The following points highlight the tow major diseases of crucifers. The diseases are: 1. White Rust of Crucifers 2. Club Root of Crucifers.
Disease # 1. White Rust of Crucifers:
White rust is common on cruciferous plants like, Brassica napus, B. alba, B. jurtcea, B. campestris; different varieties of B. oleracea, Raphanus sativus; and cruciferous weeds Nasturtium indicum and Capsella bursa pastoris. This being a common and conspicuous disease, was observed and studied by early mycologists including Persoon, Berkeley, Tulasne, and De Bary.
The disease is of relatively less- economic importance in proportion to its widespread occurrence. Earlier workers thought that white rust of crucifers belongs to the true rusts, hence the name.
Symptoms:
The disease attacks all parts of the host plant except the roots. Infection is both localized and systemic. Due to localized infection prominent white pustules of variable shape and size appear on the leaves (Fig. 357A), stem and inflorescence. Pustules may arise in close proximity and coalesce to form large patches.
Ruptured pustules become powdery in appearance, since sporangia enclosed within the pustules are exposed (Fig. 357D).
Depending on the severity of infection, the pustules may appear on one leaf surface only or on both surfaces. When the young stems and floral organs are infected, the infection becomes systemic in the tissue and stimulates hypertrophy and hyperplasia resulting the enlargement and varied distortion of infected organs.
Invaded stems often exhibit extended swellings or enlargements which may result in sharp bends, turns or even complete spirals. A proliferation from lateral buds that are normally dormant may result in a bushy growth.
The inflorescence axes before distorted, development of flowers may be suppressed, or discolouration and malformation of floral parts (Fig. 357B & C) are often resulted from systemic infection. Pustules may develop on hypertrophied organs, but they may be relatively rare on such tissue. When the white rust causes infection alone, it induces very little injury. But the attack is severe when it is associated with downy mildew.
Causal Organism:
Albugo Candida (Lev.) Kunze. It is an obligate parasite. Infection of host tissue results in the development of a copious growth of internal, intercellular, aseptate mycelium which sends in globular haustoria within the adjacent cells of the host tissue. Hyphae from the internal mycelium collect below the epidermis of the host tissue into which numerous haustoria are sent.
From these hyphae numerous short sporangiophores arise in a closely compacted palisade layer beneath the epidermis and at right angles with it.
The sporangiophores developed beneath the epidermis, raise it, to make whitish pustules or extended blister-like areas, the sori. The sporangiophores are broadly clavate from which sporangia are abstricted in basipetal succession and adhere in chains. Pads of gelatinous material formed between successive sporangia function as disjunctors.
Pressure exerted on the superimposed epidermis by the accumulation of sporangia finally causes the host epidermis to rupture along the softened middle lamellae exposing the sporangial bed.
The sporangia are disseminated by wind. The sporangia are hyaline, nearly spherical and are 14 to 16µ by 16 to 20µ in size. They usually germinate by the formation of zoospores, rarely by germ tube. The zoospores are reinform, biflagellate with laterally inserted flagella. After a period of swarming, they encyst, form-a germ tube which is capable of penetrating a suitable host through the stomata.
Towards the end of the growing season antheridia and oogonia begin to appear when the production of sporangia has almost ceased. They arise within the host tissues. The oogonia are globular, multinucleate. One or more small globular antheridia arise close to an oogonium.
Gradually the oogonial protoplast becomes differentiated into a peripheral or external multinucleate layer, the periplasm, surrounding a central uninucleate egg cell, or ooplasm.
The antheridium produces a short fertilization tube, which penetrates the periplasm and comes in contact with the egg. The antheridial contents are discharged through the -fertilization tube into the egg cell.
A single- antheridial nucleus fuses with the egg nucleus. Immediately after fertilization the periplasm is absorbed, and the fertilized egg cell develops a dark wall, becomes filled with oily and fatty food and develops to form an oospore.
The oospore wall becomes thick, turns brown, and is provided with low, blunt ridges. The mature oospores measure from 40 to 55µ in diameter. They survive in the soil and germinate after a period of rest of several months. During the germination of oospore the diploid nucleus divides into a large number of nuclei, the first division of which is reductional.
Each oospore produces a large number of secondary zoospores, enclosed in a vesicle which becomes extruded during germination of the oospore. The zoospores cause infection: to the susceptible host.
Disease Cycle:
The causal organism perennates as oospore left either in soil or in previous year’s plant debris. Thus the oospore is the source of primary inoculum and primary infections are caused by zoospores that are developed during the germination of the oospore with the return of favourable conditions. In perennial hosts, the causal organism can, however, perennate as mycelium and may be source, of primary inoculum.
In such case the primary inocula are the zoospores that are developed during the germination of the sporangia produced from the sporangiophores college botany borne on perennating mycelium. But in general, the secondary infection is caused by the zoospores produced during the germination of sporangia that are produced during primary infection. These zoospores thus constitute the secondary inocula.
Temperature conditions affect not only the germination of the both oospores and sporangia but also the susceptibility of the hosts. The optimum temperature being 10°G. Moisture on the host surface is essential for the production of inocula and infection. Host penetration is through stomata.
The greatest development of the disease is during the cool periods of the year. The existence of physiologic races has been demonstrated by many workers, but the extent of specialization and the number of races have not been thoroughly investigated.
Disease cycle of White rust of crucifers is presented in Figure 358.
Control:
One of the most effective methods of controlling the disease is the destruction of infected crop refuse of the previous year by burning to prevent the development of primary inoculum from the oospores. Next is the destruction of susceptible cruciferous weeds from in and around the crop growing areas.
Crop rotation to avoid the ill-effect of the previous year’s diseased crop is also recommended to control the disease incidence. In cases of severe attacks, destruction of diseased plants accompanied with spraying with fungicides such as, 0.8 per cent, freshly prepared Bordeaux mixture or 0.3 per cent. Blitox-50 often becomes very effective.
Disease # 2. Club Root of Crucifers:
This disease attacks a wide range of cultivated and garden plants, all of which belong to the family Cruciferae. Among the cruciferous weeds that a.re infected by this disease, mention may be made of shepherd’s purse (Capsella bursa-pastoris). The disease is widely spread throughout both tropical and temperature regions of the world.
Some of the common hosts are: cabbage, cauliflower, raddish, turnip, etc.
The first occurrence of the disease was reported from Scotland in 1780 and again in 1855. But the first scientific investigation of the disease on cabbage and the nature of its causal organism was done in Russia by Woronin in 1878. He established the fact that the disease is caused by a slime mold (Plasmodiophora brassicae) and worked out its general life history.
The disease is known under a great many common names:
In Germany it is ‘Kelch’ or ‘Kropf des Kohles’; in France it is ‘Maladie Digitoire’; in Belgium it is ‘Uingergiekt’; in Russia it is ‘Kapoustnaya Kila’ in England it is ‘Anbury’, ‘Hamburg’, and ‘Finger and Toe’; and in the United States ‘Club Foot’, ‘Club Root’, and ‘Clump Foot’.
Symptoms:
Club root, as the name suggests, is essentially a disease of the rooting system. The presence of the disease within the host tissue leads to a remarkable increase in growth in the parts affected, causing the roots, for the greater part, to become abnormally swollen. But the symptoms vary somewhat according to the nature of the host infected.
In the majority of cases the disease is manifested by a hyperplasia and hypertrophy in the root system.
The different types of symptoms are:
(i) Complete clubbing of both the main and lateral roots, the whole root system often resembles a mass of fingers and toes;
(ii) The main root becomes so much enlarged and clubbed as to assume the form of very large, irregular knots or tumours, the laterals remain healthy;
(iii) Only the lateral roots are transformed into clubs, while the main root remains free from clubbing;
(iv) Both main and lateral roots are affected, but healthy rootlets are developed from the diseased parts;
(v) Tumours or lobulated swellings of the tap root (Fig. 387A); and
(vi) Characteristic cracks or fissures and darkened areas develop in the affected parts of the root, but true hypertrophy is lacking.
A transverse section of hypertrophied root shows the infected areas to consist of several scattered groups of cells, chiefly in the cortex and medullary rays, having denser contents than normal. These cells are filled with plasmodia or with a multitude of minute spores (Fig. 387B to C).
In advanced stages of disease, due to increase in the size of the galls, disruption of the outer tissues of the host takes place and a general decay of the galled tissue sets in and the spores are released in the soil.
The disease may progress to a considerable extent before above ground symptoms become noticeable. But seriously diseased plants look sickly. Symptoms of wilting or a yellowing of the foliage are visible in them. Gradually loss of foliage takes place. Plants of this kind rarely form a head. If plants are older, when infected, they may head out but the heads are usually small and of inferior quality.
Causal Organism:
Plasmodiophora brassicae Wor. It is a parasitic slime mold. The vegetative phase consists of a plasmodium. There is no fruit body development in the life history of this slime mold. The plasmodium lives within the host cell and consumes the host protoplast and occupies the entire lumen of the infected cell.
The plasmodium at maturity cleaves down into fragments in such a manner that each nucleus with its surrounding portion of cytoplasm is enclosed by a wall and thus becomes a spore. This is how a mass of resting spores is developed. The spores are entirely free from one another, and they are held together by the host cell wall, until it is decomposed in the soil.
The spores are very small and spherical. A single diseased host cell contains a large number of these spores. The spores lie dormant in the diseased’ root cells or in the soil until the next season or until conditions are favourable for germination. The spores are liberated from the diseased root cells when the tissues decay or when the roots are eaten by animals or broken into pieces by some physical means.
When conditions are favourable for germination, the spores germinate in soil by the production of a swarm cell. Host penetration is effected by the swarm cell through-the root hair. The flagella are left behind the root hair. Only the body of the swarm cell enters the root hair. The body of the swarm cell without flagella exhibits amoeboid movement and is thus nothing but a myxamoeba.
The myxamoeba migrates to other host cells by direct penetration of the cell wall and there develops into plasmodium. If the plasmodium develops in this manner, it is probably haploid. But mycologists believe that there may also be a diploid plasmodium. They are of opinion that the myxamoeba produces haploid plasmodium in the root hair cells.
This haploid plasmodium gives rise to gametangia, again each gametangium produces a single gamete which morphologically resembles the swarm cell. The gametes are liberated out by the decay of root hair cells and gametangia. Gametic union takes place in the soil. The zygote so formed enters in the host tissue and gives rise to a diploid plasmodium from which resting spores are developed by meiosis.
Life cycle of Plasmodiophora brassicae is presented in Figure 388.
Disease Cycle:
Various factors such as soil acidity, temperature and moisture content of the soil control the disease incidence. The pH of the soil above 7’0 and a moisture Content between 45 and 60 per cent, are very suitable for the development of this disease. Loam and clay soils are generally less prone to harbour club root than light soil.
Usually low-lying, poorly drained soil favours club root, and well- drained soils inhibit it. The effect of temperature is rather indirect and its influence is related to the host development. Most pronounced development of club root is at a temperature range of 20°C. to 25°C., which is the temperature at which normal root growth occurs vigorously.
The causal organism is one of the most persistent soil-invaders. It remains viable in soil for 10 years or longer without the presence of host plants. Infected subterranean plant parts disintegrate in the soil, releasing the free spores. While the spores germinate with little or no resting period, a large percentage of them remain dormant for many years.
In the early stages of root infection, the invaded host cells are naturally those of the primary cortex, the parasite, later seeds out the primary cambium. The occupation of the cambium, however, initiates a much more serious phase of the disease than the occupation of the primary cortex. The presence of a plasmodium in a cell stimulates not only the occupied cell to meristematic activity but also the cells contiguous to it.
This is effected in two ways:
(a) by the one or more divisions of the infected cell being accompanied by a sharing of the plasmodium into the daughter and subsequent cells, before the divisional walls are laid down
(b) by bits of the Plasmodium, cut off within an infected cell, migrating through pores in the wall into contiguous cells, with a repetition of the same process within prescribed areas.
Both of these methods appear to be operative, though several authors deny the capacity of Plasmodia to penetrate cell walls.
Plasmodia portions within dividing cambial cells are supplied to practically every living cell added by the cambium. The parasitized cells, wherever they may occur, have no plan of division, and their irregular multiplication at advanced stages of infection takes place on so wide a scale that the proliferating tissues intrude upon the vascular continuity.
Such abnormal meristematic activity, at numerous centres of infection within a root, causes considerable displacement of host tissues which are therefore forced outwards and finally appear at the broken surface as clubs or galls of hypertrophied tissues.
Disease cycle of Club Root of crucifers is presented in Figure 389. 
Control:
Any effective control measure needs careful consideration the fact like:
(i) The causal organism is perpetuated by means of resting spores which remain either in soil or in infected host tissue,
(ii) The spores may remain dormant for several years.
(iii) The disease is disseminated by agencies which transport diseased plants or parts of plants, or contaminated soil,
(iv) The virulence of infection is favoured by acid soils and high moisture content of the soil.
Some of the suggested control measures are:
(i) Sanitation:
At harvesting time roots of diseased plants should not be left to decay in the soil. To guard against the spread of the disease, the diseased roots if fed to cattle should be thoroughly boiled before feeding. Soil should not be transported from infected field to new areas.
Long periods of rest from crucifers are advisable in order to starve the parasite out of the soil, and every effort should be made to eradicate susceptible weeds from the vicinity of the crops.
(ii) Crop Rotation:
Since the pathogen remains viable in soil for several years, a comparatively long rotation with non-cruciferous crops should be adopted to control the disease incidence.
(iii) Soil Treatment:
Since acid soil is favourable for disease incidence, neutralizing the acid soil with lime in the form of raw-ground lime, caustic lime, and hydrated lime often produces better result. The me of Calcium cyanamide as a substitute for lime is also effective. Often good results follow the application of disinfectants such as the highly poisonous chlorides of mercury, corrosive sublimate and calomel.
(iv) Soil Drainage:
The use of too much of free water should be avoided. Necessary soil drainage facilities are to be made to avoid water logging.
(v) Use of Resistant Varieties:
Grow resistant varieties.