Stem-Rot of Jute: Symptoms and Control | Plant Diseases

In this article we will discuss about:- 1. Introduction to Stem-Rot of Jute 2. Symptoms of Stem-Rot of Jute 3. Causal Organism 4. Disease Cycle 5. Control.

Contents:

1. Introduction to Stem-Rot of Jute
2. Symptoms of Stem-Rot of Jute
3. Causal Organism  of Stem-Rot of Jute
4. Disease Cycle of Stem-Rot of Jute
5. Control of Stem-Rot of Jute

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1. Introduction to Stem-Rot of Jute:

This disease of Jute, initially designated as die-back, was reported for the first time from Formosa in 1916 by K. Sawada of Japan. In course of time it was reported from India where it is known as Stem-Rot of Jute disease.

Stem-Rot of Jute may attack both Corchorus capsularis L. and C. olitorius L. and is common in all the jute tracts in India. No other disease causes more damage both in out-turn and quality of fibre than the stem-rot. It is a destructive disease of seed­ling jute and is usually sporadic in occurrence; but occurs in an epidemic form only tinder favourable weather conditions.

The disease attacking the jute plants both in the seedling and in the adult stages leads to the formation of gaps in the jute field and reduction in yield. When the disease incidence is mild and the deaths of the jute plants are few in the crop, there is not much cause of anxiety.

But if the death is severe, large gaps may occur and the plants develop stems of uneven thickness which take a longer time to ret and produce coarser fibres.

Again with wider spacing’s, the plants are induced to branch rendering them useless for fibre production. In the adult stage the damage done is of a more serious nature. In plants that have not succumbed to the disease, the stem usually splits and shreds.

Such stems take more time to rest and the fibre itself instead of being glossy, fine, and white is coarse, brownish, weak lacking in lusture. Again fibres from dead stem are uniformly dull, coarse and brittle.

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2. Symptoms of Stem-Rot of Jute:

The disease may attack jute plants at any stage of growth. Very young seedlings, about 2 in. high, die with the symptoms of “damping-off”, the hy­pocotyl becoming soft and completely rotted. In these diseased seedlings an abundant mycelium is found growing in the tissues of the young stem.

The earliest symptoms appear either on the hypocotyl in the form of lesions near the collar or at the node as thin blackish-brown to black streaks. Under wet conditions the younger seedlings damp-off.

But when conditions are dry and the seedlings have reached a three-leaf stage, they develop blight resulting in the shedding of the leaves and the death of the plants. Blight also occurs when the tender roots get infected. On the cotyledonary leaves the necrotic lesions are orange-citrine and roundish.

As rotting of the leaves and hypocotyl proceeds pycnidia are formed in abundance. Sclerotia are, however, formed in all the parts of the seedlings.

Again in adult plants, buffy citrine necrotic lesions occur along the apex and margins of the leaves ultimately covering the entire leaf. The leaf infection spreads to the node through the petioles; the infected leaves are shed.

Numerous pycnidia cover the entire lamina and the petiole with pycnidial ostiole on the upper surface of the leaf. Sclerotia are not developed on the affected leaves. Lesions on the stem usually occur at the nodes as small, blackish-brown depressions which may coalesce and gradually girdle the stem causing rot. The rot of the stem leads to either shred­ding, canker or wilting.

In the advanced cases, the plants wilt leaving bare dead stalks in the field with abundant pycnidia all over. In plants where lesions appear as streaks along the length of the stem without girdling it, the cortex get shredded exposing the fibrous tissue. They break down easily when strong wind blows.

In some vigorously growing plants, the lesions may become localized due to cork formation producing cankers. A furrow may be formed by coalescing several cankers. Pycnidia are usually embedded in the epidermis of the stem being visible as small black dots. Sclerotia are found in the soft tissues of the infected stem. In cankers, pycnidia and sclerotia occur sporadically.

In plants whose aerial parts are attacked, the roots very often are healthy. It is only after all parts die, the infection spreads in the roots. Sometimes, however, direct infection of roots occurs in which case the plants wilt and the infected roots are in­variably full of black sclerotia.

Infected capsules either drop off or split. In the latter case, the seeds get infected. In some of the unsplit diseased capsules seeds may also be diseased. The infected seeds are brown without any lusture and light. Sclerotia are developed within the capsule and on the seeds. Pycnidia occur on the outer surface of the capsule and sporadically on the seeds.

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3. Causal Organism of Stem-Rot of Jute:

The stem rot of Jute disease is caused by the fungus: Macrophomina phaseolina (Tassi) Goid. [=M. phaseoli (Maubl.) Ashby] whose sclorotia phase is known as Rhizoctonia bataticola (Taub.) Butler. It belongs to the form-family Sphaeropsidaceae under the form-order Sphaeropsidales of the form—class Deuteromycetes.

The fungus is characterized by colourless, septate, branched hyphae mea­suring 3-8µ across which pass freely through the host cells. It produces sub-epidermal, punctiform, black pycnidia with erumpent ostiole. The pycnidia measuring 98 — 225 x 89—275µ have multicellular wall.

Numerous conidiophores are borne in each pycnidium. The conidiophores are hyaline, simple, straight to slightly curved with tapering apex, 10—14 x 2.5-35µ, terminated by a conidium. The conidia are uni­cellular, hyaline, smooth-walled, ovcid to oblong, straight or slightly curved, 16 — 32 x 7 —10µ.

Along with the development of pycnidia, frequent dark sclerotia are produced by the hyphae. The sclerotia are 41 to 86µ in diameter.

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4. Disease Cycle of Stem-Rot of Jute:

The pathogen perennates on stubbles and in soil in the jute fields in its sclerotia form. It also harbours on the jute seeds under the seed coat and within the cotyledons. Where rotations are practised, other crops like linseed, sesamum or cowpea may form the collateral hosts. The pathogen has also been found to survive on a common weed Cyperus distans.

But primary infection is chiefly due to the seed borne inoculum than any other source.

There are two phases of disease development. During the first phase the pathogen kills a large number of seedlings and young plants in the first two months. During the second phase, which starts after the plants are four to five months old, there are no deaths, but quality of the fibre is ruined owing to the formation of cankers and shredding .

Due to primary infection, symptoms appear in the seedlings on the cotyledonary leaves and the hypocotyl within a fortnight after sowing leading to the development of pycnidia. Conidia released from the pycnidia of the diseased seedlings cause secon­dary infection on the leaves in the vicinity of the seedlings where primary infection has been established. Both rain and air play a great role for dispersal of conidia.

The conidia readily infect the leaves and the leaf infection spreads to the node through the petiole. In an infected stem, the pathogen grows in the epidermis and cortex, often invading the phloem parenchyma and the wide rays between the phloem wedges. It is also found in the central woody portion, the hyphae penetrating even the wood fibres.

Ultimately girdling of the stem occurs causing rot of the stem which leads to either shredding, canker or wilting. Usually the secondary infection is four times the primary infection.

Prolonged warm and humid conditions favour disease development leading to the severe outbreak of the stem-rot. Initially abundant leaf infection is visible during and after heavy rains which gradually leads to the spread of the disease. The most critical period for the crop is first eight weeks of its growth, for it is during this period that the disease is serious.

Again if the weather during this period is comparatively dry, the incidence of the disease is less. The interval between the appearance of the stem-rot and the death of the plant ranges between one and twenty weeks. Where the top of the plant is attacked the death is quicker. Attacked plants often survive by means of callus formation.

Root-rot usually occurs sporadically late in the season, but also appears early in the season when high temperature prevails.

Disease cycle of Stem-rot of jute is presented in Figure 386.

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5. Control of Stem-Rot of Jute:

Since the pathogen can pereruiate in soil as well as on stubbles, jute field sanitation is an important measure to cut down the source of primary inoculum.

Besides this, some of the suggested control measures are given below:

(i) Use clean seeds from localities where disease incidence has not been reported.

(ii) Seeds should be thoroughly dried and before storage should be treated with Agrosan GN or ceresan or any other Organomercuric compounds.

(iii) Betterment of cultural practice in the following manner

(a) Improvement of soil pH with lime;

(b) Application of potash between 50 to 100 Kg/ha in soil;

(c) Good drainage and improvement of porosity (in clay soil) with organic matter;

(d) Proper spacing 30 cm. x 7 cm., weeding, and thinning;

(e) Crop rotation jute with paddy.

(iv) Spraying copper oxychloride (50%Cu) at 0.75 concentration at first leaf infection produces fruitful results. Leaf infection can be reduced spraying 0.2% Lime Sulphur, 0.5% Perenox, and Bordeaux mixture (5:5:40) under field condition.

(v) Early harvesting reduces loss of fibre.

(vi) Since the fungus can survive on linseed, sesamum and cowpea, these plants should not be grown in jute fields.

(vii) Jute field weed Cyperus distans should be eradicated to reduce the source of inoculum.

(viii) Root-rot can be effectively controlled by the use of Brassicol.