The occurrence of bud necrosis in severe
form has been reported from Andhra Pradesh in 1968. The causal virus
is identified as tomato spotted wilt virus.
The earliest symptom of the disease is
seen about a month after sowing. The youngest expanding leaves show
the presence of ring spot patterns, which become necrotic later.
Necrosis of the terminal shoot bud soon starts
and extends downwards ultimately killing the main axis, while some branches
remain alive with all the shoot buds blighted.
Sprouting of auxiliary buds and lateral shoots
with malformed leaves are noticed in later stages. Flowering and pod
formation are adversely affected resulting in considerable reduction
in yield.
The virus is transmitted experimentally by grafting,
sap inoculation and by the thrips Frankliniella schultzei (Trybom)
and Scirtothrips dorsalis Hood.
Host range of the virus includes tomato, cowpea,
blackgram and green gram.
Control
Experience has shown that early sown crops
escape peak incidence of the thrips and thereby the disease.
It is also observed that optimum spacing of 30
cm between rows and 10 cm between plants resulted in decreased incidence
of the disease.
The disease is observed in 1977 in crops
grown in the sandy soils of Punjab and Gujarat.
Most of the infected plants failed to produce pods,
and even in cases of late infection, losses upto 60 per cent are recorded.
The disease is due to a sap transmissible virus.
Infected plants are severely stunted with small
dark green leaves. The young leaves show mosaic mottling and chlorotic
rings. Roots become dark coloured and the outer layers peel off easily.
The virus is transmitted by means of mechanical
inoculation and grafting.
The virus is soil-borne and is transmitted by nematodes.
The disease is restricted to sandy soils. Sowing healthy seeds in soil
samples collected from depths of 12-28 cm. of infected fields resulted
in infected plants.
The disease occur in patches in the field and reappears
in the same areas in succeeding years. Application of nematacide to
infested soils reduces the incidence and spread of the disease.
This disease is also known as white mold, sclerotium blight,
root rot and foot rot and is caused by Sclerotium rolfsii
Sacc.
The disease manifests itself on the germinating seed, seedlings
and grown up plants.
The earliest symptom is the shrivelling and rotting of kernels
which are covered with white coating.
Such white coating appears on grown up plants at the ground level
and on the lower portion of plants. Heavy rainfall is congenial for
this disease.
In humid weather, the entire plans are covered with white fungal mycelium.
Small, round, brown bodies (sclerotia) resembling mustard seeds develop
amidst the fungal net work. The plants die slowly.
The fungus is a common soil inhabitant and spreads through soil, rain
drops, hay, etc. The seed-borne phase also exists but on a minor scale
compared to soil inoculum.
Control
Deep summer ploughing and burying the infected
plant debris is recommended.
The kernels may be treated dry with Captan/Thiram/Dithane
M-45 @ 3 g/kg of seed.
The soil may be treated with PCNB (Brassicol 75%)
@ 15-20 kg/ha by broadcasting the chemical before sowing or by drenching
the soil with PCNB @ 10-12 kg/ha, 3-4 weeks after sowing.
The disease is caused by Aspergillus
niger van Tiegh. And A.pulverulentum Thonm.
The symptoms are the pre-emergence death of the
seedling with a black fungus growing on the cotyledons or young roots.
The infected seedling shows yellow-brown lesions
at the ground level, which results in the collapse of the seedling.
The entire stem at the ground level is covered
with black fungal spores. From the infected collar, disease spreads
to the tap root.
In some regions late onset of the disease causes
the rotting of the terminal portion or the crown.
This symptom is known as crown rot.
The disease is spread from season to season by
the spores adhering to the seeds and pods. In addition, this fungus
is a very common soil dweller, which can attack the newly sown crop.
Conditions, which are not conducive for quick
germination, such as deep sowing, high soil and air temperature, chemical
toxicity also, help in the high incidence of the disease.
Control
The kernels may be treated dry with Captan/Thiram/Dithane
M-45 @ 3 g/kg of seed.
A mosaic disease affecting groundnut was
reported from Delhi in 1963. A similar disease was observed in Tamil
Nadu in 1964. Crop loss ranging from 20 to 100 per cent depending on
the intensity of infection has been estimated.
Diseased leaves show circular chlorotic rings in
the early stages of infection. Later they develop dark green blisters
and chlorotic patches.
Often the leaves are malformed and puckered with
narrow pointed tips. Leaf laminae are reduced and clusters of malformed
mosaic leaves give the plant a bunchy appearance.
The disease is caused by groundnut mottle
virus. Newly formed leaves show mild mottling and vein clearing, whereas
older leaves show upward curling and interveinal depression with occasional
dark green islands. Infected plants are not severely stunted and older
plants seldom show typical disease symptoms.
The virus is seed transmitted to an extent of 0.1
to 3.5 per cent depending on the groundnut cultivars. Aphis craccivora
Koch. and Myzus persicae Sulzer. transmit the virus.
Dry root rot is caused by Rhizoctonia
bataticola (Taub.) Butl. The disease is more common in South India
and appears any time from the seedling stage upto maturity.
The infected seedlings and plants develop a dry
rot at the ground level and from there it spreads up and down.
The stem of the infected plants undergoes shredding
with minute dark bodies appearing in between the shreds.
The root system of infected plants is poorly developed.
Often the pods are also infected resulting in shrivelling of kernels.
The black bodies of the fungus (Sclerotia) occur
inside the pod also. Thus the yield is reduced by reduction in plant
population and also due to pod infection.
The fungus spreads through infected soil and seed
(externally seed-borne as well as internally pod-borne).
Control
Application of gypsum to the soil reduces the incidence
of the disease.
The kernels may be treated dry with Captan/Thiram/Dithane
M-45 @ 3 g/kg of seed.
The soil may be drenched around the base of infected
plants including one row of healthy plants with PCNB (Brassicol 75%)
M-45@ 3 g/kg of seed.
The rosette is known to be widespread causing
heavy losses and was reported first in India in 1926 as clump disease.
The disease is caused by groundnut rosette virus.
The affected plants are stunted and their internodes
are shortened. Leaves appear uniformly chlorotic and their size is conspicuously
reduced., the petiole and rachis are shortened. Plants infected early
usually do not produce pods.
Groundnut aphid (Aphis craccivora
Koch.) is the insect vector and there is no evidence of seed transmission.
Control
Reducing the build up of aphid population in the crop
by early sowing, optimum spacing and application of insecticides such
as Endosulfan @ 1200 ml/ha or Metasystox 0.1 per cent is recommended.
The symptoms which are chiefly confined to the leaflets appear as
brown to dark reddish brown pustules on the lower surface with the upper
surface developing yellow, chlorotic, irregular spots with necrotic
brown areas in the centre.
The uredosori under favourable conditions coalesce forming irregular
necrotic patches leading to premature yellowing, withering and
shedding of the foliage.
Plants infected early exhibit more disease intensity. The loss
in yield is also more in such plants.
The disease intensity is more during rainy days and when temperatures
are low.
Control
The kernels may be treated dry with Captan/Dithane
M-45/Thiram @ 3 g/kg of seed.
Dusting twice or thrice with finely powdered sulphur
@ 20-25 kg/ha or spraying with 0.2 per cent Dthane M-45/Dithane Z-78/Captan
or 0.3 per cent Sulfex at fortnightly intervals starting from 30 days
after sowing or with the first appearance of the disease controls the
disease.
The foliar pathogens such as Leptosphaerulina
crassiasca (Sechet) Jackson and Bell, Alternaria alternata
(Fr.) Keissler and Myrothecium roridium Tode ex.Fr., are of minor
importance, at present. Except on rare occasions where these minor leaf
spot infections reach epidemic proportions, chemical control methods
are not necessary.
Pre and post-emergence diseases or seed and seedling
rots
A number of fungi associated with seeds
and present in soil cause rotting of the seeds before germination and
pre and post emergence rotting of seedlings.
The fungi responsible for this include species
of Rhizopus, Aspergillus, Fusarium, Penicillium, Alternaria, Rhizoctonia,
Pythium, Curvularia and Sclerotium.
These fungi are found to inhibit seed germination
and seedling vigour.
Control
Injured, discoloured and shrivelled seed should
not be used for sowing.
The seed may be treated dry with Captan/Thiram/Dithane
M-45/Brassicol @ 3 g/kg of kernels.
The seeds may be sown at optimum depth and not
too deep. Crop rotation may be followed wherever possible.
The disease is caused by two fungi namely
Mycosphaerella berkelyii Jenkins (Cercosporidium personatum
Berk. And Curt. Deighton), M.arachidicola Jenkisn (Cercospora
arachidicola Hori). The reduction in yield is more (54%) when infected
at 20 days age of the plant than at later stages.
Symptoms appear first on the upper surface of older
leaves. C.personatum Berk. And Curt. Deigton forms dark brown
to black spots measuring about 1-6 mm in diameter, almost circular in
outline and with an indistinct pale yellow margin. C.arachidicola
Hori.
Produces reddish-brown to brown, more or less circular
to irregular lesions measuring about 1-10 mm in diameter and surrounded
by a narrow bright yellow halo.
The spots may be produced on the petioles, stipules,
stems and pegs also. They may enlarge and coalesce with one another
resulting in premature defoliation.
The extent of loss depends on the age of the crop
at the time of infection, whether conditions and the susceptibility/resistance
of the cultivar being grown.
Leaf spot development can be minimised by the
application of gypsum @ 500 g/ha as a source of calcium. High relative
humidity (90-93%), rainfall causing a film of free water on the surface
of the leaves, average minimum and maximum temperatures around 20oC
and 30oC respectively favour the disease.
The pathogens perpetuate on diseased plant debris
in the soil and on the seed. Secondary spread of the fungus is by air
borne conidia.
Control
The kernels may be treated dry with Captan/Dithane
M-45/Thiram @ 3 g/kg of seed.
Dusting may be done twice or thrice with a mixture
of copper dust 4 per cent (Blimax) and sulphur in the ratio of 1 : 4
@ 20-25 kg/ha of spraying with benomyl (0.05%) , or bavistin (0.05%)
at 20 days intervals from 40 days after sowing or with the first appearance
of the disease, especially when the weather conditions are favourable
for the spread of the disease.
Clean cultivation and destruction of infected crop
debris also helps in reducing the incidence of the disease.
The disease is caused by Aspergillus
flavus Link.ex.fr. This soil borne fungus causes untreated seeds
to rot rapidly after sowing resulting in low germination.
Infected seeds are covered by masses of yellow
or greenish spores.
The cotyledons of emerging seedlings are often
attacked and become necrotic, and their infected surfaces covered by
masses of yellow-green spores.
The fungus, which produces aflatoxins and carcinogenic
substances, may invade groundnut kernels before harvest, during post-harvest
drying and storage if the pods are not properly dried.
Control
The kernels may be treated dry with Captan/Thiram/Dithane
M-45 @ 3 g/kg of seed.
Disease Management
