Clubroot disease attacks a wide range of plants such as cabbage, cauliflower, radish, turnip, etc. belonging to family Brassicaceae (= Cruciferae). It is widely distributed all over the world, but occurs most frequently in Europe and North America. In India, the disease has been reported occurring generally in restricted hilly areas of West Bengal and Assam.
However, the first occurrence of the disease was recorded from Scotland in 1780 but the first scientific investigation of the disease on cabbage and the details of its causal organism were made in Russia by Woronin (1878) where the disease was widespread. Clubroot disease results in serious losses when susceptible varieties of crucifers are grown in infested fields. Fields once infested remain so indefinitely and become unfit for growing crucifers therein.
Symptoms of Clubroot Disease:
The most characteristic symptoms of the disease can be seen on roots and, sometimes, on underground parts of the stem. The symptoms consist of small or large spindle-like, knobby, spherical, or club-shaped malformations on the roots and rootlets. Leaves of the infected plants begin to wilt and, at later stage, the plants become yellow and stunted. Young plants may be killed by the disease within a short time after infection, while older plants may remain alive but fail to produce marketable heads.
Causal Organism of Clubroot Disease:
The pathogen is an obligate endoparasite inhabiting the host cells in the form of Plasmodium.
The life-cycle of the pathogen initiates after the perenation period is over and favourable conditions return. Perennating structures, the “cysts” (also called “resting spores”) occurring in soil germinate, each giving rise to a biflagellate zoospore (primary).
The primary zoospore moves in the film of water in soil, reaches root-hair, punctures it and its protoplast enters the cell in the form of spherical ‘amoeba’. The amoeboid structure develops therein producing Plasmodium, generally referred to as sporogenous Plasmodium.
The latter increases in size and cleaves into segments that develop into zoosporangia. Such zoosporangia may occur singly or they may be loosely aggregated. Biflagellate zoospores (secondary) are then formed and released from the zoosporangium either directly into the host tissue or to the outside of the host. Release of secondary zoospores to the outside involves either a disintegration of the root cell wall or the formation of an exit tube by the zoosporangium.
The exact function of secondary zoospores (sporangial zoospores) is not fully understood. Possibly, they function as gametes and undergo plasmogamy resulting in quadriflagellate, binucleate zygote prior to penetration and infection. The zygote causes infection of root, enters inside host cell, and develops into plasmodium, called cystogenous Plasmodium.
Though there are a number of unanswered questions regarding the origin as well as the nuclear condition of cystogenous Plasmodia, probably the most popular view is that the cystogenous plasmodia originate following plasmogamy of compatible zoospores contain genetically compatible haploid nuclei for major part of their life, and experience karyogamy and meiosis quite late. Finally, however, the cystogenous plasmodia give rise to thick-walled structures typically referred to as “cysts” (the resting spores), the perennating structures, which are released in soil by death and disintegration of the host cells.
Clubroot Disease Cycle:
(i) Perennation:
The pathogen perennates in soil by means of cysts (resting spores) produced by cystogenous plasmodia and released as a result of death and disintegration of infected host cells. It is considered that the cysts have ability to lie dormant for a number of years before they germinate to produce primary zoospores.
(ii) Primary Infection:
As is evident from the life pattern of the pathogen, the events occurring between the first infection on root-hair and symptom manifestation on root are quite interesting. The cyst germinates in soil producing primary zoospores, which enter the root-hair, produce sporogenous plasmodia which give rise to zoosporangia containing secondary zoospores, the secondary zoospores get released in soil, two zoospores fuse forming a zygote, which penetrates and causes primary infection on root. The zygote develops cystogenous Plasmodium inside the root cell.
From this point of primary infection the plasmodia move to cortical cells and reach the cambium through direct penetration of host cells. Again from here, they spread in all directions in the cambium, outward into the cortex and inward toward the xylem and into the medullary rays. They become established in some of these cells and stimulate them to over-development (hypertrophy and hyperplasia). Infected cells may attain five or more times larger size than the uninfected ones.
The over-developed roots look like “clubs” hence the name “clubroot”. The Plasmodium infected clubs not only utilize much of the food required for the normal growth of the plant, but they also interfere with the absorption and translocation of mineral nutrients and water through the root system resulting in gradual stunting and wilting of the aerial parts of the plant. However, the cystogenous plasmodia give rise to “cysts” (or resting spores), which serve as perennating structures for the rest of growing season.
(iii) Secondary Infection:
Secondary infection during the same growing season appears unusual and has not been reported so far.
Predisposing Factors:
pH of soil below 7.0 and a moisture content between 45-60% are prone to disease incidence. Usually low-lying, poorly drained soil favours this disease. Most pronounced development of clubroot disease has been recorded at temperatures ranging between 20 to 25°C. This is the range of temperature at which normal root growth occurs vigorously.
Management of Clubroot Disease:
1. At harvesting lime roots of diseased plants should not be left in the soil.
2. Following cultural devices are recommended for prevention of the disease in the field – (i) cruciferous weeds (e.g., mustard) should be eradicated, (ii) well-drained, pathogen free plots should be used, (iii) seedlings raised in pathogen-free soil should be used, and (iv) long crop-rotation avoiding crucifers should be followed.
3. Since the pathogen remains dormant in soil for several years, growing cruciferous crops in infested field should be avoided.
4. The crops should be planted in well-drained fields and adjusting its pH to 7 or slightly more by the addition of the proper amount of lime (calcium carbonate). It was observed that applying 10-20 tons/ha lime about six weeks before planting increased pH of soil to 7.9, reduced disease incidence from 98% to 0.7%.
5. Although some fungicides (e.g., chloropicrin, methyl bromide or Metam sodium or pentachloro-nitrobenzene (PCNB) have been used and they controlled the disease to some degree, all these are on the banned list now due to their hazardous and environment- polluting nature.
6. Resistant varieties should be used. All exotic cultures belonging to Brassica napus, B. nigra, and B. carinata are either free from disease or are resistant.
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