St Wilfred College

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NEMATODE DISEASE


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Introduction of Nematode

Root Knot Disease

Molya disease of Wheat & Barley

Ear Cockle of Wheat


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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.


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1) ROOT KNOT DISEASE OFVEGETABLES

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.


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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.


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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.


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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.


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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, produceseggs 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.


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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.


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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.


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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.


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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


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Preparations of the fungus Trichoderma harzianum; bu treating transplants orinfested soils with spores of the treating transplants or infested soils with spores of

the fungus Dactylella oviparasitica, which parasitizes the eggs ofMeloidogyne

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.


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2) MOLYA DISEASE OFBARLEY 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.


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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 plantsbecome 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.


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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.


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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.


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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.


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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 damageby 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.


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3) EAR

COCKLE OF WHEAT The ear-cockle of wheat is a well known disease caused byAnguina 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.


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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 andcrinkled 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.


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THE PATHOGEN

The nematode causing this disease is known as Anguina tritici (Steinback)

Filipjev.


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DISEASE CYCLE

Each nematode larva is slender with a cylindrical to spindleshaped 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 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

avaerage, 87 x 44 mirons in size.


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DISEASE CYCLE

The second stage larvae which emerge from the eggs are about 0.75 micronslong. 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.


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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).


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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.


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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 surethat 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.

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