Maize Disease PDF

Course Title: Diseases of Field and Horticulture Crops and their Management-I (PP-353) Topic: Diseases of Maize Dr. L. SANAJAOBA SINGH Assistant Professor (Plant Pathology)...

Course Title: Diseases of Field and Horticulture Crops and their Management-I (PP-353) Topic: Diseases of Maize Dr. L. SANAJAOBA SINGH Assistant Professor (Plant Pathology) College of Agriculture, Kyrdemkulai, CAU, Meghalaya  1. Stalk Rot: Caused by Fungi and Bacteria. In fungi, Stalk rot symptoms are caused by three different fungi viz Fusarium spp., Macrophomina sp. and Cephalosporium sp. Bacterial stalk rot: Erwinia chrysanthemi pv. Zeae but Erwinia dissolvans pv. Zeae and Pseudomonas syringe pv. lapsa also found associated with stalk rot symptoms. In India, Bacterial stalk rot is reported by Prasad from Pusa (Bihar). This disease is quite destructive in high rainfall areas and occurs in epidemic form in the foothills. The disease reduces both fodder as well as grain yield.  Fusarium Stalk Rot: Symptoms:  Fusarium spp. are responsible for producing stalk rot symptoms in dry and warm climate.  The initial disease incidence is more severe in low and tropical areas later is more prevalent in cooler highlands. Senescence  The symptoms appear when the crop enters senescence phage. It affect the roots, crown region and lower internodes. Affected plants have shredded pith that may be a whitish-pink to salmon color and die prematurely. Brown streaks may be observed on the lower internodes. Permanent wilting of the leaves and drying of the whole plant. Stalks feel spongy when squeezed and may be easily crushed or crimped at lower internodes. Plants may lodge when pushed sideways or impacted by wind. The disease is more severe under high plant population.  Pith shredding Fusarium Stalk Rot symptoms Pathogen/ Etiology: Fusarium moniliforme ; F. graminearum ; F. semitectum The pathogens are seed borne with up to 75% of all seed planted being infected. The importance of seed infection to subsequent development of root rot and stalk rot is not clear. The pathogen also overwinters as mycelium in debris on or in the soil, where it can infect the plant directly through the roots causing root rot and lower stalk rot. Two types of conidia are produced, macroconidia and microconidia. Macrocondia are hyaline, curved near the tips, three to five septate and 2.5-5 X 15-60 µm. Micro conidia are abundant single celled, 2-3 X 5-12 µm and borne in chains. Conidiophores are unbranched with branched manophialids Favourable condition:  Temperature may be one factor that determines the extent of invasion of the stalk rot fungi of maize.  Dry and warm climate favour during silking stage of maize predisposed to infection.  The water stress at flowering and high soil temperature help in increasing of the magnitude of the stalk rot symptoms at post flowering stage of maize crop.  Disease incidence was greater in sandy soil than in loam or clay soil. In general, stalk rot incidence and severity increase with increased fertility.  High Temperatures ranging from 80° to 100° F.  Disease cycle: The fungi overwinter as mycelium in corn residue, other dead plant residue, and in corn seed. This fungus is often found growing in healthy stalks and may cause rot only under certain conditions. Spores are spread by wind and splashing water; infection takes place through the roots, wounds in the stalk, or leaf scars. Disease development is favored by warm temperatures (80-100°F) and when a wet midseason follows early season dry weather.  Management: Used of Hybrid Ganga and single cross hybrid CM 202 x CM 111 have shown field resistance Crop rotation. Rotation and tillage will reduce inoculum. Use a tillage system that chops and incorporates residue to break it down Do not use plant populations higher than recommended for the hybrid Soil test and follow fertilizer recommendations; maintain proper nitrogen to potassium balance. Reduce stresses when possible - stalk rots are favored by plant stress following pollination Control leaf diseases with fungicides if necessary Control corn rootworm and corn borer. Scout preharvest to determine stalk condition. Schedule harvest based on stalk quality as well as grain moisture  Bacterial Stalk Rot: Symptoms: Symptoms start from the lower nodes of the plants and affect the stalk up and down to a limited extent. Initial disease symptoms include discoloration of the leaf sheath, which spread further to stalk, leaves and plant topples down in severing condition and a foul odour is detected.  occasionally, the rot cause soft dark decay of rind, but generally the interior of the stalk is rotted. The rind will loses it natural green colour and become pale straw colour giving a cooked appearance. The infected stalks become soft and turn into dry mass of shredded, easily disjoint fibres. Later the stalk breaks and the plant collapses. The first stage of maceration involves the entry of the bacteria to the parenchymatous tissues of plants that have been physiologically compromised, such as by bruising, excess water or high temperature. The next stage involves local maceration as a result of depolymerization of plant cell walls, followed by necrosis of the entire plant.  Due to the complexity of plant cell walls, which consists of polysaccharides, the main ones being cellulose, hemi-cellulose and pectin, a variety of enzymes are accordingly produced by Erwinia chrysanthemi for the efficient breakdown of cell walls. The major enzymes have been found to be pectinases which degrade various components of pectin using different reaction mechanisms. Symptoms of Bacterial Stalk Rot Pathogen/ Etiology: Erwinia chrysanthemi pv. zeae Facultative anaerobe and induce various enzyme resulting in causation of parenchymatous necrosis and vascular wilt. a motile, gram-negative, rod shaped bacterium. It is varying from 0.8-3.2 x 0.5-0.8 μm (average 1.8 x 0.6 μm). There are 3-14, but more usually 8- 11, peritrichous flagellae. The bacterium is produced off white, slimy and shiny colonies on King‟s B Medium.  Favourable environmental conditions: Preferred high temperatures (30 -35 º C) and high relative humidity for infection and disease development. High temperature and humidity important for physiological and metabolic activity of bacterium therefore its growing well and producing sufficient pectolytic enzymes which is important for plant cell degradation. It can be a problem with areas of heavy rainfall or where overhead irrigation is used and the water is pumped from a lake, pond, or slow-moving stream. Disease Cycle: The pathogen is soil borne and lives saprophytically on disease plant debris for about nine month and in the rhizosphere of non-host plants. Natural and slightly acidic soil are favourable for its survival. The pathogen enters the host through injured areas, wounds, stomata or hydathodes, weak spot resulting from extension of endogenous roots and injured brace root. Insect injury, accumulation of water around the stem base and relative high humidity favour infection. high nitrogen without P₂O₅ and K enhance the disease incidence, whereas, high doses of P and K reduce it.  Managements:  Host-plant resistance: Host-plant resistance is the most economic approach to manage this disease. Identification and use of resistance sources in breeding programme have been employed by various researchers. Complete resistance to this pathogen has not been reported. Inbred line CM 104, CM 105, CM 112, CM 202, CM 600, hybrid Ganga Safed 2 and multiple disease resistant (MDR) population MDR 1, MDR 2, TX 325 c and Sona Surya 72 are resistant.  Cultural practices: The pathogen infection can be suppress via organic manure amendment which stimulates the population of beneficial microflora and avoid flooding and excessive irrigation. Ridge sowing method also helps to the farmer to manage that disease.  Chemicals: Streptomycin (dihydro streptomycin sulphate) and terramycin (terramycin hydrochloride) singly and in combination were effective singly and in combination against the bacterium. The antibiotic was effective at all the concentra-tions (25, 50, 100, 250, 500 and 1000 ppm) against Erwinia species but E. chrysanthemi pv. zeae was highly sensitive.  The copper fungicides with combination antibiotics significantly inhibit the growth of pathogen under both conditions (in vitro and in vi-vo).  Bleaching powder were used such as sprinkling of chlorinated water between plant rows or on basal internodes of plants or broad-casting of dust or granules (coated and uncoated; containing 22 and 28% chlorine, respectively) between thé rows were effective to reducing the disease incidence significantly.  2. Downy mildew / Crazy top Symptoms The most characteristic symptom is the development of chlorotic streaks on the leaves. Plants exhibit a stunted and bushy appearance due to shortening of the internodes. White downy growth is seen on the lower surface of leaf. Downy growth also occurs on bracts of green unopened male flowers in the tassel. Small to large leaves are noticed in the tassel. Proliferation of auxillary buds on the stalk of tassel and the cobs is common (Crazy top). Symptoms Pathogen/ Etiology: Sclerophthora macrospora The fungus grows as white downy growth on both surface of the leaves, consisting of sporangiophores and sporangia. Sporangiophores are quite short and Anamorph: Zoosporangia ellipsoid to obovoid, hyaline, stout, branch profusely into series of apical papillate, 60-114 x 28-50 pointed sterigmata which bear um, germinating in water to release kidney-shaped zoospores hyaline, oblong or ovoid sporangia with 2 flagella. (conidia). Teleomorph: Oogonia globose Sporangia germinate directly and to subglobose, wall thickened, infect the plants. In advanced stages, hyaline, 20-48 x 10-29 um, oospores are formed which are producing oospore filling oogonia. Antheridia hyaline, spherical, thick walled and deep kidney-shaped, paragynous. brown. Oospores germinate directly to produce zoosporangia.  Favourable condition:  Low temperature (21-33°C), High relative humidity (90 per cent) and drizzling.  Young plants are highly susceptible. Disease Cycle:  The primary source of infection is through oospores in soil and also dormant mycelium present in the infected maize seeds. Secondary spread is through airborne conidia.  At the onset of the growing season, at soil temperatures above 20°C, oospores in the soil germinate in response to root exudates from susceptible maize seedlings. The germ tube infects the underground sections of maize plants leading to characteristic symptoms of systemic infection including extensive chlorosis and stunted growth. If the pathogen is seed borne, whole plants show symptoms.  Oospores are reported to survive in nature for up to 10 years. Once the fungus has colonised host tissue, sporangiophores (conidiophores) emerge from stomata and produce sporangia (conidia) which are wind and rain splash disseminated and initiate secondary infections. Sporangia are always produced in the night. Germination of sporangia is dependent on the availability of free water on the leaf surface. Initial symptoms of disease (chlorotic specks and streaks that elongate parallel to veins) occur in 3 days. Conidia are produced profusely during the growing season. As the crop approaches senescence, oospores are produced in large numbers.  Management:  Grow resistant varieties and hybrids viz. CO1, COH1and COH2.  Deep ploughing.  Crop rotation with pulses.  Rogue out infected plants.  Treat the seeds with Metalaxyl at 6g/kg.  Spray the crop with Metalaxyl + Mancozeb @ 1kg on 20th day after sowing.  Brown leaf spot of maize Symptoms:  The disease attack the leaf blades, leaf sheath as oval shaped light green bleached or yellow water soaked lesions, which become reddish brown to brown having lighter margins.  Numerous spot developed in a small area giving the leaf blade or sheath a rusty- brown appearance. The spot may coalesce and form a large spots.  The browning of the host tissue is due to necrosis of the affected cells and accumulation of large number of spore of the fungus.  Eventually the affected leaves dry and die prematurely. The fungus attack the lower portion of the plant more than the upper portions.  Stem infection weakens the tissues, which break at the infection point. Pathogen/ Etiology: Physoderma zeae maydis It is an Obligate parasite. The fungus produces coenocytic hyphae and sporangia which are flat, smooth and brown in colour measuring 24-26 x 22-24 µ. The infected lesion contain a large number resting sporangia. The resting spore survive in the disease plant debris or in the soil and carry over the disease from one season to next season. Under the favourable condition, the sporangia open through the lid, liberating uniciliate, hyaline, thin walled zoospore (5-7 x 3-4 µ).  Favourable Conditions: The disease is common in low lying and ill drained filed. High temperature (28-29 °C) and abundant moisture during the early growth period of the host favour the disease development Disease Cycle:  The thick-walled, brown sporangia (resting spores) formed within infected cells enable P. maydis to over season in corn debris or in the soil.  The sporangia are released from infection pustules, disintegrating corn debris, and soil and are carried to susceptible plants by air currents, insects, splashing rain or flowing water, and humans.  Free water is required for infection. When moisture is present in the whorl or behind the leaf sheaths and temperatures are relatively high (23° to 30°C), a sporangium “germinates” to release 20 to 50 swimming zoospores.  The zoospores move about in water for 1 to 2 hours before settling down, becoming amoeba-like, and penetrating young meristematic tissue with fine infection hyphae.  The resulting mycelium enters mesophyll or parenchyma cells and forms larger, vegetative structures (Sammelzellen). Infection commonly occurs in a diurnal cycle (diel cycle), resulting in alternating lateral bands of infected and healthy leaf tissue as it emerges from the whorl. Zoospores of P. maydis can infect corn tissue only during certain hours of the day and within a few hours after being released.  The development of symptoms and the germination of new sporangia occur approximately 6 to 20 days after infection, completing the disease cycle.  Figure: Stages in the life cycle of Physoderma maydis (a ). Two sporangia (Plural)/ sporangium (singular) (resting spores), top view and side view. (b) stage in opening of a sporangium, showing the early stage of zoospore formation. Note the dehisced operculum (lid) being carried up by the enlarging sporangium. (c) Mature zoospores escaping through the ruptured apex of the resting spore. zoospores (d) Three zoospores with a single flagellum from a germinated resting spore. (e) Germinating zoospores, amoeboid stage. amoeba (f) Rhizomycelium within a corn epidermal cell showing young sporangia at the ends of short hyphae. (g) Corn leaf cell filled with mature resting sporangia. (Sammelzellen).  Management:  Filed sanitation reduce the inoculum potential.  Crop rotation reduce the intensity of the disease.  Balance fertilizers should be applied.  Cultivation of resistant varieties is practically feasible and most effective method to manage this disease. Inbred lines AA, BSR 182, C103d, C123, CM 106, CM 108, Cube, GE 440 etc. have been found resistant to the disease.  Fungicides like captan 50 WP and Fermates 76% (ferbam sprayed) in the whorls of maize plants, twice a week for 4 weeks before silking are effective in the management of disease. Benlate, Bavistin and plantvax are also effective.