Economically Significant Fungal Diseases of Potato and their Management


Abstract The cultivation of potato is often affected due to attack of various diseases caused by fungi, bacteria, viruses and nematodes etc P. infestans over-summers as dormant mycelium in infected tubers in the cold storage. The presence of late blight infection in apparently healthy tubers collected from diseased field provides new dimension to the epidemiology of this disease. Fungicides like azoxystrobin, fenamidone, famoxadone, iprovalicarb and mefenoxam and their combinations with contact fungicides like mancozeb have shown promising efficacy against potato late blight. Early blight (Alternaria solani), can survive as conidia or mycelium in dried infected leaf bits in the soil. Sprays of mancozeb, zineb, ziram, propineb and others like chlorothalonil, captan, copper oxychloride, Bordeaux mixture, captan etc. have been reported to be effective against this disease. In Black Scurf (Rhizoctonia solani) the fungus perpetuates in the form of sclerotia on the seed tubers or in the soil. It can survive in the soil for many years and has wide host range. Successful management of fungal potato diseases can be achieved mainly by integrated desease management, using resistant potato varieties, following the proper cultural practices and by chemical treatment of the crop and ,sometimes, of the seed. This review deals with the important fungal disease problems in potato, their etiology, epidemiology and different strategies for effective management.

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Key words: Potato, fungus, fungicides, tubers


Potato (Solanum tuberosum L.) is an important vegetable crop and is cultivated over an area of about one million hectares in India, with the total production of more than 1.5 million tons. Important potato growing states are Uttar Pradesh, West Bengal, Bihar, Assam, Himachal Pradesh, Madhya Pradesh, Punjab and Karnataka. One to three crops per year are taken under varied agroclimatic conditions. In India, about 80 per cent of potato crop is cultivated under subtropical and 20 per cent under temperate to sub-temperate climate. The cultivation of this crop is often affected due to attack of various diseases caused by fungi, bacteria, viruses and nematodes etc (Khurana et al., 1998).

Late Blight

This disease is caused by Phytophthora infestans. Late blight is the most destructive disease of potato throughout the world and was recorded in the beginning of nineteenth century in the Andes Mountains of South America. The disease is believed to have been introduced into Europe from South America in early 1840s from where it spread to other countries and caused a famine in Ireland (known as Irish famine) during 1845-46 resulting into deaths of millions of Irish people and an equal number migrating to other parts of the world, particularly North America. The systemic development of Plant Pathology as a discipline started after this famine. Late blight has the tremendous potential to cause up to 70 % reduction in the yield in a susceptible cultivar. The losses ranging from 20-25 % in Punjab, 40-50% in Haryana, 15-20% in Uttar Pradesh and 5-10 % in Bihar and West Bengal have been reported (CPRI, 1987). In India, annual losses due to late blight have been reported to range between 10-75% (Dutt 1979). The extent of damage depends largely at which stage the crop is attacked and it is usually heavy when infection occurs on the young crop stage before tuberization that sometimes can result into complete yield losses in epidemic years and the losses vary between 15 to 100 per cent depending on cultivar, crop stage and the fungicides sprayed (Thind and Mohan 1998).


The symptoms of late blight appear on leaves, stem and tubers. Initially small, water-soaked lesions develop near the tips and margins of the leaves which rapidly grow into large, brown to purplish black, necrotic lesions under favorable weather conditions. During morning hours, whitish downy growth of the pathogen consisting of sporangiophores and sporangia can be seen on the edges of the lesions mostly on the underside of the leaves. Light brown to dark brown lesions appear on stem and petioles which may elongate later and girdle the affected parts. The affected stems become weak and collapse, causing death of the plant parts above the lesions. Sometime the tender growing stem tips and nearby young foliage are attacked in the young crop and the plants stop their growth and wither soon. Since the disease is polycyclic in nature, the entire crop in a field may be killed in one or two weeks and the field gives blighted appearance. The tubers may get infected by rain-washed sporangia from the diseased foliage. The infected tubers show irregular, small to large, slightly depressed areas of brown to purplish skin which extend deep into the internal tissue of the tubers. The infected tuber tissue which is firm and dry in the beginning is often invaded by secondary pathogens, mainly bacteria, in the field or poorly ventilated storage places resulting into soft rot of tubers.

Causal Pathogen

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Late blight is caused by Phytophthora infestans (Mont.) de Bary which belongs to division Mastigomycotina, class Oomycetes, order Peronosporales and family Pythiaceae. The mycelium is coenocytic, hyaline, branched having simple to club shaped haustoria. Sporangiophores originate from internal mycelium and emerge through stomata on the leaves and tubers. These are slender, hyaline, sympodially branched, indeterminate, septate having side branches with swollen bases. Sporangia are formed on the tip of sporangiophores and are hyaline, thin walled, lemon shaped, papillate having up to 30 nuclei, measuring 21-28X12-24 µm. The sporangium turns to the side on maturity and sporangiophore growth continues with characteristic swollen nodes. This fungus is heterothallic and requires two mating types A1 and A2 for sexual reproduction. In India although A1 mating type is of common occurrence, prevalence of A2 type has been recorded in Shimla hills after 1984 (Singh et al., 1993). Antheridia and oogonia are produced after A1 and A2 mating types come in close contact. Antheridia are amphygynous while oogonia are spherical. Oospores are 24-46 µm in diameter, thick walled and develop after fertilization. Oospore formation varies depending upon particular A1 and A2 combinations and also on infected potato genotypes (Cohen et al., 1997) but self production of oospores in A1 population is also reported. There has been shift from simple 0 and 4 races to complex 4-8 gene races of P. infestans after 1965 in India. (Arora 1990) reported that development and fitness of complex races is dependant on cultivars planted and favorable weather conditions.


Various measures which aim to reduce the primary inoculum and spread of the disease can help in effective management of potato late blight. These include transgenic approach, sanitary measures, use of healthy seed, cultural practices, host resistance and use of fungicides.

Transgenic approach

Potato (Solanum tuberosum L.) late blight, caused by Phytophthora infestans (Mont.) de Bary, is one of the most damaging diseases in any crop. Deployment of resistant varieties is the most effective way to control this disease. However, breeding for late blight resistance has been a challenge because the race-specific resistance genes introgressed from wild potato S. demissum Lindl. have been short lived and breeding for "horizontal" or durable resistance has achieved only moderate successes. The high-level late blight resistance in a wild potato relative, S. bulbocastanum Dunal subsp. bulbocastanum, is mainly controlled by a single resistance gene RB. Transgenic potato lines containing the RB gene have showed strong late blight resistance, comparable to the backcrossed progenies derived from the somatic hybrids between potato and S. bulbocastanum. RB gene into potato using traditional breeding methods, an alternative to deploying the RB gene through genetic transformation (Lara et al., 2006)

Sanitary measures

Infected seed tubers, diseased haulms left in the field and cull piles, which may serve as primary source of inoculum, should be destroyed by burning or proper burying them deep in the soil. Application of certain chemicals such as sodium chlorate or chlorthiamid granules is also useful for this purpose. Volunteer or self sown plants and weeds which may harbour late blight infection can be destroyed by application of some suitable herbicides.

Use of healthy seed

Since infected seed is the major source of primary inoculum for late blight, apparently infected tubers should be sorted out before and after storage and the cull piles destroyed by burning or burying deep in soil. Potato tubers to be used for seed should be taken from a disease free crop. The use of healthy tubers for seed will ensure healthy and disease free crop.

Cultural practices

Some alterations in the cultural practices may prove beneficial in reducing late blight incidence in the field. Proper hilling and earthing up of potato tubers should be practiced to minimize chances of tuber infection. Wider row to row and plant to plant spacing ensures better penetration of air and sunshine to lower parts of the plants thus creating unfavorable conditions for development of the disease. Cultivation of the blight resistant and susceptible varieties together reduces the rate of spread of the disease epiphytotic (Bhattacharyya and Singh 1990). Cultivation of potato with some other crop like wheat also slows down spread of the disease. In the north-western plains of India like Punjab and Haryana, early planted crop (in September) generally harvested pre-maturely after about two months remains free from late blight. Main season autumn crop planted in early October is harvested in January-February and is often attacked by late blight. In Himalayan hills the disease generally appears in late June and in plains in mid-November to mid December. So planting of early maturing varieties in early April in hills and in late September or early October in plains following by dehaulming of plants at 1% disease intensity should prove beneficial.

Host resistance

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Use of resistant varieties is regarded as the best means of late blight management. Initially the resistance was derived from Solanum demissum which soon broke down due to development of specialized races of the pathogen. Early studies had shown that the resistance in potato plants to P. infestans was inherited as dominant character and the R genes control hypersensitive response in a race specific manner. Later it was realized that the pathogen exists as race complexes and has the ability to produce new races rapidly. In India earlier simple races like race 0 and 4 were prevalent, but now with the introduction of new varieties multigene races are occurring both in hills and plains and eleven multigene races are reported using potato differential lines with 0 to 11 R resistance genes. Now the efforts are directed to produce varieties having polygenic field resistance. Such resistance sources are available in species like S. demissum and S. stoloniferum and such resistance is governed by a number of minor and independent genes. Field resistance is associated with characters like longer incubation period, reduced pathogen growth within the host tissue, reduced sporulation and late plant maturity. (Louwes et al., 1992) have also reported S. circaefolium sub sp. circafolium to be a good resistance source as well against late blight.

The Central Potato Research Institute, Shimla has developed and released several blight resistant varieties of potato for cultivation in different parts of the country including hilly and plain areas which include Kufri Jyoti, Kufri Sherpa, Kufri Badshah, Kufri Jeevan, Kufri Jawahar, Kufri Muthun etc. However, an important area is still under Kufri Chandramukhi which is highly susceptible to late blight. In Kufri Jyoti and Kufri Badshah varieties the blight appears about 20 days later than Kufri Chandramukhi and these varieties show less foliar infection (15-35%) till end of the season while Kufri Chandramukhi is completely killed within a month (Anonymous, 1991). (Bjor and Mulelid, 1991) reported cultivar Pimpernal without R genes to possess resistance to tuber blight. Das et al. (1996) have developed blight resistant clones of commercial varieties using gamma radiation.

Chemical control

Fungicides form an important input for managing late blight of potato because host resistance in commercial varieties is often broken down by multigene races of the P. infestans. Several fungicides have been reported to provide good control of late blight in India and other countries. Bordeaux mixture and Burgundy mixture which were used earlier were later replaced by copper oxychloride, captafol, mancozeb, zineb, propineb and other dithiocarbamates, chlorothalonil etc. (Dutt, et al., 1982; Malathi and Jeyarajan, 1995). These have to be used as prophylactic applications before infection is established. Mancozeb is now an accepted fungicide for late blight control in India and is reported effective by several workers. A preventive fungicide application schedule appears more effective (Thind, et al., 1989) for contact fungicides and spraying with these fungicides before usual dates of disease appearance when the crop is about six weeks old in north Indian conditions gives better control.

In the past two decades, several systemic fungicides with significantly better efficacy have been found promising for late blight control. Metalaxyl, an acylalanine fungicide, has proved most effective against this disease (Schwinn and Staub, 1987). Oxadixyl, banalaxyl, ofurace and dimethomorph are other specific fungicides having high efficacy against this disease (Thind and Mohan 1997; Mohan and Thind 1999). Dipping of sprouted tubers in 0.1 per cent metalaxyl for 30 minutes suppresses the disease (Singh and Bhattacharyya, 1990). However, excessive and irrational use of these phenylamide fungicides may lead to the development of resistance in the pathogen. Metalaxyl resistant populations of P. infestans have been reported in many countries (Dowley and O'Sullivan, 1991; Deahl et al., 1993) including India (Arora, 1991; Thind, et al., 2001.). To avoid the development of fungicide resistance, mixture formulations of systemic and contact fungicides are generally recommended. Ridomil MZ (metalaxyl + mancozeb) is one such mixture being commonly used against late blight (Alam et al., 1991; Thind and Mohan, 1997). Other mixtures which are in use for late blight control are ofurace + mancozeb, cymoxanil+ mancozeb, dimethomorph + chlorothalonil, dimethomorph + mancozeb, oxadixyl + mancozeb, oxadixyl + copper oxychloride, banalaxyl + mancozeb and few others. Recently, newly developed fungicides like azoxystrobin, fenamidone, famoxadone, iprovalicarb and mefenoxam (a new enantiomer of metalaxyl) and their combinations with contact fungicides like mancozeb have shown promising efficacy against potato late blight (Thind et al., 2004a,b).

Forecasting based fungicide applications reduce the cost of disease management by reducing number of applications. A preventive spray schedule of contact fungicides like dithiocarbamates is recommended as soon weather conditions like temperature and relative humidity become favourable. Phenylamide fungicide mixtures need to be sprayed only when heavy disease risk situation prevails in the event of intermittent rains and cloudy weather.



The disease mainly affects foliage and may uncommonly occur on stem and tubers. The symptoms first occur on lower leaves as dark brown, oval or angular spots scattered on the leaf surface. The spots are usually surrounded by a chlorotic zone which may extend much beyond the lesion due to the presence of toxin 'alternaric acid' produced by the pathogen. Under suitable climatic conditions, they enlarge rapidly to 3-4 mm diameter, become irregular and may evolve entire leaf lamina. Concentric rings may appear on the lesions giving them target board appearance. Large number of spots on a single leaf results in senescence and dropping. During frequent rains, large dark brown lesions are produced resembling those of late blight but without apparent whitish growth of the fungus. Infection on petioles and stems shows small or elongated dark brown necrotic lesions and the tissue may break at the infection point. Lesions on tubers are dark sunken, round to irregular in shape and surrounded by raised borders with underlying flesh giving dry and leathery appearance. Tuber infection is uncommon in plains.

Causal Pathogen.

Early blight is caused by the demataceous Alternaria solani (Ellis & Mart.) Jones & Grout belonging to sub-division Deuteromycotina, class Hyphomycetes, sub class Sporomycetidae, order Moniliales and family Dematiaceae. It has pale to olivaceous brown septate mycelium. Conidiophores may arise singly or in small fascicles through stomata from the mycelium present in the dead centres of spots and are up to 110 x 6-10 µm in size. Conidia are usually solitary, obclavate, oblong to elliptoid, tapering to a beak almost of the same length or even longer as that of the conidial body. Conidia are muriform, pale to olivaceous brown, smooth, 150-300 x 15-19 µm having 9-11 transverse and 0-few longitudinal septa. No perfect stage of the fungus is known.


Different methods such as sanitary measures, cultural practices, use of fungicides and host resistance can be used for managing early blight.

Field sanitation and cultural practices

Diseased haulms and crop debris should be removed from the infected fields after harvest and destroyed in order to reduce the primary source of inoculum for the next crop. Balanced fertilization of the crop ensures healthy and vigorous plant growth which contracts less disease. Poorly fertilized plants are liable to be attacked more by the disease. Tubers should be allowed to mature in the field before harvest and injury to the tubers should be avoided. Use of disease free tubers for planting, removal of diseased crop debris from the fields and 3-4 years crop rotation help in reducing the primary inoculum.

Host resistance

Resistance to early blight has been identified in Solanum species such as S. phureja and S. chacoense that has been exploited for breeding of resistant cultivars (Stewart, et al., 1994). Among various cultivars being grown in the plains of India, Kufri Sindhuri shows good resistance against the attack of early blight.

Use of fungicides

Most of the fungicides recommended against late blight can effectively control early blight of potato as well. Sprays of dithiocarbamate fungicides such as mancozeb, zineb, ziram, propineb and others like chlorothalonil, captan, copper oxychloride, Bordeaux mixture, captan etc. have been reported to be effective against this disease (Thind and Jhooty 1982; Steinberg, et al., 1996). These fungicides give better control when used as preventive applications at the initiation of the first symptoms. Tebuconazole, a triazole fungicide, has also demonstrated good efficacy against early blight. Recently developed strobilurin fungicide azoxystrobin has been reported to provide good efficacy of both late blight and early blight of potato and tomato.

Integrated disease management

More than one management practices can be integrated for achieving better level of disease control. Genotypes having moderate level of resistance can give desired control of early blight with fewer fungicide applications compared to susceptible cultivars and result into economical yield returns (Shteinberg et al., 1993). The intensity of fungicide applications can be adjusted in such a way that moderately resistant cultivars can be sprayed at longer intervals while in case of varieties with age related resistance it would be better to increase the frequency of sprays towards the end of the season. Some antagonistic organisms can also be used in the IDM programme. Two strains of Trichoderma species have been reported antagonistic to Alternaria solani (Martinez and Solano, 1995). A strain 679-2 of Pseudomonas species can also inhibit this pathogen through production of a water soluble metabolite and there was no adverse effect of copper fungicides. This antagonist can be easily integrated with other disease control measures (Casida and Lukezic 1992).



Stem canker and blight phase and the scurf phase are the two distinct phases of the disease. There may be pre-emergence death of the plants or the germination may be delayed when the pathogen attacks growing tips of the sprouts. If the infection is less, a large number of sprouts may arise and the affected hills show yellowing of plants which generally remain stunted. In stem canker phase, the growing tips of sprouts show browning. Sunken, circular or elongated brown necrotic spots may also be observed on the mature sprouts at the point of infection near mother tuber. Severely affected sprouts are killed. Later, when shoots emerge, similar necrotic lesions are observed on the stem which may extend downwards and may completely girdle the stem. In case of severe cankerous lesions, the tops show stunting, rusetting and purpling of leaves. Green aerial tubers may also appear on the branches and petiole axes and the disease phase is called 'aerial tubers'.

The most prominent symptom of black scurf is the presence of black crust on tubers due to the formation of sclerotia of the fungus. The pathogen produces a large number of sclerotia superficially on the surface of growing tubers. These sclerotia may be hard or spongy forming a black crust of scurf on the tuber surface. These are normally seated on the skin and do not cause any damage to the tuber inside. Black scurf phase is more common than stem canker in India. Dry rot symptoms on tubers are also seen if the pathogen enters through wounds.

Causal Pathogen

Black scurf is caused by the fungus Rhizoctonia solani Kuhn. (teleomorph Thanatephorus cucumeris (Frank) Donk). The mycelium is septate, brownish, dolipore type, 5-14 µm wide. The lateral branches of the mycelium are constricted at branching point and possess septum near the junction. The sclerotia are small, brown to black and unlike other fungal sclerotia are undifferentiated into rind and medullae. Outer cells of sclerotia are thick walled and dark in colour. Basidial stage of the fungus has also been reported in some parts of the country on dead potato haulms, which appears as flaky pellicle on the substrate under cool and humid environment.The basidiospores appear onsterigmata arising from barrel shaped to clavate basisdia and are usually four in number. These are ellipsoid to oblong and flattened on one side Different strains of the pathogen have been identified based on cultural and sclerotial characters. Based on anastmosis grouping (AG), R. solani infecting potato has been assigned to A4 type.


The black scurf pathogen survives in soil as well as through seed potato tubers and has a wide host range. Successful management of the disease can be achieved by following proper cultural practices and chemical treatment of the seed.

Cultural practices

In general, planting of healthy and disease free tubers is helpful in reducing the incidence of the disease. Change in the date of planting is another important criterion. If the time between planting of tubers and sprout emergence is reduced, less infection is observed. In the hills, the crops should be sown in spring to reduce stem canker and necrosis of sprouts. On the other hand, in the plains, early plantation of main crop followed by early harvest is recommended. Two to four years rotation with cereals, brassicas and legumes is helpful for the management of this disease. Green manuring with Dhaincha (Sesbania cannabina) reduced the black scurf on tubers by 40 per cent while maize and sunhemp (Crotolaria juncea L.) were reported effective by (Bhattacharrya, et al., 1977). The increase in organic matter content of the soil helps in reducing the population of the fungus through enhanced activity of the antagonists such as Trichoderma spp. Likewise, soil amendment with neem or margosa cake or with saw dust has been found to reduce black scurf (Sikka et al., 1971; Singh et al., 1972). Other practices like shallow planting and good drainage also help in disease reduction.

Seed tuber treatment:

Treatment of seed tubers with chemicals before planting or before storing results in effective disease control. Dipping of seed tubers in 0.25 - 0.5 per cent solution of organo-mercurials such as Emisan-6, Agallol or Aretan for 5-10 minutes is widely practiced by the farmers. But these mercurial fungicides are being banned now because of toxicity and pollution problems. Certain oxathiin fungicides are also reported to be effective against stem canker phase of the disease. (Tanii et al., 1982) reported significant control of the disease by dusting or spraying of tubers with Validamycin. (Khanna et al., 1991) reported good efficacy of carbendazim to control the disease.

Dipping of seed tubers with 1% acetic acid plus 0.05% zinc sulphate or with 3% boric acid has also been reported effective (Somani, 1986). The treatment with boric acid is more effective, less toxic and safer than organo-mercurials which are not only hazardous but also affect the emergence of sprouts especially when the temperature is above 30oC. Recently, Thind et al. (2002) have reported almost complete control of black scurf by dipping infected seed tubers in 0.25 per solution of Monceren (pencycuron), a phenyl urea based fungicide, for 10 minutes before sowing.



All the underground plant parts except roots are attacked. The plant cells multiply rapidly at the infection site and produce hypertrophied tissue masses resulting into wart type symptoms on tubers and beads like projections on stems or stolons varying in size from small protuberances to large intricately branched structures. Warts are normally soft, pulpy, spherical and similar in color to tubers. The colour may change to green on exposure to sunlight. Sometimes whole tuber may be covered with warts. The colour of warts changes to dark in shade as the tubers mature. Sometimes secondary micro-organisms invade the wart tissues causing their decomposition.

Causal Pathogen

Potato wart is caused by the fungus Synchytrium endibiotichum (Schill.) Perc. Which is holocarpic and endobiotic in nature. The fungus produces sporangia which release a large number of uniflagellate planospores. When planospores originate from different sori, these behave as planogametes and copulate to form zygospores which act as resting sporangia of the pathogen. One race and one biotype of the pathogen have been reported from Darjeeling hills in India. (Phadtare and Sharma 1971) have reported certain other hosts to be infected by the fungus.


The disease mainly being soil borne in nature is difficult to be managed. Various measures including quarantines, cultural practices, host resistance some chemicals have been found effective in reducing the disease level.

Quarantine measures

Since the disease is soil borne, its eradication is very difficult. Strict domestic quarantine measures enforced in India have helped to restrict the disease in Darjeeling district of West Bengal only where it was first reported. Considering the risk of spread of the disease through contaminated soil particles, the seed as well as table potatoes are not allowed to be taken out from this district and this has helped to contain the disease effectively.


The pathogen can remain viable in the infested soil for several years. This warrants practicing crop rotation with non-host crops for 8-10 years where the disease has become endemic. The pathogen population in the soil can also be reduced through steam sterilization of the soil.

Host resistance

Some potato lines such as Ronda, Edina, Mira from European countries have shown considerable resistance to potato wart. Varieties developed by CPRI, Shimla like Kufri Jyoti, Kufri Sherpa, Kufri Jeevan, and Kufri Muthun have demonstrated resistance to late blight as well as wart and can play significant role in reducing the disease level in endemic areas.

Chemical treatments

The use of fungicides like mercuric chloride, copper sulphate, formaldehyde etc. as soil application, though effective, but is quite expensive and can result into some non-target effects. These can be applied to limited extent to check the establishment of the pathogen into those areas where it has recently been introduced.



Initial symptoms of common scab appear on tubers as small brownish and slightly raised spots which later on enlarge, merge with each other and give corky appearance. Scab symptoms on tubers are categorized as shallow and deep pitted. In shallow scab, the affected tubers show superficial roughened areas, sometimes raised above but often slightly below the skin of the tubers. The lesions of scab consist of corky tissue which is the result of abnormal proliferation of the cells of tuber epidermis due to invasion by the pathogen. The lesions may vary in shape and size and the color is generally light to dark brown. In deep pitted scab, the lesions are dark brown or almost black and measure 1-3 mm or more in depth. They are also corky in appearance and may join together involving entire surface of the tuber. Other forms of scab are proliferated lenticels with hard corky deposition and concentric series of wrinkled layers of cork around central black core.

Causal Pathogen

Common scab of potato is generally considered to be caused by Streptomyces scabies (Thaxter) Waksman and Henrici. However, many species of Streptomyces are now reported to be responsible for causing common scab, though S. scabies is generally recognized as its major cause. Other species of Streptomyces responsible for causing mild common scab are S. griseus (Krainsky) Waksman & Hewici, S. collinus Lindenbein, S. aureofaciens, S. longisporoflavus, S. griseoflavus, S. alborgriseolus, S. violanceorber and S. flaveolus (Dey and Singh, 1983). However, names of some of these species are not included in the Advanced Lists of bacterial names. Glucose asparagines agar, Czapek's agar and Tyrosine-caesin-agar are suitable media for the isolation of Streptomyces species. The mycelium of the pathogen is slender, branched with few or no cross walles. The spores are cylindrical or ellipsoid produced on special hyphae that develop cross walls from tip and spores are pinched off. These Streptomyces species are gram positive and aerobic.Among other species in India, (Singh and Singh, 1991) reported S. aureofaciens for inciting various types of shallow or deep scab symptoms on potato tubers.


As the disease is both tuber and soil borne, it is difficult to control it. However, some management practices have been adopted to check this disease. Healthy and blemish free seed tubers should be selected for sowing in order to reduce the primary source of inoculum.


The tubers can be disinfected by dipping them for 10-30 minutes in 0.25 per cent aqueous solution of mercurial fungicides such as Emisan or 0.5% solution of Agallol or Aretan (Singh and Soni, 1987). The treatment has been commonly accepted by farmers in India. However, due to environmental pollution and health hazards, mercurial fungicides are now being banned. Other tuber treatment chemicals like 3 per cent boric acid and certain antibiotics like Streoptocycline and Plantamycin have also given satisfactory control.


Since soil pH and soil moisture are important factors in the development of disease, they have been exploited for minimizing the losses. Successful control of potato scab has been achieved by frequent irrigations of the field at weekly intervals from tuberisation until maturity (Singh and Singh, 1981). Green manuring and cultivation of certain legumes before planting potato has been emphasized as important cultural practices in controlling common scab. Green manure probably increases the activity of certain actinomycetes and other bacteria which are antagonistic to S. scabies. Delay in sowing also reduces disease incidence. Four year crop rotation with wheat-oat followed by potato-onion-maize also helps in reducing scab in the infested fields (Singh and Jeswani, 1987).In Russia, S. scabies was reduced by application of high rates of potassium in combination with nitrogen and phosphorus fertilizers. In India, Singh and Singh (1993) confirmed the role of nitrogenous fertilizers in the control of common scab (S. aureofaciens) of potato. Growing potatoes in acidic soils also reduces scab and addition of sulphur can bring the pH to near 5.5. Application of gypsum is reported effective to reduce common scab (Singh and Soni 1987).

Host resistance

Limited information is available on the use of resistant varieties to manage this disease as no commercial variety is known to possess high resistance to scab. Good level of resistance to scab has been reported in Solanum chacoense and S. phureja. Solanum andigena x S. tuberosum hybrids and red skinned varieties have been found to possess considerable resistance to scab (S. scarius) and are being used in the resistance breeding programme (Nagaich, 1983). (Singh and Singh 1992) have reported Kufri Sindhuri and some other accessions as resistant to scab caused by S. aureofaciens.

Conclusions are irelevant