Wart disease, often called “black wart”, causes severe damage to potato specifically in regions of cool climate throughout the world. This disease was first discovered and described in Hungry in the year 1895.
In India, the disease was first reported by Ganguly and Paul (1953) from Darjeeling and is restricted to the same district and adjacent areas. It is because the pathogen fails to overcome hot climatic conditions, and does not succeed in spreading the disease to other parts of the country.
Symptoms of Wart Disease:
Symptoms appear only on underground parts (tubers, buds on stems, stolons) of shoot and basal part of the stem near ground level. They are characterized by warty, tuberous, and dirty cauliflower-like outgrowths on infected parts. The outgrowth is roughly spherical and usually not a solid structure. It is soft pulpy and can be cross-sectioned more readily than a tuber. However, the roots are never infected and do not show any symptoms.
Casual Organism:
The fungal pathogen is an obligate parasite. Its vegetative body (thallus) is “endobiotic” (living entirely within the cells of its host) and “holocarpic” (complete vegetative thallus converted into reproductive structures). The unicellular, naked vegetative thallus grows in size, rounds up, and secretes a bi-layered thick-wall around it. This structure is called a “prosorus”, which enlarges and attains a size probably largest among fungi (upto 80 µm in diam) and settles at the bottom of the host cell.
The prosorus now germinates producing a vesicle, which develops into a “sorus”, a structure containing many sporangia under a common wall. Each sporangium of the sorus produces many uniflagellate zoospores in it. When the zoospores mature, they are set free into the soil.
They hop and swim in the film of soil water, contact susceptible underground-parts of the host, come to rest and withdraw their flagella, and enter the host cell bodily through a pore dissolved by their enzyme activity. This represents the vegetative thallus of the pathogen.
With the arrival of dry weather or approaching towards the end of the crop season the zoospores start functioning as “planogametes” instead of infecting the host. The planogametes fuse in pairs (or occasionally in groups of 3 or 4) forming a bi-flagellate zygote. The planogametes from same sporangium (or gametangium) never fuse with each other. However, the bi-flagellate zygote swims for some-time in the film of water in soil, approaches to and settles on the host surface, and enters inside the host in the same manner as the zoospores do.
Karyogamy occurs in zygote before penetration and the thallus developed as a result of zygote-germination is diploid. The diploid vegetative thallus lies at the bottom of the infected cell and transforms into a “resting sporangium” instead of prosorus. The resting sporangium is dark-brown in colour and forms folds and ridges on its surface.
Resting sporangia are released into the soil due to decay of infected parts and may remain viable in soil for many years. When incurable conditions come back, the resting sporangia enjoy meiosis and produce large number of haploid zoospores (uniflagellate) in soil. These zoospores, enter inside the host and transform into vegetative thallus.
Wart Disease Cycle in Potatoes:
(i) Perennation:
The pathogen perennates through resting sporangia present in infected plant debris in soil, or released in soil due to decay of plant debris. With the arrival of dry weather or approaching towards the end of crop-season the zoospores being produced during primary as well as secondary infections turn towards sexual course of reproduction, function as planogametes, and produce finally, resting sporangia.
The latter are very resistant to extremes of temperature, high and low, and may remain viable in soil even in the absence of a potato crop for many years. Resting periods of 9 to 12 years have been recorded in many instances.
(ii) Primary Infection:
When potato crop becomes available in the field and meteorological conditions turn to be favourable, the perennating structures (resting sporangia) germinate producing zoospores in soil. The zoospores approach the underground shoot-parts, withdraw their flagella, and bodily enter the host cells wherein they (now called vegetative thallus) settle down at the bottom of host cells.
Now, each of the host cells containing vegetative body of the pathogen swells and the neighbouring cells start dividing repeatedly (hyperplasia) followed by swelling (hypertrophy). Ultimately, the wart is formed on the infected plant part and thus symptoms are manifested.
(iii) Secondary Infection:
The protuberances (outgrowths; warts) that are formed due to primary infection are the centres of secondary inoculum. The zoospores, which are produced by the sporangia within the host tissue (particularly warts) during primary infection get released in soil, and ultimately cause secondary infection on healthy tubers or other underground shoot. If conditions are favourable, the zoospores are produced repeatedly and bring many secondary infection cycles in one growing season.
However, both primary as well as secondary infections may occur at the same time in the soil during favourable environmental conditions. This results in severe disease incidence and destruction of potato crop.
When the weather dries or the crop-season approaches towards end, the zoospores produced as a result of primary and secondary infections stop causing any fresh infection and start functioning as planogametes. The latter fuse and, finally, result in resting sporangia production, which survive during unfavourable conditions and serve as source of primary infection during next growing season.
Predisposing Factors:
A temperature between 12 to 24°C and a high degree of soil moisture are the factors that help quick germination of resting sporangia and zoospores in soil resulting in severe infection. It has been reported that a periodic flooding followed by drainage at a relative soil humidity of 45% and aeration are very favourable for the disease incidence. However, slightly acidic soil proves most favourable for disease development.
Management of Wart Disease:
1. Once introduced in an area, it becomes difficult to control the disease because of any effective control measures evolved.
However, some of the following practices can reduce disease incidence:
(i) Seed stock from infested fields should be discarded,
(ii) The quarantine regulations should be observed strictly, and
(iii) Thoroughly cleaning the cultivation plots and burning the previous year’s plant debris should be undertaken.
2. Besides, soil treatment by fumigants (e.g., mercuric chloride, ammonium sulphocyanate, copper sulphate, 5% formalin) is thought to eradicate the pathogen from an infested area, but they are too expensive and impracticable to apply on large scale.
3. The only practical and effective measure to manage the disease is the use of resistant varieties. Kufri Muthu, Kufri Sheetman, Kufri Sherpa, Kufri Khasi Garo, Kufri Bahar and Kufri Kumar are recommended varieties. More recently, red-skin Kufri Kanchan variety has been found resistant to the wart disease. Kufri Swarna variety is also resistant to the disease.
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