Here is a list of fifteen major plant diseases with their control measures.
1. Tip Burn of Paddy or Pansukh of Rice:
The names, tip burn, dakhitla, chatra, ukra, kadamoraor pansukh, have been given tea leaf-drying disease of rice known in India for quite some time. It has been described by Dastur (1937) and Mishra and Chakravarty (1955).
The first symptom of the disease is the drying of the leaves. They become less lustrous to bronzing and later become scorched at the top. The drying progresses down along the margin, resulting in the drying of the complete leaf. In advanced stages, the entire plant dries and wilts. The leaves and stalks turn brown. This disease spreads speedily in the field.
The cause of the disease is not properly understood. The disease is common in wet soils or in Poorly-drained fields where the water is allowed to remain stagnant for more than a fortnight. This is because water reduces the supply of oxygen to the roots.
The use of ammonium sulphate has been recommended-by Dastur (1937) to control this disease. According to him the disease is caused by the lack of available nitrogen. He recommended that the fields be drained during the early stages of plant growth and then 15-25 kg of ammonium sulphate/acre be applied. According to Sinha and Singh (1956), green manuring reduces the incidence of tip burn and increases the yield.
2. Blossom End Rot of Tomato:
This disease of tomato fruit is a nutritional disorder thought to be caused by a derangement of the water balance between the leaves and fruits during the growth of the plant. It is characterized by a lesion at the blossom end of the fruit, which occurs while the latter is still green or while it is ripening on the vine. A water-soaked spot appears at the point of attachment of the senescent petals.
It enlarges quite quickly until it is about 2 cm or more in diameter, and at the same time the diseased tissue shrinks, depressing the, surface of the lesion. The colour of the fruit becomes darker and secondary organisms commonly invade the tissues. The diseased portion of the fruit becomes delimited as a sunken, leathery, dark coloured area.
If tomatoes are grown at relatively constant low moisture content, the disease does not develop. If plants are grown at relatively high moisture content, succulent growth is very quick, the rate of transpiration is very high and disease incidence is greater.
Sandy soils are more favourable to blossom end rot. Foster (1937) found that increased amounts of nitrogen are more favourable to the occurrence of the disease when other conditions are also conducive, while higher doses of phosphorus reduce the incidence of disease. The relation of nutrient salt concentrations to the growth of tomato and to the incidence of blossom end rot of the fruit has been studied by Robbins (1937).
At the lowest concentration, where growth is greatest no disease occurs, while at the highest concentration, where there is greatest fluctuation in the rate of transpiration, 80 per cent of the fruits become diseased. That transpiration has an influence by the blossom end rot of tomato was proved by Schroeder (1949).
Schroceder was able to check the disease with emulsified hydrocarbon sprays. Releigh and Chuck a (1944) found that the incidence of disease was greater when the nutrient solution was high in nitrogen, sulphur, magnesium, potassium or chlorine and when it was low in calcium. Lyon et al. (1942) found that the blossom end rot has a correlation with the calcium content.
The most common technique of controlling blossom end rot is to maintain an equable environment and to keep the soil properly moist. This should be taken care of especially when the fruit begins to develop.
3. Heat Canker of Linseed:
It is a non-parasitic disease caused by high soil temperatures near the soil surface.
Heat injury of the cortical tissues of the hypocotyl and stem near the soil line is common flax and other succulent herbaceous plants. If the soils are dark coloured and the surface temperature becomes high enough to kill the cells of young cortical tissues before the plants are large enough to shade the surface, the cortical tissues collapse, which caused in the death of the young seedlings. Due to the collapse of tissues, sunken brown lesions develop on the stems. There is an enlargement of-the cortical tissues above the cankers.
High temperatures can be avoided by early planting. The rows should be drilled from the north to the south. This results in maximum shedding. Damage from this disease can be stopped by higher rates of seeding, using a nurse crop, mulching the soil surface and irrigation.
4. Black Heart of Potato:
The conditions under which this disease develops vary largely. It is known that a number of rather distinct sets of environments produce practically the same result or cause this disease, such as high temperature in transit, poor air circulation in storage and high soil temperature during the growing season.
Bartholomew (1913) explained the fundamental nature of black heart and made a pathological study of the black heart of potato tubers.
He found that he could produce black heart in tubers by exposing them to high soil temperatures for 24-48 hours in an oven heated to 40-42°C. Mann and Joshi (1920) made a chemical study of heart rot or black heart in potato tubers.
They could produce this disease by first coating the tubers with collodion or paraffin or replacing the air in a container with carbon dioxide or nitrogen. Black heart can also be produced by placing tubers in sealed containers. This shows that oxygen is very necessary to prevent the occurrence of black heart on potato tubers.
The centres of potato tubers attacked by black heart show black portions when sliced open, or after being sliced open, the potato tubers undergo a fairly quick change white or pink to brown to dark brown or black. Borthplomew (1915) has studied the growth of the disease.
When a tuber exposed to 40°C for 24 hours is cut open, the interior tissue appears normal in the beginning, but upon exposure to air, pink discolouration occurs which slowly becomes dark brown or black.
This was shown to be an enzymatic effect in which some of the amino acids, specially tyrosine, pass through a series of intermediate compounds to the deeply coloured, relatively stable and insoluble compounds known as melanins.
High temperatures bring about sub-oxidation by stimulating respiration under conditions in which cells in the interior of the tubers cannot secure a sufficient supply of oxygen. Ventilated storage over long periods predisposes potatoes to black heart.
Davis (1976) showed that a disease similar to black heart could due to electric cummt, freezing, immersion in toulene or glycerine and by certain pathogens.
The disease can be significantly checked by avoiding very high or low temperatures and by properly storing potatoes in well airy storage godowns.
5. Mango Necrosis or Black Tip:
The disease was first reported from Bihar and is now well known in Bihar, Uttar Pradesh, West Bengal and Punjab. It is commonly found near the brick kilns in Uttar Pradesh, Bihar, West Bengal and Punjab in northern India.
Black tip of mango is characterized by the necrosis of one third or half of the fruit. The most susceptible varieties are ‘Daseri’, ‘Safeda’ and ‘Langra’. The diseases start as a small, circular, pale patch at the tip of the mango fruit and soon enlarge, become black and cover the tip of the mango fully.
The outer skin of the affected portion becomes fiat and hard. Internally, in the vessels of the mesocarp, are found certain brown deposits which have been provisionally identified as belonging to the group of tannins, flavotannins, flavophenols or their derivatives.
Earlier it was thought that black kiln fumes are direct cause of the disease. Sen (1943), Das Gupta and Verma (1939), Das Gupta and Sinha (1944), working on the disease in Bihar and Uttar Pradesh, advised that the smoke of these gases polluted the air with toxic gases such as sulphur dioxide and that these gases caused the necrosis of the fruit tissues.
In laboratory experiments the disease could be produced by exposing -mango fruits to smoke and sulphur dioxide. Later on Das Gupta and Sen (1960) in their final report stated that there is a deficiency of boron in the mango fruits exposed to brick kiln fumes.
The disease was, however, not attributed to a lacking of boron in the soil but to disturbances in boron metabolism due to the interaction of brick kiln fumes with, certain cell metabolites of mango.
The disease can be checked by spraying borax at 2.7 kg/100 gallons three times in the season, viz., pre-flowering, flowering and immediately after fruit setting.
6. Zinc Deficiency Disease of Citrus:
This disease is very common in many citrus gardens in India. It is also known as mottling foliocellosis.
The main symptom is the production of alternate chlorotic regions and dark green patches in the leaf. The portions near the leaf veins are generally brown and the rest of the leaf is chlorotic.
Due to continual deficiency of zinc in the soil, there is severe stunting of the plant reduction in leaf size, narrowing of the leaf and severe chlorosis. The fruit size is also reduced. The plants become weak and are exposed to root infections and this slowly results in their death.
The application of zinc sulphate to the soil gives a very slow response. Spraying zinc sulphate and lime mixture (zinc sulphate 2.268 kg and quick lime 2.268 kg in 100 gallons of water) is recommended for a quick response.
7. Powdery Mildew of Peas (Pisum sativum L.):
This is distributed all over the world. The disease spreads in epidemic form almost every year when the plants are in the pod stage towards the end of January and in February.
Unlike the downy mildew which is favoured by moist weather, this mildew disease is at its worst when conditions are dry. Several other leguminous crops, such as Medicago, Vicia, Lupinus, Lens esculenta, Trifolium dubium, etc., are attacked.
Uppal observed heavy decrease in pod formation in pea due to serious infection of powdery mildew in Bombay and reported that even one picking was not possible, whereas 6-7 pickings were obtained from a normal crop.
According to Munjal et al. (1963), it attacks cabbage, sugar beet, turnip, clover and lentil. Losses depend on the stage of maturity of the pea crop when infection occurs.
In the early stages, small irregular powdery spots appear on the upper surface of leaves. When plants are, in the flowering and pod stage (in January and February), the disease assumes drastic proportions. The powdery whitish spots completely cover the leaves, petioles, stem and even the pods. The plant shows a greyish white appearance, and the leaves turn yellow and are finally shed. The yield from the crop may be greatly diminished.
The organism responsible for the powdery mildew of peas is Erysiphe polygoni DC. The mycelium consists of delicate and persistent hyphae which are attached to the leaves, by means of appressoria. Hyphae penetrate the epidermis and swell into a lobed and round sac in the epidermal cells. Conidiophores arise vertically from the leaf surface.
Conidia usually form singly (rarely in chains), are ellipsoid, and 31-38 x 17-21 μ. Later in the season, cleistothecia appear as sharp, black specks scattered on the surface of the while mycelium; globose, 85-126 μ in diameter.
Appendages very variable in number and length, mycelioid, sometimes knotty and frequently geniculate, rarely irregularly branched, brown, usually as long as the diameter of the ascocarp, at the most 2-3 times as long. Asci- 3-10, usually 4-8, ovate to broadly ovate or subglobose, 50-60 x 30-40 μ. Ascospores 3-5 rarely 6, 22-27×13-16 μ.
The fungus is an obligate parasite and the disease perennates through cleistothecia in the soil. Ascospores from the perennating cleistothecia first infect the lowermost leaves near the soil. The conidia formed abundantly during primary infection, are responsible for the secondary spread ‘of the disease. This is also suspected to be seed borne.
Field sanitation and cleanliness is important. Diseased plant debris should be collected and burnt in the field. For vegetable crops early varieties are preferred. Dusting with sulphur (200 mesh) is recommended.
Uppal and Starker (1954) found that 1 per cent Karathane dust was superior to sulphur dust in controlling this disease. Singh and Mishra recommended sulphur for controlling the powdery mildew of pea. Shrivastava reported that sulphur dust, Cosan, Blosal, Karathane WD and Thiovit sprays controlled the disease in Rajasthan.
Khatua made a field assessment of systemic and contact fungicides for the control of powdery mildew of pea and showed that the most effective fungicides were Calixin and Karatbane followed by Milstem and Sultaf.
Aureofungin, Morocide and Mucuprax were also effective. The use of seed from disease free areas is recommended Seed treatment with organosynthelic fungicides, especially Captan, Cerenox and Thiram also gives good control.
Out of the 670 genotypes tested, P185, P388 and 6588 proved resistant. It was interesting to note that all the strains which exhibited resistance to powdery mildew belonged to the table pea group (Pisum sativum). The germplasm lines could be utilized for breeding pea varieties resistant to powdery mildew.
8. Powdery Mildew of Apple:
This disease is not indigenous to any specific region. It is very common in the apple orchads of northern India. Nursery plants are damaged more than the adult plants. Peaches (Prunus persica), quince (Cydonia vulgaris) and Photinia spp. are also attacked.
The disease generally appears soon after the buds change into new leaves and shoots. Sometimes buds are so heavily infected in the previous season that they are killed before they develop into leaves.
The affected leaves are longer and narrower than normal leaves and are covered with a whitish growth. In nursery plants, the disease prevents the formation of wood in the stem. Fruit buds suffer more damage than vegetative buds.
The disease is caused by Podosphaera leucotricha Ellis and Ever. The ectophytic mycelium sends saccate haustoria in the epidermal cells. Aerial conidiophores aries from this mycelium on leaves and shoots.
Cleistothecia play a very small part, if any, in the spread of the fungus. In most places, the fungus survives in the form of resting mycelium or encapsulated haustoria in the buds. Secondary spread is by wind-borne conidia.
Effective fungicides include microfine sulphur, lime sulphur, wettable sulphur and Karathane.
Lime sulphur sprays should be undertaken according to the following schedule:
(i) 1:15 dilution when the buds are green,
(ii) 1:35 dilution at the open cluster stage,
(iii) 1: 60 dilution at the blossoming or full pink stage,
(iv) 1: 1 00 dilution when about half the petals have fallen.
Breeding resistant varieties appears to be the best control measure. Some good sources of resistance for breeding varieties are known. Susceptibility to mildew in apple varieties is controlled by one completely dominant gene and is related to weather conditions. There is no evidence of matroclinous inheritance of resistance.
9. Powdery Mildew of Cucurbits:
This is spread all over world. The disease occurs in India almost every year. The same fungus has been reported to attack potato seedling, lettuce, sunflower, castor (Ricinus communis), Antirrhinum orontium, and Sonchus asper.
Humid conditions are good to the disease. The first symptoms are tiny, white, superficial spots on leaves and stems which become powdery as they become large. The superficial white powdery mass may in the last cover the entire host surface.
Black, pin-point-like bodies representing the ascigerous stage of the fungus, appear late in the season on the host surface but are not generally formed in the Indian climatic conditions. Severe infection may lead to premature defoliation of the plant. The fruits remain undersized.
Powdery mildew is a serious widespread disease of cucurbits in India. Erysiphe cichoracearum DC and Sphaerotheca fuliginea infect cucurbits in various parts of the world. Erysiphe cichoracearum is the main causal organism of this disease.
Mycelium is usually well developed and evanescent, but sometimes persistent and effused. Conidia in long chains, are ellipsoid to barrel-shaped and vary in size, 25-45 x 14-26 μ.
Cleistothecia are formed in autumn, gregarious or scattered, globose, becoming depressed or irregular, 90-135μ diam. wall cells usually indistinct, 10-20 μ wide. Appendages are numerous, basally inserted mycelioid, interwoven with mycelium, hyaline to dark brown, 1—4 times as long as the diameter of the ascocarp, rarely branched.
Asci 10-25, ovate to broadly ovate, rarely subglobose, more or less stalked, 60-90 x 25- 50 μ. Ascospores 2, very rarely 3,20-30 x 12-18 μ. Sphaerotheca humuli var. fuliginea Poll.— this fungus usually occurs in the conidial state, particularly on Cucurbitaceae, and has often been confused with Erysiphe cichoracearum.
The conidia on germination form a characteristic forked germ tube distinguishing them from those of E. cichoracearum which on germination produce appressoria.
The patches formed by this fungus are reddish brown. The cleistothecia are distinct in structure from those of Erysiphe. Powdery mildew of cucurbits caused by S.fuliginea is a serious disease in northern India.
Sohi and Nayar obtained perithecial stage of S. fuliginea on several varieties of Luffa leucantha and Cucumis sativus under glasshouse conditions from Aligarh in Uttar Pradesh.
The means of existence of the fungus between successive crops is not very clear. In the areas where cleistothecia are formed, these might be the main mode of perennation from one season to the next.
It is possible that the fungus survives in its conidial stage on wild hosts in a suitable locality and from there the conidia are wind borne to cultivated areas. Heavy dew favours penetration by the germ tube. Penetration is confined to the epidermal cells where spherical haustoria are present.
Blumer distinguished 13 formae species of E. cichoraccarum based on a single species or a single section of a genus.
A safe control measure for controlling E. cichoraccarum in the greenhouse is 1 per cent Bapolysulphide with temperature at 24-25 °C and air humidity at 80 per cent. Sprays with colloidal sulphur and Thiram effectively control Sphaerothecafuliginea.
Karathane has been reported to be effective against powdery mildew of Cucurbits. Systemic fungicides, that is, Benomyl and Bavistin have been found to be equally effective in controlling this disease.
10. Powdery Mildew of Grapevine:
This is spread worldwide. The damage to vines is extensive in Europe and western USA. There are frequent reports from Europe of the complete destruction of the grape crop.
In Afghanistan, the loss in 1958 was estimated at 50-80 per cent, which is equivalent to five million dollars. In India, this disease is common and destructive in Maharashtra, Gujarat, Madras and Andhra Pradesh.
The disease shows its appearance on leaves as white patches on both the surfaces. The affected young leaves distorted. Similar symptoms are also seen on young blossoms and young berries.
When flowers and berries are affected, there is considerable decrease in yield. Young berries, when infected, turn dark, become irregular in form and develop cracks. Diseased vines have a wilted and dwarfed appearance.
The pathogen responsible for this disease is Uncinula necator. Mycelium is usually semi persistent, very thin and effused or forming patches, sometimes evanescent. Conidia are usually in long chains, ellipsoid to almost cylindric.
Cleistothecia are rarely formed, usually epiphyllous, sometimes hypophyllous, globose, depressed, more or less scattered, 84-105 μ in diameter, wall cells 10-22 μ wide. Appendages 8-30 equatorially inserted, 1-6 times as long as the diameter of the ascocarp, septate, thin walled, brown towards the base, flexuous and flaccid apex more or less helicoid when mature often strongly so. Asci 4-6, rarely 6-9, broadly ovate 50-60 x 25-40 μ. Ascospores 4-7, ovate to ellipsoid, 15-35×10-14 μ.
Conidia and mycelium overwinter in diseased buds, fallen berries or on overwintered stems. Cleistothecia, when formed, are also capable of overwintering.
Old cultural practices including the cutting and trimming of developing shoots to reduce shading and allow free air circulation of vines are important for control. Pruning, after the shedding of leaves, thinning out and cutting back of laterals, and removal and destruction of all diseased parts, are important aspects of a clean cultivation. Dusting with sulphur is a general practice for control in regions where temperatures are not high. Bordeaux mixture and fixed coppers are also recommended.
11. Powdery Mildew of Wheat (Triticum spp.) And Barley:
The diseases occur all over the world. In India it causes severe damage in some areas when the weather is cool and cloudy. The disease is common in the sub-montane areas of northern India and in certain parts of Rajasthan, Haryana and Punjab. It occurs on wheat, barley, rice and oats and also on grasses, such as species of Agropyron, Bromus, Dactylis and Elymus.
A greyish-white powdery growth is produced on the leaf. Such symptoms are also found on leaf sheaths and floral parts. The pathogen grows numerous superficial colonies.
The mycelium forms a flocculent growth which is white when the conidia are being formed and then changes to grey or black when the cleistothecia are formed. The leaf size and the number of leaves get reduced in infected plants. The leaves that are not shed become weak, twisted and deformed.
Physiology of the Diseased Plants:
Infection results in temporary stimulation of respiratory activity of the tissue and in chlorosis underneath and around the fungus. There is also an increment in transpiration of the host and further water loss due to the transpiration of the fungus.
The host plant then becomes thin and weak which is reflected in reduced yield and in some reduction in the normal plumpness of the kernel. After chlorosis of the tissue beneath the fungus mycelium has occurred, the reproductive activity of the mycelium declines, and sporulation is more advanced around the advancing edge of the lesion.
Chlorophyll may then reappear, giving rise to conspicuous green spots. Apparently this chlorophyll does not become active in photosynthesis. Studies of changes in the respiratory pattern in resistant and susceptible barley are reported by Millerd and Scott and Bushnell and Allen.
The pathogen responsible for the powdery mildew of cereals is Erysiphe graminis DC. ex Merat. The primary mycelium forms superficial, scattered, elongate to ellipsoid effuse patches, which are at first white but change to pale brown or grey; the haustoria are elliptic with long finger-shaped appendages radiating from both ends. Conidiophores arising from the primary mycelium are rather small with a terminal generative cell and a swollen basal cell. Conidia are in long chains, ellipsoid and are 25-37 x 12-17 μ.
Secondary mycelium is persistent lanuginose and is interlaced. It is at first white, but turns grey-white to brown, is sparingly branched, shiny, 40-60 μ wide bearing numerous un-branched thick walled rather rigid bristles, 200-100 μ long and 4-7 μ broad, forming a thick felt. Cleistothecia immersed in the felt, at first globose, become strongly depressed often cupulate, 135-250 μ in diameter; wall cells small, indistinct.
Appendages poorly developed, rudimentary, mycelioid, subhyaline to pale brown. Asci 8-25, ovate to more or less distinctly pedicellate, 70-108 x 25-40 μ. Ascospores 8, rarely 4, elliptic subhyaline to pale brown, 20-24 x 10-14 μ, formed only after the host plant has completely dried up.
The disease is spread through soil through cleistothecia where conditions are favourable. Conidia do not retain their viability at high temperatures. Conidia are produced in large quantities in a relatively cool and moist environment. They are spread readily by air currents and are the chief secondary inoculum during the usual cereal growing season.
Upon germination, the germ tube forms an appressorium in juxtaposition with the host cuticle. A hyphal peg invades the cuticle and the sub-cuticular wall and forms a haustorium in the epidermal cell.
There is no further growth of the pathogen within the host tissues. The rest of the mycelial thallus as well as the conidiophores, conidia and cleistothecia are entirely extramatrical (i.e. on the exterior of the host substrate).
Ehrlich and Ehrlich studied the ultrastructure of the haustorium with the aid of an electron microscope. They suggested that a sheath is formed around the haustorium from the host or pathogen or both, which may become a source of host metabolites used by the fungus and of substances secreted by the latter, which in turn may enter the host cell matrix.
Mycelium of the pathogen grows best at 20° or 21 °C. Low temperatures of 5-9 °C are more favourable for the germination of conidia. Best temperatures for the discharge of ascospores of E. graminis f. sp. hordei are 8°, 16-29° and 24 °C.
Ascospores grow best at 16-20°C. According to Mosemann and Powers, cleistothecia can survive up to 13 years at low temperatures. Arya holds that a temperature of 30°C or above has deleterious effect on the disease. Ascospores are formed most rapidly at 22-27°C if the cleistothecial material is exposed to alternate drying and wetting in the soil.
Although most of the powdery mildews are favoured by dry weather, the powdery mildew of cereals is an exception in this respect and thrives at low as well as high humidities. According to Prabhu, a 100 per cent relative humidity and a temperature of 15-20 °C are optimum for conidial germination.
Cherewick found that disease development could be diminished by sprinkling plants with water. Yarwood (1939) attributed this response to a reduction in sporulation as a result of injury to the conidiophores. The seriousness of the disease is increased by the application of nitrogen fertilizer.
The complete disease cycle in India is still not known. According to Mehta and Arya and Ghemawat, asci and ascospores, even if formed, have practically no chance to germinate and cause infection.
However, in his later work, Arya showed that asci does not mature in the cleistothecia of fallen leaves, but ascospores form in them after 10 months if the leaves are subjected to alternating dry and wet soil conditions.
Such conditions are available in low lying fields. According to Mehta, the disease is introduced in the plains in the form of conidial infection blown down from the hills where the fungus can survive in a cooler environment.
The existence of distinct physiologic races of E. graminis was first proved by Marchal. He differentiated seven forms on the basis of the principal host genera which were affected, that is, E. graminis tritici, hordei, avenae, secalis, poae and agropyri. E. graminis hordei were described by Mains and Dietz, and within E. graminis tritici.
The disease can be controlled by the use of sulphur dusts or sprays having potassium or sodium sulphide (1 per cent solution in water) or copper sulphate (1.05 per cent solution in water), to which is added a suitable spreader.
These methods are not economical on commercial basis. Resistant varieties will provide the best control measure of the disease. No work on this, aspect has been done in India. According to Arya, varieties NP710, NP718, K53, K53, E750, C591 are moderately resistant.
12. Root Knot of Vegetables:
The root knot nematodes, Meloidogyne spp., stand out as the most dominant group of plant parasitic nematode in almost every vegetable field and cause enormous losses every year in the nursery as well as planted fields. The common species are Meloidogyne arenaria, M. incognita and M.javanfca.
They attack such crops as various cucurbits, potato, tomato, brinjal, chillies, ladyfinger (Okra), groundnut, carrot, radish and Colocasia. M. arenaria is commonly associated with yellow decline disease of chillies in the district of Coimbatore. As a result of infestation, plant growth is reduced and the leaves turn yellow.
In potatoes the disease is not easy to recognize in the field as often no above-ground symptoms are produced. Sometimes plants are situated, sickly, and may even show signs of premature and sudden drying.
The nematode infestation on the tuber appears as tiny tubercles but heavy and localized infestations stimulate excessive cell division leading to gall formation. The disease may be complex with brown rot or bacterial wilt caused by Pseudomonas solanacearum and in such cases plants usually die suddenly. In tomatoes the symptoms are somewhat more pronounced. The plants develop slowly and appear stunted if the infestation has been early and severe.
The leaves are yellowish-green to yellow, tend to droop and wilt suddenly if wilt organisms are present. Sometimes the leaves get scorched from the margin inwards. The main root and the laterals in all cases bear spherical to elongated galls. The presence of these galls is the most characteristic symptom.
Symptoms similar to those on tomato are also noticed on brinjal (egg-plant), chillies, ladyfinger (Okra), cow pea, and French beans. In the case of chillies the plant growth is reduced and the leaves turn yellow.
The eggs of, Meloidogyne spp. are ellipsoidal and measure 67-128 x 30-52 microns. Differentiation of the larvae takes place within the eggs. The eggs are laid in the body of the female or in a gelatinous matrix extruded from the vulva. Up to 600 eggs are laid by each female. Numerous females of the nematodes are present in the foot galls. These survive in the soil and leaf debris.
The second stage larvae liberated after the hatching of the eggs move about in the soil but their movement is very slow. During their movement in the soil these larvae are influenced by various physical, chemical and biotic soil environments. High temperatures such as 40- 50°C kill these larvae quickly. Hence, during hot summer months most of them in the top 5-7 cm layer of soil are killed.
The movement of these larvae is very much slowed by the presence of excess soil moisture, clay content of the soil, and lack of aeration; sandy, light soils favour their movement best. Consequently, the disease is common in light textured soils. When these larvae approach the roots of plants they are attracted by the root exudates and are held in a mass around the roots. Finally, root infection is caused by these second stage larvae.
The invading larvae first penetrate the meristematic tissue and migrate until the head becomes established in an intercellular space near the endodermis. The females remain in this position permanently. The males soon die. Around the mouths of the feeding females giant cells are formed due to host-parasite interaction.
These giant cells are a characteristic feature of root knot infection. Roots are infected over a temperature range of 12 °C-35 °C. In general, a temperature of 25-28 °C is best for infection, rapid multiplication and increased size of galls.
Because of the very widespread and serious nature of this problem on vegetable crops, much attention is being given to control these nematodes by the use of chemicals and resistant varieties.
The use of chemical fumigants has been attempted in certain cases with marked success. Nematocides, such as DD, DBCP, Phorate and Carbofuran have been found to be very effective in experiments, but their use is still restricted due to the high cost of the chemicals.
The addition of neem cake, and similar nori-edible oil cakes at the rate of 25 quintals per hectare has been found to reduce root knot incidence in repeated field trials.
Application of saw dust at the rate of 25 quintals per hectare along with standard NPK fertilizers is cheaper and equally effective in reducing the disease.
It is essential that all the sources of nematodes, such as weed hosts, should be eliminated from the field. The soil should be deep ploughed during summer and allowed to dry. Flooding has been found to be effective in eliminating root knot nematodes from the soil. Lowland rice culture preceding the vegetable crop reduced the incidence of root knot in the latter.
13. Molya Disease of Barley and Wheat:
This disease was first reported on wheat and barley in Rajasthan. The disease has been described by Prasad et al. (1959) and Swamp and Singh (1961). It is now known to be widespread in the States of Rajasthan, Haryana and Punjab.
The damage may be as high as 50 per cent in certain infected areas. Barley is more susceptible than wheat. This disease is known as cereal root eelworm in England and occurs on wheat, oats and barley.
The disease occurs in patches in the field. If the same crop is cultivated year after year the diseased patch increases until the whole field is infected. The infected plants become dwarfed and pale, with a matted root system. Mild swelling occurs near the root tips. Glistening white bodies are seen adhered to the roots. These bodies (cysts) become brown and may remain attached to the roots or fall off in the soil after the roots decay.
Prasad (1959) and Swarup and Singh (1961) have identified the nematode causing this disease to be Heterodera avenae (H. major). The lemon-shaped, brown cysts of the nematode lying in the soil measure about 400-500 microns in width and 600-700 microns in length. The number of eggs in each cyst is variable. On attaining its full length the embryo undergoes the first moult within the egg and gives rise to the second stage larvae.
At the anterior end the stylet starts to form by this time. Inside the cyst the larvae become fully developed. These escape via the vulva and other apertures in the cyst wall. The free second stage larvae thus released migrate through the soil in search of a suitable host.
The second stage larvae are attached to the root usually by their necks, with most of their bodies outside the root. The sexes can be distinguished in the third stage of larvae. The male develops a single testis while the female develops paired ovaries.
The male larva, when fully formed, is of a rather narrow and slender structure, tapering slightly at the anterior end and has a short, rounded tail. It has a short stylet. Within a short time the fourth moult occurs and the fully developed male larvae of the fifth stage wander in the soil for some time and then die.
Penetration of the host occurs just behind the root tip. After the fourth moult, adult female larvae are formed which grow into lemon-shaped structures. Over the surface of the adult female (cyst), a sub-crystalline layer is secreted. The cyst helps the nematode to survive in the soil. In the adult female larva, the body cavity is entirely filled by the ovaries which tend to obliterate other structures.
The host range of Heterodera avenae (H. major) is confined to the family, Graminae, Jding some grasses, and these may serve as alternate hosts’ (collateral hosts). The main hod of survival of the nematode in the soil is by means of cysts.
A long rotation of at least four years is recommended. The rotation is more effective if the soil is kept fallow and dry during summer.
Green manuring of infested soil with chopped cabbage leaves heavily reduces the larvae he soil. The activity of some nematode trapping fungi, such as Arthrobotrys oligospora and Dactylaria thoumasla is reased as a result of green manuring.
Soil fumigation with D-D mixture has been found to be quite efficacious in controlling the ease.
14. Citrus Nematode Disease:
The citrus nematode Tylenchulus semipenetrans is invariably present in citrus plantations all over India especially with trees in various stages of decline and dieback. The population lie in the soil and on the roots is often directly correlated with the stage of decline of the trees. Experimental evidence is, however, lacking on the exact role of a nematode in the citrus decline complex under Indian conditions.
The affected trees are generally stunted with little bearing and exhibit dieback of twigs. The roots of such trees are dark in colour with shortened rootlets, swollen and irregular in appearance.
Saccate, sedentary females are root parasites. The larvae which survive in the soil infect the roots. The females swell and deposit eggs in a gelatinous secretion. Swellings are not formed.
Due to its complex nature, it is difficult to control this disease. DBCP at the rate of 14B kg/hectare, when applied to declining sweet orange trees, not only resulted in a decrease of nematode population but also in an increase in yield by 200 per cent. Baines et al. (1957) obtained 100 per cent control of Tylenchulus semipenetrans by using vapam at a concentration of 100 ppm in the field.
There are several other important nematode diseases, such as the reniform nematode on castor, the root knot nematode in groundnut and Heterodera cajani on sesame amongst the oil seed crops.
Root knot nematodes constitute another problem in plantation crops, such as cardamum, pepper-vine, ginger and turmeric in the state of Kerala.
The lesion and burrowing nematodes pose the most serious problems to the coffee areas in South India. Radopholus similis is another nematode in banana in Tamil Nadu, Kerala and some parts of Karnataka. Tylenchorynchus brassicae has been reported by workers in Aligarh which causes damage to cauliflower in Uttar Pradesh. Sethi (1965) and Chandrasekhran and Seshadri (1969) have shown the association of a number of nematodes with sorghum crops.
15. Ear-Cockle of Wheat:
The ear-cockle of wheat is a well-known disease caused by Anguina trilici. This is known in India as “sehun” disease and is common in different parts of northern India (Uttar Pradesh, Punjab and western part of Bihar).
The nematode of this disease was first noticed in England in 1743 but its significance was realised only in 1775-76. It is often present in association with the yellow ear rot (tundu or tannan disease) caused by the bacterium Coryinebacterium tritici.
In Uttar Pradesh, Singh et al. (1953) reported that the disease causes an annual loss of 30 per cent. Apart from loss in yield, the disease has been known to produce toxic effects on man and animals when quantities of galls are consumed along with the flour. Though this disease has been completely eradicated from Europe and the American continents this nematode still persists in developing countries like India.
The disease does not produce galls but its effects are visible on the stems, leaves and floral organs. Affected plants may be dwarfed and their leaves twisted and crinkled which prevents the normal emergence of the younger leaves from within, causing them to be buckled.
The infected heads are partially or completely replaced by cockles that are hard, dark brown or black. These stony structures vary in size from region to region. They are filled with nematode larvae which can be seen by soaking the gall in water and then macerating it.
Severely affected plants may even die. Even if seedling symptoms are absent, plants may bear galls in their ears. The plants show a spreading nature and tend towards more tillering. Early ear formation has also been noticed. Basal enlargement of the stem and formation of galls on awns, glumes and staminate tissues have been reported by Gupta (1966).
The nematode causing this disease is known as Anguina trilid (Steinback) Filipjev.
Each nematode larva is slender, with a cylindrical to spindle-shaped body slightly blunt at the anterior end and tapering to a point at the posterior end to form the tail. The body consists of an outer covering enclosing an inner tube, the alimentary canal, which ends at the mouth. The mouth opens into a buccal cavity containing a buccal spear, 9-11 microns long, which is hollow and pointed. This spear helps the larva to get out of the egg and also to pierce the host tissues.
Below the buccal cavity the digestive canal continues as the oesophagus with an anterior and a posterior bulb, the latter joining the intestine. The intestine opens into the rectum and then into the anus.
There is too much variation in the sizes of larvae from samples collected at different places. The adult males measure 3-5 mm in length while the adult females are 2-2.5 mm long and wider than the males. The eggs are, on an average, 87 x 44 microns in size. The second stage larvae which emerge from the eggs are about 0.75 microns long.
The larvae in the wheat galls have extreme longevity. They can survive up to 28 years under dry conditions and up to 8-9 or even 14 years under moist conditions. In soil the galls become moist and the larvae break free of the softened walls of the galls.
The liberated larvae make their way to the growing point of the wheat plant while it is still near the soil base. These larvae around the growing point feed ectoparasitically and are carried upwards with the lengthening of the culms, until the embryonic flower tissues are formed, when they enter the endoparasitic mode of life by invading these tissues. There, they undergo rapid metamorphosis, becoming adult males and females.
Copulation follows and after egg laying the adults soon dies. The eggs soon hatch into second stage larvae which remain inside the gall to carry on the life cycle. Occasionally, the larvae enter the leaves and mature there to form galls. The nematode is susceptible to desiccation and high temperature under moist conditions.
Plants can become infected with nematodes in the initial stages of growth only, that is, before the seedlings have emerged from the soil. Larvae free from bacteria have been found to produce only the cockle disease. Bacteria are unable to produce the rot independently. However, in combined infection, the nematode larvae are completely killed by the yellow rot bacterium.
Since the parasite is introduced into new areas mostly through galls mixed with seeds, proper seed selection is the best method of controlling this disease. The diseased ears should be picked out and burnt.
Healthy seeds can be picked out from a mixed lot by using a sieve that can retain normal plump grains and allow the small round galls to pass through. Infected and healthy seeds can also be separated by being immersed in water or brine solution.
The galls do not sink but float on the surface and can be removed. In fields where the disease has occurred once, cultivation of wheat should be stopped for two to three years. The disease does not occur on barley and oats.
Either of these crops can be grown in such fields. Gupta (1966) tested certain nematicides against the disease. Nemaphos (granular) proved to be most effective when used at the rate 4.5 kg per acre.
Nematode infection of wheat plants is influenced by temperature. The incidence of ear cockle is higher with lower temperatures. Hence, crops sown early usually escape infection. In areas where the disease has established itself it is better to resort to early sowing.
The screening of wheat varieties to locate sources of resistance is still in the initial stages and offers good promise for the future. No wheat variety under cultivation in India is immune to the disease. Varieties Sonora 63, Lerma Rajo, N.P. 908 and S. 227 show a certain degree of tolerance to the disease. The disease can be controlled by intensifying extension work and educating the cultivators.