St Wilfred College 3b2z4x

NEMATODE DISEASE

 Introduction of Nematode  Root Knot Disease  Molya disease of Wheat & Barley  Ear Cockle of Wheat

INTRODUCTION  Nematodes belong to the kingdom Animalia Nematodes are worm like in appearance but quite distinct taxonomically from the true worms. Most of several species of nematodes line in fresh or salt water or in the soil, and

feed on micro organisms and microscopic plant and animals. Numerous species of nematodes attack and parasitize human and animals in which they cause various disease. They obtaining their food with spears or stylehs and causing a variety of plant disease worldwide. There are some nematodel disease which are following.

1) ROOT KNOT DISEASE OF VEGETABLES  Root knot nematodes occur through out the world, especially in areas with warm or hot climates. They attack more than 2,000 species of plants including almost all cultivated plant & reduce world crop production by about 5% loses in individual fields. Root knot nematodes damage plant by devitalizing root tips and causing the formation of swellings of the roots.

SYMPTOMS ABOVE GROUND SYMPTOMS

 Are reduced growth and fewer small, pale green or yellowish leaves that tend to wilt in warm weather. Blossoms and fruit are few and of poor quality affected plant killed prematurely. UNDER GROUND SYMPTOMS  Infected roots develop the typical root knot galls that are two to several times as large in diameter as the healthy root. Several infection along the root give the root a rough, clubbed appearance. Roots infected by nematode also develp a bushy root

system. Usually, however, infected roots remain smaller and show necrosis and rotting. When tubers or other fleshy underground organs such as carrots, potatoes and yam are attacked, they produce small swellings over their surface, which become quite prominent and cause distortion or cracking.

THE PATHOGEN  Meloidogyne spp. The male and female root knot nematodes are easily distinguishable morphologically. The males are worm like and about 1.2 to 1.5 millimeters long. The females are pear shaped and about 0.40 to 1.30 m.m. long.

DISEASE CYCLE  Each female lays approximately 500 eggs in a gelatinous substance. There are various juveniles stage. The first and second stage juvenile are worm like and develop inside each egg. The second stage juvenile emerges from the egg into the soil. This is the only infective stage of the nematode. If it reaches a susceptible host, the juvenile enters the root, becomes sedentary, and grows thick like a sausage. The nematodes feed on the cells around its head by inserting its styler

and secreting saliva into the cells. The saliva stimulates cell enlargement.

DISEASE CYCLE  The nematode than undergoes a second molt and give rise to the third stage juvenile, which is stouter and goes through the third molt and gives rise to the fourth stage juvenile, which can be distinguished as either male or female. These undergoes the fourth and final molt and the male emerges from the root as the worm like adult male, which becomes free living in the soil, while the female continues to grow in thickness and somewhat in length and appears pear shaped. The female continues to swell, with or without fertilization by a male, produces

eggs that are laid in gelatinous protective coat inside or outside the root tissues. Depending on the position of the female may hatch immediately or a few of them over winter and hath in the spring.

DISEASE CYCLE  A life cycle is completed in 25 days at 27oc, but it takes longer at lower or high temperatures. When the eggs hatch, the infective second stage juveniles migrate to adjacent part of the root and cause new infections in the same root or infect other roots of the same plant or roots of other plants. Roots know nematodes are spread primarily by water or by soil clinging to farm equipment or infected propagating stocks transported into uninfested areas.

DEVELOPMENT OF DISEASE  Second stage juveniles enter roots behind the root tip and keep moving until they reach positions behind the growing point. There, they settle with their head in the developing vascular cylinder. In older roots the head is usually in the pericycle. Cells near the path of the juvenile has become established, some of the cells around its

head begin to enlarge. Their nuclei divide, but no cell walls are laid down. The existing walls between some of the cells break down. The existing walls between some of the cells break down and disappear, giving rise to giant cells. Enlargement and coalescing of cells continues for 2 to 3 weeks, and the giant cells invade the surrounding tissues irregularly. Each gall usually contains three to six giant cells, which are due to substances contained in the saliva secreted by the nematode in the giant cells during feeding.

 The giant cells attract nutrients from surrounding cells and serve as feeder cells for the nematode. The giant cells crush xylem elements already present but degenerate when nematodes cease to feed or die. In the early stages of gall development the cortical cells enlarge in size and latter, they also divide rapidly. Swelling of the root results from excessive enlargement and division of all types of cells surrounding the giant cells and from enlargement of the nematode. As the females enlarge and produce their egg sacs, they push outward, split the cortex, and may become exposed on the surface of the root or remain completely covered,

depending on the position of the nematode in relation to the root surface.  In addition to the disturbance caused to plants by the nematode galls themselves, damage to infected plants is frequently increased by certain parasitic fungi, which can easily attack the weakened root tissues and the hypertrophied, undifferentiated cells of the galls. Moreover, some fungi e.g. Fusarium, Rhizoctonia, and the oomycete Pythium, grow and reproduce much faster in the galls than in other areas of the root, thus inducting an earlier breakdown of the root tissues.

CONTROL MEASURES  Root knot can be controlled effectively in the green house with stream sterilization of the soil or soil fumigation with nematicides. In the field the best control of root knot is obtained by fumigating the soil with approved chemical nematicides. Each treatment usually gives satisfactory control of root knot for one season. In several crops, varieties resistant to root – knot nematodes are also

available. Transgenic plants producing inhibitors to certain nematode proteinases have shown promising resistance to the nematode and their use may prove practical in the future. Several cultural practices, such as crop rotation, fallow soil, soil solarization, and certailn soil amendments, are also helpful in reducing root – knot losses. Biological control of root knot has been obtained experimentally by treating nematode – infested soil with endospores of the bacterium Pasteuria penetrans, which is an obligate parasite of some plant parasitic nematodes, or with

Preparations of the fungus Trichoderma harzianum; bu treating transplants or

infested soils with spores of the treating transplants or infested soils with spores of the fungus Dactylella oviparasitica, which parasitizes the eggs of Meloidogyne nematodes; and in some experiments by treating transplants or infested soils with spores of the vesicular arbuscular mycorrhizal fungi Gigaspora and Glomus. Fairly good experimental control of root knot has also been obtained by mixing essential oils from plant spices into nematode – infested soil before planting and through an increase in plants of their local and systemic – induced resistance to root knot

nematodes by mixing in the soil or spraying the plants with amino – butyric acid and other amino acids.

2) MOLYA DISEASE OF BARLEY AND WHEAT  The disease was first reported on wheat and barley in Rajasthan. The disease has been described by Prasad et. Al. (1959) and Swarup and Singh (1961). It is now known to be widespread in the states of Rajasthan, Haryana and Punjab. The damage may be as much 50% 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.

SYMPTOMS  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 of fall off in the soil after the roots decay.

THE PATHOGEN  Prasad et al. (1959) and Swarup and Singh (1961) have identified the nematode causing this disease to be Heterodera avenge (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.

DISEASE CYCLE  On attaining its full length and the embryo under goes the first moult within the

egg and give 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 suitable host.  The second stage larvae are attacked 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.

DISEASE CYCLE  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.

CONTROL MEASURES  Crop rotation with a non – cereal crop can prevent the disease. Since the disease is more prevalent in light soils with poor water holding capacity, it is suggested that the maintenance of good soil structure of fertility will be helpful in reducing damage by this disease. Two or three deep ploughing of the infested fields during summer and soil fumigation with D.D. at the rate of 400 litre per hectare, or D.B.C.P. at the rate of 30 litres per hectare will help control molya nematode.

3) EAR–COCKLE OF WHEAT  The ear-cockle of wheat is a well known disease caused by Anguina tritici. This is known in India as “Sehun” disease and is common in different parts of northern India (Uttar Pradesh, Punjab, and Western parts of Bihar). The nematode of this disease was first noticed in England in 1743 but its significance was realized only in 1775-76. It is often present in association with the yellow ear rot (tundu or tannan disease) caused by the bacterium Clavibacter tritici.

SYMPTOMS  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.  Several affected plants may even die (Gupta, 1966). Even if seedling symptoms are absent plants may bear galls in their ears. The plants show a spreading nature and

tend towards more tillering.

THE PATHOGEN  The nematode causing this disease is known as Anguina tritici (Steinback) Filipjev.

DISEASE CYCLE  Each nematode larva is slender with a cylindrical to spindle –shaped body. 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 eggs and also to pierce the host tissues. Below the buccal cavity the digestive canal continues as the esophagus with an anterior and a posterior bulb, the latter ing 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 avaerage, 87 x 44 mirons in size.

DISEASE CYCLE  The second stage larvae which emerge from the eggs are about 0.75 microns long. The larvae in the wheat galls have extreme longevity. The can survive up to 28

years under dry conditions and up to 8-9 or even 14 years under moist conditions . In soli 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 die. 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.

DISEASE CYCLE  The nematode is susceptible to desiccation and high temperature under moist conditions . Plants can become infected with nematodes in the initial 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 (Gupta, 1966).

DISEASE MANAGEMENT  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.

CONTROL MEASURES  Use only gall-free seed from a healthy crop. Remove the galls from seeds by winnowing or using a sieve of proper size. Galls can also be removed by soaking the seed in 2 per cent to 5 per cent common salt. When salt water is used, make sure that the treated seed is washed by plain water 2 to 3 times and then dried before sowing. The disease is caused by the nematode, Anguina tritici. In a diseased head, grains are replaced by nematode galls (cockles). The galls are filled with nematode larvae.