Potato: Solanum tuberosum L.
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.
- Use of disease free seed tubers for raising the crop is important
for minimizing the fungal inoculum.
- 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.
- 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.
- 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
- Seed potatoes should be checked thoroughly before storage. All
blighted tubers must be removed and buried deep in the soil.
- Ridges should be made high enough to cover all daughter tubers
and reduce chance of their infection upon exposure.
- 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.
- When the disease affects 75% crop foliage, the haulms should be
cut, removed from the field, and buried deep.
- The mycelium in the infected tuber can be killed by exposing
tubers at 40 °C for four hours or 30 °C for 65 hours.
- The dipping of tuber seed material in 1 percent Bordeaux mixture
is useful in checking disease.
- 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.
- 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
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
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 µm 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
µm x 8 - 10 µm bearing four sterigmata which arise as blunt knobs and become
later horn shaped, 7.5 – 12 µm x 2.5 - 3.5 µm. Spores ellipsoid or oblong
ellipsoid, thin walled, flattened on the inside, truncate to apiculate, 9 - 12.5
µm x 5 - 7 µm.
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.
- Combination of tuber disinfection and improved cultural practices
successfully checks the incidence and severity of black scurf.
- 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.
- Crop rotation with maize or 'dhaincha' (Sesbania aegyptiaca)
for green manure also checks the disease build up.
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
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
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
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
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.
- 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.
- 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.
- 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.
- The application of chemical fungicides was not found effective in
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.
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.
- 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
- Splitting of the tubers at the time of the planting should be
avoided as splitting spreads the disease even to health tubers.
- The pathogen is heat susceptible and covering the soil with
polythene sheet for raising the soil temperature has been found effective in
- 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.
- Application of stable bleaching powder (12kg/ha) mixed with
fertilizer in furrows while planting reduces wilt incidence by 80%.
- The tuber seeds should be treated with 0.02 percent
streptocycline for 30 minutes.
- Practicing crop rotation for 2-3 years with crops like maize,
finger millet, cabbage, cereals, garlic, lupin and onion can reduce the disease
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
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.
- 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.
- 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
- The long crop rotation
with non-host crops (wheat, pea, oats, barley, lupin, soybean, sorghum
and bajra) can give disease control to
- The application of green
manures may be helpful in checking the disease development.
The sowing of resistant varieties like kufri sindhuri
is useful for disease control.