant. Plants infected early may produce nubbins or be totally barren.
In China, SCMV has been reported as seriously affecting maize production.
This disease results from combined infection by two viruses: maize chlorotic mottle virus (MCMV) and either maize dwarf mosaic virus (MDMV) or wheat streak mosaic virus (WSMV). No lethal necrosis will develop if only MDMV and WSMV occur together. Infected plants are short. The leaves show chlorosis and die at about flowering time (Photo 92). There is no ear development in plants infected during early stages of growth.
96 92 97 93 94 98 Maize mosaic virus I (MMV) The disease has been found in many countries worldwide. The vector is the planthopper Peregrinus maidis, which will transmit the virus for most of its life after feeding on an infected plant. The vector also transmits maize stripe virus. Hosts for MMV include maize, sorghum, and a few other graminaceous species. Plants are most susceptible when infected 4 to 6 weeks after emergence. The most conspicuous symptoms are dwarfing and striping along the veins (Photos 93, 94).
Degree of dwarfing depends on plant age at infection. Because internodes are shortened, leaves appear “crowded” and erect. Fine continuous stripes develop along the veins beginning at leaf bases.
Later symptoms include shorter-than-normal leaves with a rough and fleshy appearance. Stripes may be dark yellow, and may finally become necrotic. Prior to total necrosis of the tissues, foliage turns red or dark purple.
This disease has been reported in tropical locations in Africa, Asia, and the Americas, including Hawaii, India, and Australia.
Initial symptoms on the leaves are small chlorotic specks that later develop into narrow parallel chlorotic stripes along the younger leaves. The chlorotic bands can vary in width and extend from the base to the tip of the leaves (Photos 95, 96). Infected plants usually show stunting and bending of the tassel. Normally ear development and yield are reduced.
The virus is transmitted by the planthopper Peregrinus maidis, and the vector will transmit the virus for most of its life after feeding on an infected plant. The vector can also transmit maize mosaic virus.
100 95 96 101 97 98 102 Maize streak virus (MSV) The disease, reported first from East Africa, has now extended to many other African countries. The virus is transmitted by Cicadulina spp. leafhoppers.
Cicadulina mbila (Naude) is the most prevalent vector, and will transmit the virus for most of its life after feeding on an infected plant. Early disease symptoms begin within a week after infection and consist of very small, round, scattered spots in the youngest leaves. The number of spots increases with plant growth; they enlarge parallel to the leaf veins. Soon spots become more profuse at leaf bases and are particularly conspicuous in the youngest leaves. Fully elongated leaves develop a chlorosis with broken yellow streaks along the veins, contrasting with the dark green color of normal foliage (Photos 97, 98). Severe infection causes stunting, and plants can die prematurely or are barren. Many cereal crops and wild grasses serve as reservoirs of the virus and the vectors.
103Maize rough dwarf virus (MRDV)
This virus has been known for several years in countries in Europe and Asia, as has its variant, “Mal de Rio Cuarto,” in central Argentina and Uruguay.
Infected plants show stunting; secondary veins become chlorotic and thick. The leaves become leathery and younger leaves roll upwards with characteristic overgrowths (enations) on the veins on the underside (Photo 99). Symptoms can be detected in seedlings at approximately one month of age. In later stages, infected plants develop a reddish color and form either no ear or simply nubbins which are often bent at the tip. The tassels and upper leaves are malformed and underdeveloped (Photo 100).
The virus is transmitted by several delphacid planthoppers including Laodelphax striatellus for MRDV and Delphacodes kuscheli for MRCV.
Transmission is for most of the life of the vector after feeding on an infected plant, and females can pass the virus to the next generation through the eggs.