Skip Navigation Links Potato: Solanum tuberosum L.
Family: Solanaceae




1. EARLY BLIGHT

The disease is very commonly found on potato, tomato and other solanaceous crops and is worldwide in distribution. The pathogen has very wide host range. The disease is appear in early season that why it is known as early blight. The pathogen is producing similar disease symptoms on its hosts.

Symptoms: The disease mainly infects leaves and tubers. Initially the symptoms occur on the lower and older leaves in the form of small (1-2 mm) circular to oval, brown or dark brown spots. These lesions have the tendency to become large and angular at later stage. Mature lesions on foliage look dry and papery and often have the concentric rings. The spots coalesce to form a large patch which results in leaf blight. The entire foliage is blighted in severe disease incidence. The pathogen produces slightly sunken, dark coloured and linear lesions on stems and leaf petioles. The symptoms on the tuber comprise of brown, circular to irregular and depressed lesions with underneath flesh turning dry, brown and corky. Lesions tend to enlarge during storage and affected tubers later become shriveled.  

Causal Organism: The early blight disease of potato, tomato and other solanacaeous crops is causing by Alternaria solani (Ell. and Mart.) Jones and Grout. The mycelium of the pathogen is septate, branched and light to dark brown. The conidiophores emerges from the stomata are septate, dark coloured, borne singly and measuring 50-90 x 8-9 µm. The conidia are borne in chains on the conidiophores which are muriform, with transverse and longitudinal septa, dark brown, constricted at the septa, long beaked and measuring 120-290 x 12-20 µm. The pathogen produces alternaric acid, a non-specific toxin, in the host tissues which is responsible for chlorosis.

Disease Cycle: The pathogen responsible for disease is mainly soil borne. The primary infection of the disease is occurs through tubers. The fungal mycelium and conidia may remain in dormant stage in host plant debris for a year or more. The other collateral hosts play an important role in the dissemination and perpetuation of the pathogen. The disease incidence may increase if abundant humidity is present followed by low temperatures.

Disease Management:

  1. Use of disease free seed tubers for raising the crop is important for minimizing the fungal inoculum.
  2. The crop must be given balanced doses of fertilizers, especially nitrogen. Spraying the crop with urea (1.0%) at 45 days after sowing and giving subsequent sprays 8-10 days after the first spray helps the crop to easily escape the severe onslaught of early blight disease.
  3. In the hilly regions, spraying of Copper Oxychloride (0.30%), Zineb (0.30%), Brestan 60, Dithane M-45 and Bordeaux mixture (1.0%) is recommended for control of early blight disease.
  4. Solanaceous crops, which act as the collateral hosts for the disease organism, hence their cultivation nearby potato fields, must be avoided. The cultivation of resistant varieties such as Kufri naveen, Kufri sindhuri and Kufri jeevan is recommended to protect the crop from pathogen.

 

2. LATE BLIGHT

The potato crop is native to north andes (south America) and the late blight is an endemic disease. This is one of the worst disease and responsible for great famine of Europe in 1840. The disease is reported from India in 1870-1880 from Nilgiri hills. The disease caused severe losses in crop yields and is estimated in Punjab (20-25%), Haryana (40-50%), Uttar-Pradesh (15-50%) and Bihar and West Bengal (5-10%).

Symptoms: The disease affects all plant parts, viz., leaves, stems and tubers. It first appears on leaves as small pale green spots, which enlarge into large water soaked lesions under humid and cloudy weather. The dirty brown lesions later become turn black. A white mildew (cottony growth) ring forms around the dead areas on the lower side of leaves. In dry weather, water soaked areas turn necrotic brown. On stems, light brown elongated lesions are formed which may encircle the stem. The fungus infects the tubers formed inside the soil causing dry rot and brown discolourations of the tissues. The frequently metallic tinge develops on the margins of the affected tissue. The tubers carrying the pathogen are the real carriers and serve as the source of the disease in the subsequent season. Infected seed tubers grow into healthy plants but under favourable conditions for the disease (10-12OC and RH > 80%) development, the disease infects the stem and lower leaves.  

Causal Organism: The causal pathogen of the late blight disease is Phytophthora infestans (Mont.) de Bary. The hyphae of the pathogen are branched, hyaline and coenocytic. The pathogen produced branched sporangiophores in clusters through stomata which bear thin walled, hyaline, lemon shaped and papillate sporangia. The sporangia are disseminating through wind and germinate by germ tubes, causing further infection. The pathogen produces thick walled oospores through sexual reproduction and germinates by sporangia which have biflagellate sporangiospores.

Disease Cycle: The primary infection of the disease is initiated through infected tubers and secondary spread of the disease is found by conidia produced abundantly on the host. The conidia are disseminated by air and irrigation water. The pathogen produced sexual spores within the tissues during adverse environmental conditions. When host plants and tubers come in contact with the fungal pathogen, it attacks the plants and remains in dormant condition. When such infected tubers stored and use for the seed material in next growing season, the pathogen again become active in the presence of soil and cause further infection in the host plants. The disease cycle is continued in the same way year after year. The pathogen can not remain viable saprophytically in the soil but present in the field by infecting other solanaceous hosts.

Disease Management:

  1. Seed potatoes should be checked thoroughly before storage. All blighted tubers must be removed and buried deep in the soil.
  2. Ridges should be made high enough to cover all daughter tubers and reduce chance of their infection upon exposure.
  3. If the weather conditions (temperature 10-20OC, RH>80%) are favourable for the disease development irrigation should be stopped immediately. The light irrigation is given, if essential.
  4. When the disease affects 75% crop foliage, the haulms should be cut, removed from the field, and buried deep.
  5. The mycelium in the infected tuber can be killed by exposing tubers at 40 °C for four hours or 30 °C for 65 hours.
  6. The dipping of tuber seed material in 1 percent Bordeaux mixture is useful in checking disease.
  7. Protective sprays with a contact fungicide, viz., Mancozeb (0.2%) before appearance of the disease is effective. Subsequent sprays if necessary should be repeated at 8 to 10 days interval. In case of severe blight attack, one or two sprays of Metalaxyl (0.25 %) are given to check the further spread of the disease. Mancozeb is applied at an interval of 15 days after the Metalaxyl application. Some other effective fungicides are Dithane Z-78, Dithane M-45, Oxadixyl, Brestan and Difolatan.
  8. The cultivation of resistant varieties such as kufri kundan, kufri kumar, jeevan, kufri neela, kufri muthu, kufri jyoti, kufri khasigaro, kufri badshah, kufri sherpa, kufri kishan, kufri sindhuri and kufri kuber is best way to control disease completely.

 

3. BLACK SCURF AND STEM CANKER

The black scurf is a serious disease of potato in all potato growing areas of India including hilly regions. The disease is causing considerable yield loss in potato crop. The disease also reduced market value of tubers.

Symptoms: The disease commonly affects the tubers, sprouts, stems and stolons. The most common symptom is black scurf comprising of dark brown to black irregular lumps sticking on the surface of tubers which are sclerotia of fungus. These irregular lumps are closely adhered to the tuber surface and do not wash off easily. Other symptoms on the tuber include skin cracks, crater like depressions, pitting, stem-end necrosis and shape deformity. The disease often causes sprout injury both in storage and in fields after planting. The affected sprouts show discoloration of tissue. The heavily infected sprouts cannot emerge from soil leading to space in germination. The emerging sprouts when infected later develop cankers causing girdling of stem bases. Such affected plants show upward rolling of leaves with pinkish or purplish margin. Often small green or reddish aerial tubers are also formed in the axils. The infection also spreads to roots and developing stolons resulting in rotting of cortical tissues. Such infected roots later shed away hence infected plants have poor root system. Infected stolons give rise to deformed tubers.  

Causal Organism: The causal pathogen of black scurf disease of potato is Rhizoctonia solani Kuhn. Fructification delicate, thin hypochnoid pellicle, white to buffy, hyphae branching at right angle with some cruciform cells, without clamps, 7.5 – 14 µm in diameter, basal long celled with barrel shaped segments, branching abundantly and bearing the basidia in small imperfectly symmetrical cymes. Basidia subcylindric and barrel or obpyriform shaped, 14 -18 µm x 8 - 10 µm bearing four sterigmata which arise as blunt knobs and become later horn shaped, 7.5 – 12 µm x 2.5 - 3.5 µm. Spores ellipsoid or oblong ellipsoid, thin walled, flattened on the inside, truncate to apiculate, 9 - 12.5 µm x 5 - 7 µm.

Disease Cycle: The pathogen is seed tuber and soil borne. The infected tubers bear the pathogen on its surface black to chocolate coloured hard fungal sclerotia. When such contaminated seed tubers are used for plantation purposes, the pathogen become active and infect the growing young shoots and killed them. The killing of young shoots showing gaps in the fields and nearby growing plants are also get infected and showing dark brown canker at the collar regions. The canker formation at collar region is results in the wilting and death of the plants. The translocation of food material from leaves other regions is interrupted which results in stunting and purpling of the leaves. The pathogen produced black sclerotia on the tubers and remains viable up to next growing season.

Disease Management:

  1. Combination of tuber disinfection and improved cultural practices successfully checks the incidence and severity of black scurf.
  2. In the hills tuber treatment with an organomercurial compound (Agallol) & soil application of PCNB @ 30kg/ha is most effective. In the North India plains, treatment of the diseased seed with Thiabendazole, TBZ + 8 Hydroxyquinoline, acetic acid + zinc Sulphate, Carbendazim and Boric Acid effectively controls the disease. The progeny tubers of such treated seeds are usually free from black scurf. A continuous use of treated seed for 2-3 crop seasons is found to completely check the disease.
  3. Crop rotation with maize or 'dhaincha' (Sesbania aegyptiaca) for green manure also checks the disease build up.

 

4. WART

It is one of the most dreaded diseases of potato. The disease was first time reported from Hungary in 1895. Now the disease has been reported from Bolivia, Canada, India, Europe, Mexico, Peru, South Africa, U. S. A. In India, the disease is frequently occurred in North-East Himalaya. The losses from the disease are very high due to it affects tubers.

Symptoms: The most favourable conditions for the development of the disease are periodic flooding followed by lack of proper drainage and aeration. The wart affected plants bear bigger leaves and littler taller haulms which are green in colour and no disease symptoms are seen on the shoots. The disease is characterised by 'cauliflower-like' dark brown colour warty growths on tubers, stolons and stem bases but not roots. The size of the wart depended on the disease intensity. In severe disease infection and under wet conditions, it may be seen in the form of greenish-yellow crust on the stems and leaves at or near the soil level. All the tubers on diseased plant do not necessarily develop warts. Diseased tubers may show formation of either one or more tumours. Such tubers sometimes are completely transformed into warty mass. The tumors may turn brown to black with age.

Causal Organism: The fungal pathogen responsible for wart disease of potato is Synchytrium endobioticum (Schilb.). The pathogen produces thin walled sporangia in summer and winter. The resting sporangia are released by the decay of infected tissues and may remain viable for many years in the soil. The sporangia germinate through vesicles and produce zoospores which are uniflagellate. These zoospores lose its flagellum before infecting potato tubers. The naked protoplast enters in to tubers through pores. When it reaches in lower part of the cells, the surrounding cells start repeated division and form characteristic tumourous tissue. A golden brown and double layered wall is secreted around the thallus and produced prosorus which ultimately produced zoospores which liberated in to the soil and again infect the tubers.

Disease Cycle: The wart disease is soil borne and causal pathogen survives in the soil for many years in the form of resting sporangia. They can be obtained in dry soil up to after 15 months and in dry debris after 60 months. The transportation of infested soils and infected plant tubers by different ways are the means of spreading of the pathogen. The short duration of water saturation is essential for the germination of resting spores, sporangia and movement of zoospores. The optimum temperature for initiation of infection is 12-24 °C and pH ranges 3.9-8.5.

Disease Management:

  1. Wart affected tubers used as seed are the chief means of the disease spread. The disease may also spread through seed of wart immune varieties grown in wart infested land, contaminated soil carried on the feet of men, animals or farm implements, and manure containing diseased material.
  2. The disease incidence can be minimized through practicing of long crop rotation (5 years or more), using disease free potatoes as seed material and burning of wart affected lumps and potato peelings are effective in checking the spread of the disease.
  3. The cultivation of resistant varieties to wart disease is only useful way to control the disease. Some such resistant varieties are Kufri muthu, Kufri sheetman, Kufri sherpa, Kufri khasi garo, Kufri bahar, Kufri kumar, Kufri kanchan and Kufri swarna.
  4. The application of chemical fungicides was not found effective in disease management.

 

5. BACTERIAL WILT OR BROWN ROT

The brown rot of potato is a vascular disease caused by bacterium Pseudomonas solanacearum. The disease is wide spread in tropical, subtropical and warm temperate regions of Africa, Asia, Australia, Central and North America, Europe and West Indies. The disease is become a serious problem India and found almost at all potato growing areas. The disease has been reported from sixteen states of India and the yield loss may be varies depending on the climate, host susceptibility and availability of inoculum. The pathogen has very wide host ranges.

Symptoms: Brown rot or bacterial wilt is a destructive disease of the potato. The pathogen affects both the above and underground plant parts. It causes losses in two ways: (i) premature wilting and death of the plants leading to total loss of yield, and (ii) rotting of the tubers in transit or storage. The earliest symptom is slight wilting of the top which is soon followed by total wilting. The wilting of the plant is caused by a toxin produce by bacterium. In advanced stage, if the base of the stem of the affected plants is cut transversely and squeezed, the bacterial mass is seen to ooze out as a dull white slimy mass on the cut surface. The tuber produced two types of symptoms viz. vascular rot and pitted lesions. In vascular rot, the vascular tissues look like a water soaked circle, which subsequently may turn brown. At advance stage of infection, the tubers shows brown discolouration on the skin. The lesions on tuber are produced due to infection through lenticels (skin pores). Initially water soaked spots develop which enlarge forming pitted lesions.

The bacterium is mainly confined to the vascular tissues of the host plants but in advanced stages, it may invade the cortex and pith regions, causing tissue discolouration. The infected tubers may start rotting in wet soils and may exude bacterial mass from the eyes which adhere in the soil.

Causal Organism: The brown rot and wilt of potato is caused by bacterium Pseudomonas solanacearum (Smith) Smith which is currently known as Ralstonia solanacearum (Smith) Yabnuchi et al. The bacterium is gram negative, motile with polar flagella and aerobic. The bacterium does not contain virulence if cultured in laboratory media. The bacterium has five races and five biovars.

Disease Cycle: The disease is soil borne and bacterium live in the soil on diseased plant debris. The disease is spread from diseased to healthy tubers through cutting knives used in preparation of tuber seeds and irrigation water. The infection can be takes place by wounds caused by cultural practices, insects and nematodes. The potato tubers carry the bacterium through their vascular tissues, on the surface and in the lenticles. The disease is favoured by high temperature (21-38 °C) and high soil moisture (50-100 percent water holding capacity). The bacterium may remain viable in the soil for sixteen months and in the disease plants for nine months.

Disease Management:

  1. The infected seed tubers including apparently healthy seed tubers from diseased crop are important in spread and carry over of the disease. Hence, disease free seed tubers obtained from disease free areas should be used for planting.
  2. Splitting of the tubers at the time of the planting should be avoided as splitting spreads the disease even to health tubers.
  3. The pathogen is heat susceptible and covering the soil with polythene sheet for raising the soil temperature has been found effective in disease control.
  4. The irrigation water should not move from diseased to healthy areas and infected plants should be removed and burnt. The deep ploughing after crop harvesting in May or June exposes the soil inoculums to summer heat strokes and kills them effectively.
  5. Application of stable bleaching powder (12kg/ha) mixed with fertilizer in furrows while planting reduces wilt incidence by 80%.
  6. The tuber seeds should be treated with 0.02 percent streptocycline for 30 minutes.
  7. Practicing crop rotation for 2-3 years with crops like maize, finger millet, cabbage, cereals, garlic, lupin and onion can reduce the disease inoculum.

 

6. SCAB

The common scab of potato is reported from all over the world. The disease is the most prevalent and important in neutral or slightly alkaline soils. In India, the disease is become widespread in Assam, Bihar, Haryana, Himachal Pradesh, Punjab, Maharashtra, Meghalaya, Uttar Pradesh and West Bengal. The disease can causes up to 40 percent yield losses that is due to rough and blemished skin.

Symptoms: The symptoms of the disease appear on the tubers as shallow or deep lesions. The shallow scabs of the affected tubers are showing superficial roughened areas on the skin, sometime above and below the plane healthy skin. The arising tissues are often become dark coloured and corky which are vary in shape and size. The deep scabs produce more dark and 1-3 mm large lesions.    

Causal Organism: The common scab of potato is causing by Streptomyces scabies. This is slender, branched, aerial, grey coloured mycelium with few or no cross septa. The conidiophores are branched, septate, spirally coiled with terminal branches. The fragmentation of the hyphae forms spores or conidia in chains and disseminated after breaking. The spores are barrel shaped or cylindrical and smooth. The spores germinate through germ tubes.

Disease Cycle: The pathogen is transmitted through soil water, wind blown soil and infected potato seed tubers. However, the main source of disease dispersal is infected tubers. The pathogen penetrates inside the tissues through lenticels, wounds, stomata or directly in young tubers. The pathogen grows inside between the cells, the cells die and pathogen then live there as saprophyte. The pathogen is secretes a chemical substance which stimulate the cell division in the surrounding cells of lesion and produce several layered cork cells. The pathogen is multiplied inside the dead corky cells and large scab lesions develop. The disease development is favoured by dry soils.

Disease Management:

  1. The pathogen is difficult to control because of long survival both on seed tubers and in soils. However using disease free certified seed tubers could minimize the disease incidence.
  2. Before planting the seed tubers are treated with organomercurial compounds  such as Emisan-6, Agallol or Aretan (0.015%for 20 minutes) or Boric Acid (3% for 30 minutes) and dries in shade. The same treatment is repeated before the storage of the tubers.
  3. The long crop rotation with non-host crops (wheat, pea, oats, barley, lupin, soybean, sorghum and bajra) can give disease control to some extent.
  4. The application of green manures may be helpful in checking the disease development.
  5. The sowing of resistant varieties like kufri sindhuri is useful for disease control.