Diseases of Potato

Early blight
Introduction:

The disease is world-wide in distribution wherever potato is cultivated.

The disease affects young crop and may cause yield loss upto 40% if not
contained. The disease appears both in tropical and temperate regions.

Symptoms:

Small pale brown spots first appear on leaves. Lowest leaves are
attacked first followed to upper parts of the plant. Concentric rings on leaves
surrounded by chlorotic areas are the characteristic symptom of the disease.
In dry weather spots become hard and leaves are curled but in humid weather
big rotted patches are formed and leaves may fall down. Similar patches are
developed on stem resulting in the whole plant to collapse. The rotting may
reach upto the tuber. Affected plants develop less and smaller size tubers.

Pathogen:

Alternaria solani is the causal pathogen. The conidiophores of the pathogen

emerge through stomata from the spots and bear conidia. The conidia are
beaked, muriform with 5-10 transverse septa alongwith a few longitudinal
septa. Conidia germinate within 35– 45 minutes at 28-300 C.

Favourable Conditions:

It occurs in high intensities in areas where dry warm weather alternates

with the intermittent rains. It is serious in late planted crop in Bihar, Uttar
Pradesh and Punjab. Reduction in plant vigour and senescence increases
susceptibility to early blight.

Disease Cycle:

The mycelium of the pathogen remains viable on dry infected leaves for
10– 12 months. Conidia are also viable upto 17 months at room temperature.
Initial infection therefore takes places either by mycelium or conidia surviving
in soil on dead plant debris. Contamination of seed tubers with conidia or
mycelium may be another source of primary inoculum. The infection starts
from lower most leaves and further spread of the disease takes place from the
conidia formed on these leaves. The conidia are disseminated by water, wind
and insects. Under favourable conditions of rains followed by warm and dry
weather the disease spreads very rapidly.

Disease Management:
1. As the pathogen is soil– borne, crop rotation should be followed for 2– 3
years with non– solanaceous crops.
2. Dead haulms should also be raked band burnt after harvesting.
3. Provide conditions favourable for vigorous growth of the crop.
4. Use of certified seed are important measures to avoid infection.
5. Regular sprays with fungicides at an interval of 10– 21 days depending on
severity of the disease should be done.
6. Fungicides like Dithane M– 45 @ 0.2%, Blitox– 50 @ 0.25%, Captan @ 0.2%
etc. have also been recommended for disease control.

Late blight

Introduction:

Usually infection starts in 6 weeks old plants. First reported from Andes
mountains of South America. In India, the disease was first reported in
Darjeeling district in India (1880). The famous Irish famine of 1845– 46 was
due to failure of potato crop by a disease which was later identified as late
blight of potato. In this famine, millions of people died due to starvation as
potato was staple food of Irish people. Several epiphytotics have been reported
due to late blight in different parts of the world. In India, the disease is found
in all the potato growing areas. The disease also occurs on tomato.
Symptoms:
The disease usually appear late in the season than early blight. Initially
starts from leaf tips or margins and spread inward. Brownish black areas
develop on leaves which can cover the whole leaf surface. The disease spreads
very fast when high humidity is there and cover the whole leaf within 1– 4
days. The disease can cover all the leaves and stem of the infected plant and
sometimes the whole crop is blighted. The tubers can also be infected while
in soil or during harvesting or in storage. Most of the tubers of infected plants
are rotted showing brown to purple discoloration on the skin of tubers. Moist
atmosphere is suitable for wet rot and dry weather causes dry rot.
Pathogen:
The pathogen, Phytophthora infestans is the causal pathogen of the
disease. The mycelium is endophytic and intercellular. Sporangiophores
develop from the mycelium and come out through stomata or lenticels of
tubers. Sporangia are pear shaped and papillate and develop at the tips of
sporangiophores. The sporangia germinate and form secondary sporangia
which produce zoospores upon germination. The zoospores are biflagellate
and cause infection to the host. Sexual reproduction is not known. Several
physiologic races are known in the pathogen.
Favourable Conditions:
 Late blight progress rapidly when relative humidity is > 90 % and
temperature between 10- 250C.
In hills, occurrence of the disease generally coincides with the onset of
monsoon rains. In plains it appears whenever low temperature prevails in
combination with high humidity brought about by rain, dew or irrigation.

Disease Cycle:

Primary infection most likely comes through seed tubers particularly

under Indian conditions. The mycelium from contaminated tubers grows
upward in the stem and cause sporulation on small dwarfed shoots. Infection
of foliage takes place from the spores produced in primary lesions. The
sporangia are spread through wind, water and leaf eating insects to the
healthy crops in the region. The spores are washed out to the soil from affected
leaves and infect tubers. The tubers also got contaminated when come in
contact of infected leaves during harvesting or in contact with infected tubers
in the storage.

Disease Management:

1. Use of certified seeds, sanitation, delayed harvesting, storage in cool, dry

and well aerated stores are the major precautions to avoid infection.
2. Spraying of crops with fungicides starting well ahead of disease appearance
time can provide good control. Dithiocabamates (Zineb, Maneb etc.) are
more widely used to control the disease.
3. Spray with Dithane Z–78 and Dithane M– 45 @ 2– 2.5 kg/ 1000 litre of
water / ha have been recommended.
4. Prophylactic measures

a. Metalaxyl @ 0.1% or Mancozeb @ 0.25% or Chlorothalonil @ 0.2% or

Bordeaux mixture @ 1% can be applied at 7 to 10 days intervals in the
hills and 10 to 15 days intervals in plains.
b. Dip sprouted tubers in Metalaxyl @ 0.2% for 30 min.
5. Late blight resistant varieties have been developed by Central Potato
Research Institute, Shimla for different regions of India as given below:
North– western plains: Kufri Jeevan, Kufri Alankar, Kufri Navtal, Kufri
Badshah and Kufri Swarna.
North– eastern region: Kufri Naveen, Kufri Khasigaro, Kufri Himalini,
and Kufri Sherpa.
Shimla hills: Kufri Jeevan, Kufri Jyoti and Kufri Muthu
Nilgiri hills: Kufri Naveen and Kufri Moti.
 Wart

Introduction:

Wart disease of potato is caused by a microscopic soil borne fungus.

Most infested soils are in home gardens. Wart disease presents biological,
social, and legislative problems. This pamphlet attempts to put some of these
problems in perspective.The disease losses seen in temperate regions. In
India, the disease is restricted to Darjeeling. Tubers are disfigured by the
growth of warty galls, which may not be apparent until after harvest. Severe
infestations can destroy the potato crop by preventing tuber production.
Financial impacts are compounded by quarantine measures and loss of
export markets.

Symptoms:

Potato wart symptoms can be found on all underground plant parts

except roots.

Stem – Galls form at the base of the stem; initially white, but turning black
when decaying; may be as small as a pin or as large as a fist; surface is rough
and corrugated– warty in appearance
.
Tubers – Eyes develop cauliflower– like swellings; when formed underground,
they are the same colour as the potato skin, darkening with age, or green if
exposed to light. Typical warts are soft and pulpy and easier to cut than a
healthy tuber.

Stolons– Symptoms similar to tubers.

Aerial buds – Small greenish warts form in the position of the aerial buds at
the stem bases.

Pathogen:

The organism responsible for wart disease of potato is a tiny, single

celled fungus, Synchytrium endobioticum.

Favourable Conditions:

The disease favours high soil moisture, optimum temperature of 210 C

(12 – 280C) and slightly acidic to neutral pH.

Disease Cycle:

The causal agent, Synchytrium endobioticum, is an obligate parasite

which does not produce fungal– like mycelium. Infection causes host cells to
proliferate into a warty gall containing spore– baring structures called
sporangia. In the spring, when temperatures are above 80C and given
sufficient moisture, sporangia in decaying warts each release zoospores,
which infect potato growing points including buds, stolon tips and leaf
primordia. The infection cycle continues while conditions are favourable.
Resting, or winter sporangia are formed as the galls decay, and can remain
viable in soil for up to 40– 50 years. There are over 20 strains, or pathotypes,
of S. endobioticum that occur around the world, including four known in
Newfoundland. Potatoes that are resistant to one pathotype may be
susceptible to another.

Disease Management:

1. Wart affected tubers should not be planted.

2. Strict quarantine measures.
3. Grow wart resistant varieties like Kufri Kanchan, Kufri Jyoti and Kufri
Muthu.

Bacterial Brown Rot or Wilt Disease of Potato

Introduction:
First bacterial disease reported in India. First recorded in 1891 from
Pune district of Maharashtra. Also referred as bacterial wilt or ring disease or
bangle blight. Occurs in Assam, West Bengal, Orissa, hills of Uttar Pradesh
and Nilgiris.

Symptoms:

Diagnostic symptoms are wilting, stunting and yellowing of plants and

browning of xylem. A brown ring is formed within tuber due to discoloration
of vascular bundles. In severe cases, eye buds become black and if infected
tubers are cut, grayish white bacterial ooze comes out of the vascular bundles.

Pathogen:

The disease is caused by a bacterium, Ralstonia solanacearum. The

bacterium is rod– shaped, motile and gram– negative type.

Favourable Conditions:

The disease favours high soil temperature (25–350C) and soil moisture
>50% for disease development.

Disease Cycle:

The pathogen survives in soil, infected tubers and alternate cultivated

and wild hosts. Soil is a potential source of primary inoculum. Infected and
surface contaminated potato tubers also serve the source of primary
inoculum. The pathogen invades the potato by way of stolons and also spread
by contaminated knife while cutting tubers for sowing. In Nilgiri hills the
bacterium may survive on potato crop grown throughout the year.

Disease Management:

1. Crop rotation with maize or soybean for 3 yrs.

2. Use disease free tubers for sowing.
3. Deep summer ploughing.
4. Treat seed tubers with streptocycline @ 0.02% for 30 min giving 4 mm
deep sharp cut.
5. Disinfestation of cutting knives with sodium hypochlorite (10%).

Common Scab of Potato

Introduction:

The disease is widely distributed in cool and hilly places. The disease
decreases the maket value of tubers due to rough skin.
Symptoms:
Superficial or deep seated lesions are formed on the skin of tubers. The
areas of lesions become rough and are raised over the skin. The lesions have
darker corky tissues of different shape and size. Sometimes the lesions join
together covering the complete surface of the skin.
Pathogen:
The causal pathogen of the disease is Streptomyces scabies. The spores
are smooth walled and cylindrical measuring 0.8– 1.0 x 1.2– 1.5μ in size.
Disease Cycle:
The pathogen survives in soil and get distributed through movement
of soil by wind and cultural operations but main distribution is through
contaminated seed tubers. Infection occurs through newly formed
unsuberized lenticels, stomata, wounds and may be directly through the
cuticle when skin is thin. The pathogen develops in dead cells and causes the
development of lesions. The pathogen is most active in dry soil, and hence the
disease can be suppressed by irrigation. Optimum infection takes place at 20-
220 C.
Disease Management:
1. Use of healthy seed tubers, seed treatment with mercurial fungicides like
agalol– 6 and aretan etc. by dipping for 5 min in 0.25% solution are useful
for elimination of disease.
2. Crop rotation, growing of legume crops before potato planting.
3. Application of 20– 30 kg / ha of PCNB (Brassicol) will reduce common scab.
 Potato Leaf Roll Virus (PLRV)

Symptoms:
Reddening of leaf margins and tips of leaves, leaf rolling, usually leaflets
rolled upwards and starts from lower and oldest leaves are the major
symptoms of the disease on leaves of potato caused by PLRV. Affected plants
remain stunted and yield of tubers is greatly reduced.
Pathogen:

Potato leaf roll virus (PLRV) is the causal pathogen and belongs to
luteovirus group. The virions are isometric, 24 nm in diameter and have 30%
nucleic acid and 70% proteins. The genome is ssRNA, linear and unipartite.

Transmission:

The most efficient and important vector of PLRV is Myzus persicae. The
virus is also transmitted by grafting.

Disease Cycle:

The primary inoculum comes through infected tubers used as seed and
also from natural hosts. Further spread of the PLRV takes place by insect
vector.

Disease Management:

1. Disease free seed tubers for planting

2. Spray Imidacloprid @ 1.5 ml/ lit of water to control spread through aphid
vectors.

Potato spindle tuber viroid

The Potato spindle tuber viroid (PSTVd) was the first viroid to be
identified.

Symptoms:
Plants appear erect, spindly and dwarfed. Leaves small, erect and
leaflets dark green. Tubers elongated with tapering ends. Tuber eyes are
numerous and more conspicuous.

Transmission:

The disease is spread through infected seed tubers and mechanically

spread by knives used to cut seed tubers. Also transmitted by pollen and seed
and contaminated mouth parts of grasshoppers, flea beetles and bugs.

Management:
1. Use of PSTVd free potato seed tubers.
2. Disinfestation of cutting knives.