Wednesday 17 July 2013
Tuesday 16 July 2013
Banana ; BUNCHY TOP;PANAMA DISEASE; SIGATOKA LEAF SPOT
Groundnut;TIKKA DISEASE OR LEAF SPOT; RUST
| Groundnut: Arachis hypogaea L. Family: Fabaceae 1. TIKKA DISEASE OR LEAF SPOT
Tikka disease is reported from all groundnut growing countries of the world such as Africa,
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pora arachidicola and
Cercosporidium personatum. The perfect
stages of both these fungal pathogens (Mycosphaerella
arachidicola and M.
berkeleyii) play important role in
primary infection and pathogen survival. The yield loss from tikka disease has
been reported from 20-50 per cent but may be increased with association other
diseases. The all groundnut varieties grown in
Causal Organism: The causal organism
of tikka disease are Cercospora
arachidicola Hori (perfect stage of the pathogen:
Mycosphaerella arachidicola W. A.
Jenkins) and Cercosporidium personatum
(Berk & Curt) Deighton (perfect stage of the pathogen:
Mycosphaerella berkeleyii W. A.
Jenkins). The mycelium of C.
personatum is intercellular, brown,
septate, branched and slender with haustoria. The conidia are hyaline, 18-60 x
6-11 µm, 2-7 septate and borne singly on short, 26-54 x 5-8 µm conidiophores.
The conidiophores are produced in bunches from the hymenial layer of
sub-epidermal region. The mycelium of C.
arachidicola is inter and
intracellular, brown, septate, branched and without haustoria. The conidiophores
are 22-45 x 3-5 µm, yellowish brown, septate and conidia are hyaline or pale
yellow, obclavate, 4-12 septate measuring 38-108 x 3-6 µm.
Disease Cycle: The tikka disease of
groundnut is soil borne. The pathogen C.
arachidicola and
C. personatum disseminated by wind which is
blown from leaf to leaf. The primary infection of disease is caused by conidia
found on the plant debris in the soil. The spores remain viable in the soil for
a long time and infect the succeeding crop under favourable environmental
conditions. High humidity and relatively low temperature is essential for
initiating the fungal infection. It is observed that the high nitrogen
fertilizer increases disease intensity.
Disease Management: The disease can
be controlled by long crop rotation and sanitation practices. The intercropping
with pigeon pea and use of phosphatic fertilizers also reduced the disease
incidence. The early sowing crop varieties reduce the disease. The use of
Dithane Z-78 (0.2%), Dithane M-45 (0.2%), Cosan, Breston (0.1%) and copper
sulphate mixture (15-25 kg/ha) effectively controlled the disease. Some other
effective systemic fungicides are benomyl, bavistin, brestanol and cercobin.
2. RUST
The rust of groundnut is distributed in Central and
Symptoms: The disease is found on 6
weeks or more old plants. The small orange coloured uredial pustules appear on
lower surface of the leaves. At later stages, these pustules may appear on upper
leaf surface and other aerial parts of the plant except flower. The ruptured
epidermis exposes a powdery mass of uredospores. The infected leaves are showed
small, brown and necrotic lesions on the upper leaf surface. The severely
infected leaves wither and drop prematurely. The seeds formed on infected plants
are small and shriveled.
Causal Organism: The rust of
groundnut is caused by Puccinia arachidis
Speg. The uredial and telial stages of the pathogen are known till now. The
uredospores are one celled, subglobose, ovoid to round, light brown, thin
walled, 2-3 germ pores and measuring 24 x 21 µm with short and hyaline pedicels.
Disease Cycle: The uredospores are
short lived in infected plant debris. The continuous cultivation of the crop in
Disease Management: The application of a mixture of Carbendazim (0.5 %) and Mancozeb
(0.25 %) at 2-3 weeks interval on 4-5 weeks old plants effectively controlled
the disease.
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Cotton: Gossypium spp.; RHIZOCTONIA ROOT ROT; WILT;VERTICILLIUM WILT; ANTHRACNOSE
| Cotton: Gossypium spp. Family: Malvaceae |
Chilli:. ANTHRACNOSE
Chilli: Capsicum annuum L.
Family: Solanaceae
Family: Solanaceae
1. ANTHRACNOSE
Anthracnose disease is a major problem in India and one of the more
significant economic constraints to chilli production worldwide, especially in
tropical and subtropical regions. The disease causes both pre- and post-harvest
fruit decay. Chilli anthracnose usually develops under high humid conditions
when rain occurs after the fruits have started to ripen with reported losses of
up to 84%. Economic losses caused by the disease are mainly attributed to lower
fruit quality.
Chilli anthracnose was first reported in India on chillies from the
Coimbatore . Anthracnose incited by Colletotrichum spp
is one of the most damaging diseases of chilli in India . The severity of the disease varies depending on
cultivars grown and the weather conditions prevailing in a particular region. In
severe instances, the pre harvest and post harvest infections together account
for more than 50% of the crop losses. Three species, namely
C.
capsici,
C. gloeosporioides and
C.
acutatum were known earlier to cause
anthracnose in chilli. However C. capsici was the most predominant species in
the major chilli growing states namely Karnataka and Andhra Pradesh.
Symptoms: Anthracnose is the common name for plant diseases
characterized by very dark, sunken lesions, containing spores. The disease
appears as small circular spots that coalesce to form large elliptical spots on
fruits and leaves. Under severe conditions, defoliation of affected plants
occurs. The disease has been observed to occur in three phases, they are: (i)
Seedling blight or damping off, ii) Leaf spot and die back, and (iii)
Anthracnose or fruit rot. Capsicum fruit rot reduces fruit dry weight and
quantities of capsaicin and oleoresin. In anthracnose or fruit rot caused by
C. capsici, the ripe fruits turning red are mostly affected. The
disease is characterized by the appearance of small black circular spots on the
skin of the fruits that spread in the direction of the long axis, thus becoming
more or less elliptical. As the infection progresses, the spots get either
diffused and black, greenish or dirty grey in colour or they are markedly
delimited by a thick and sharp black outline enclosing a lighter black or straw
coloured area. In some cases, the lesions are brown and then turn black from the
formation of setae and sclerotia. Severe infection results in change of fruit
colour from red to straw or white. Numerous acervuli are scattered on the
discoloured area of the infected fruit. When a diseased fruit is cut open, the
lower surface of the skin is covered with minute, spherical, black stromatic
masses or sclerotia of the fungus. A mat of fungal hyphae covers the seeds. Such
seeds turn rusty in colour. Affected fruits are deformed, white in colour and
lose their pungency. Ultimately, the diseased fruit shrivels and dry up.
The disease symptoms of die-back starts from growing point of flower bud and the
tops of the affected branches wither and turn brown. The disease infection move
downwards and shows die-back. The infected parts get enamel white colour which
is punctuated by scattered, black, bristly and minute elevations (acervuli) of
the pathogen. The symptoms often appeared after rainy season and prolonged dew
on the plants.
Disease Cycle:
The fungus is both
internally and externally seed-borne. Sowing such contaminated seeds results in
pre emergent and post emergent damping-off of seedlings in nursery and field.
These infected seedlings form the primary sources of inoculum. The fungus
survives in an active form on the stems and branches causing die-back symptoms.
The wet conditions caused due to monsoon rains that occur during the
June-October period help in the outbreak and spread of the disease.
The pathogen survives between seasons in plant debris or on weed hosts.
Alternative hosts include other solanaceae (tomato, potato, eggplant) plants.
Fruits are infected when spores of the fungus or infested debris are rain
splashed onto chilli plants. New spores are produced within the infected tissue
and are then dispersed to other fruits. Infection usually occurs during warm,
wet weather. Temperatures around 26 °C are optimum for disease development,
although infection occurs at both higher and lower temperatures. Severe losses
occur during rainy weather because the spores are washed or splashed to other
fruits, resulting in more infections. The disease is more likely to develop on
mature fruits, although it can occur on immature fruits as well.
Disease Management:
Rot and die back caused by Colletotrichum capsici
is the major disease of chilli in India . The integrated management techniques are
recommended, as no single specific management program including crop rotation
can eliminate chilli anthracnose.
Cultural control-
- Planting of contaminated seed or transplants facilitates disease
spread. Use of healthy pathogen-free chilli seed or transplants should be
adopted.
- Early removal of affected plants will control the spread of the
diseases.
- Transplants should be kept clean by controlling weeds and
solanaceous volunteers in the vicinity of the transplant houses
- Stagnation of water should not be allowed in nursery beds and
fields in order to avoid fungal infection. The field should have good drainage
and be free from infected plant debris.
Use of resistant cultivars-
- The use of resistant varieties for anthracnose disease viz., IIHR
275-13-5, IIHR345-6, IIHR 332 -109, CC4, Ujwala, Perennial, H-1, H-4, H-6, CA
87-4. S- 20-1, Lorai and BG-1 will be useful in disease control.
Use of chemicals-
- The disease can be controlled by seed and foliar spray treatment
with perenox, azoxystrobin, chlorothalonil, copper, difenoconazole, famoxadone,
iprodione, procymidone, tolylfluanid and carbendizim.00
- The fungicide traditionally recommended for anthracnose
management in chilli is Maneb (2.5g per liter) (Smith, 2000), although it does
not consistently control the severe form of anthracnose on chilli fruits
- The strobilurin fungicides azoxystrobin, trifloxystrobin and
pyraclostrobin (1ml/liter) and difenconazole (1ml per liter) have recently been
labeled for the control of the anthracnose disease. The first foliar spray is
given at the first pair of leaf stage and subsequent sprays done twice at 20-day
intervals.
Biological control-
- Antagonistic Pseudomonas fluorescens as seed treatment and
as well as spray treatment @108 CFU.g-1 were found to be effective against C.
capsici (Srinivas et al., 2005; Jeger and Jeffries, 1988)
- Trichoderma species are able to effectively control C.
capsici infection in chilli.
- Other biological control agents that have been tested for
efficacy against Colletotrichum include Bacillus subtilis and
Candida oleophila.
Use of plant extracts-
-
Plant products have been tested in many laboratories. Seed and spray treatment showed that the crude extract from rhizome, leaves and creeping branches of sweetflag (Acorus calamus L.), palmorosa (Cymbopogon martinii) oil, Ocimum sanctum leaf extract, and neem (Azadirachta indica) oil could restrict growth of the anthracnose fungus.
Sunflower; LEAF SPOT; RUST
| Sunflower: Helianthus annuus L. Family: Asteraceae 1. LEAF SPOT
The disease is commonly found on all varieties of sunflower in the winter
season.
Symptoms: The pathogen produces brown
coloured spots on the leaves, stem, sepals and petals. The lesions on the leaves
are dark brown with pale yellow margins and yellow halo, at first the spot is
small and become larger as the disease advanced with irregularly circular shape
(up to 2-3 cm in diameter).
Causal Organism: The fungal pathogen
causing leaf spot of sunflower is
Alternaria helianthi Hansf. The mycelium is septate, branched and bearing
conidiophores. The conidiophores are cylindrical, pale grey-yellow, straight or
curved, geniculate, simple or branched, 2-5 septate and measuring 31-80 x 8-11
µm. The conidia are cylindrical to long ellipsoid, straight or slightly curved,
pale yellow to pale brown, 1-11 transversely septate, occasionally longitudinal
septa, constricted at the septa, rounded at both ends and measuring 42 – 110 x
15 – 28 µm. The conidia are produced singly on the conidiophores. The fungal
pathogen grows well and produced abundant conidia on culture media.
Disease Cycle: The disease is
appearing each year through soil borne fungal inoculums. The pathogen is
survived in plant debris.
Disease Management: The disease can
be effectively controlled by spraying of Mancozeb (0.3%) thrice with 7-10 days
intervals, Dithane M-45 (0.2%) or Thiovit or any other copper fungicide with ten
days intervals.
2. RUST
The rust disease of sunflower is common, widespread and most severe. The severe
infection of disease reduces yield considerably.
Symptoms: The small reddish brown
spots covered with rusty coloured dust are appear on the lower leaves and then
spread to all leaves even to other green parts of the head. The leaves turn
yellow but only sometimes fall down from the plants. The pycnia and aecia stages
usually occur on volunteer seedling plants which are growing among the debris of
the previous crop. The inoculum from the affected crop is spread by wind to the
healthy cultivated crop.
Causal Organism: The fungal pathogen
of sunflower rust is Puccinia helianthi
Schw. which is an autoecious pathogen and produces uredia and telia on the
leaves. The uredosori are dark cinnamon brown and uredospores are round
elliptical or ovoid, wall dark cinnamon brown, finely echinulate with two
equatorial pores and measuring 17 – 21 x 24 – 27 µm. The teleutospores are two
celled, elliptical or oblong, 21 – 31 x 28 – 50 µm, obtuse or rounded at the tip
and base, constricted at the septum, chestnut brown, smooth and colourless
pedicel which is longer than spore.
Disease Management: The sanitation practices like crop rotation, destruction of
volunteer seedlings and trash of previous year crop may be helpful in checking
the disease. The spraying of fungicides such as Thiovit, Dithane M-45 or Nickle
chloride is effectively control the disease. The cultivation of resistant
sunflower varieties like MSFH-1, MSFH-6, MSFH-8, MSFH-9, BSF-1 and VSF 182 is
the best way to control the disease completely.
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Tomato; WILT
Tomato: Lycopersicon esculentum Mill.
Family: Solanaceae
1. WILT
The wilt is one of the serious diseases of tomato reported from several
countries of the world including
Symptoms: The first symptom of the
disease is appearing as clearing of the veinlets and leaf chlorosis. As the
disease advanced, the petiole and leaves are droop and wilt. The entire plant
may wilt and die in few days. If the roots and stem cut transversely, a dark
brown or black discolouration of the vascular tissues may be seen.
Causal Organism: The wilt of tomato
is causing by Fusarium oxysporum f.
lycopersici (Sacc.) Snyder and Hansen.
The fungal pathogen produce both inter and intra-cellular mycelium which
produced macro- and micro-conidia. The mycelium is delicate, peach coloured,
sparse or abundant then floccose becoming felted and sometimes winkled in older
cultures. Microconidia: borne on simple phialides arising laterally on the
hyphae or from the short sparsely branched conidiophores, abundant, variable,
oval to ellipsoid and straight to curved, 5 – 11 x 2.4 - 3.5 µm. Macroconidia:
borne on more elaborately branched conidiophores or on the surface of
sporodochia, thin walled, 3 – 5 septate, fusoid- subulate and pointed at the
both ends, hooked apex and a pedicillate base; 3 septate, 33 – 41 x
3 – 5 µm; 5 septate, 37 – 58
x 3 – 5 µm. 3 septate conidia were more abundant. Chlamydospores: smooth,
abundant, terminal and intercalary, solitary or occasionally in pairs.
Disease Cycle: The fungal pathogen is
present in many soils as saprophyte. The pathogen infects host plants if grown
in infested soils. The pathogen attacks root, rootlets and spread upwards in the
host vascular tissues. The pathogen multiplies rapidly within the vascular
tissues and clogs them which interferes the upward movement of solutes and
nutrients, resulting in wilting of host plants. The pathogen also produced
toxins (fusaric acid and lycomarasmin) inside the host tissues that may play a
vital role in disease development.
Disease Management: The pathogen is
soil borne and persists saprophytically for many years. Thus, the disease
control is very difficult. The cultivation of resistant varieties is the only
effective method for disease control.
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Banana; BUNCHY TOP; PANAMA DISEASE; SIGATOKA LEAF SPOT
Banana: Musa paradisica var. sapientum
Family: Musaceae
2.
Family: Musaceae
1. BUNCHY TOP
The disease was recorded first time in 1879 from Fiji . The disease has also been reported from
Egypt , Sri Lanka , Australia ,
Pacific islands, Malaysia
and India .
It is believed that the disease has been introduced in India from Sri Lanka through infected suckers. The disease is
reported from Kerala in1940 and spread in banana growing neighbouring states
like Tamilnadu, Karnataka, Andhra Pradesh, Maharashtra, Bihar, Orissa and
Assam .
Symptoms: - The disease is
transmitted to the plant by the aphid vector
Pentalonia nigronervosa and dwarf
varieties of banana are very susceptible to the disease. The primary symptoms of
the disease are seen when infected banana suckers are planted. The suckers put
forth narrow leaves, which are chlorotic and mosaic. The affected leaves are
brittle, with dark green patches and margins rolled upwards. The characteristic
symptom of bunchy top virus is the presence of dark green streaks along the
secondary veins or midrib of petiole. The diseased plants remain stunted and do
not produce fruits. The infected plant leaves shows characteristic rosette or
bunchy top symptoms. The disease does not kill the plant but once the plant gets
infected it does not recover from the disease.
Causal Organism: - The disease is
caused by Banana virus I or Musa virus I or Banana bunchy top virus transmitted
by the aphid vector Pentalonia
nigronervosa.
Disease Cycle: - The virus is found
systemically in all parts of the plant including rhizomes and suckers. The first
symptom of the disease is appeared after 5-6 weeks of inoculation from insect
vector. The vector usually feed at basal portion of pseudostem of host plant but
may be found on upper portion of the host plant. The aphids may migrate at long
distances. The aphid retains the infective potential for a period of 13 days and
transmits the virus to healthy host in a period of 90 minutes.
Disease Management:
- Removal of clumps, suckers and diseased plants is very important to stop dissemination of disease.
- Planting material should be disease free and not collected from disease prone areas.
- The vector (aphid) should be controlled to check spread of the disease by spraying with 0.1-0.5% Metasystox.
- The disease affected banana plants should be killed with herbicide (2,4- D or 2, 4, 5 – T). The infected rhizomes dug out and cut into small pieces with further spray of herbicide to check germination, which may harbour the virus.
2. PANAMA
Fusarium wilt of banana (panama disease) is one of the most devastating diseases
of banana in the world. The disease is prevalent in
Australia , Coasta Rica , Hawaii , India , Jamaica ,
Panama , South America ,
Surinam
and West Africa . The disease affects many
economically important varieties. The disease has been reported in India from Andhra Pradesh ,
Assam , Bihar, Karnataka, Kerala, Maharashtra,
Tamilnadu, and West Bengal
states.
Symptoms: - The pathogen attacks
banana plants of all ages and spreads mainly through the soil. The pathogen gets
entry in the plant body through roots damage caused by the nematodes. The fungus
blocks the vascular system and causes wilting. It is most damaging in poorly
drained soil. Banana plants affected by fusarium
will show yellowing of leaves starting with the oldest leaves. The newly emerged
leaf remain green and erect for a long period but later it also shows blotchy
and yellowing symptom with wrinkling lamina. Other petioles may remain erect but
will soon become yellow then brown and dry. In some cases the outer leaf sheaths
of the pseudostem may split longitudinally near soil level. If the pseudostem
cut longitudinally, many black or brown coloured streaks can be seen which run
upward to leaf bases and all other directions. The cut stem smells like rotten
fish. Plants affected by panama will generally not develop sufficiently for a
mature bunch to be produced and the disease can cause total crop loss. The
disease spread is favoured by warm soil temperature, poor drainage, light soils
and high soil moisture. Red or brown dots or streaks are also seen.
Causal Organism: - The pathogen
causing wilt or panama disease of banana is
Fusarium oxysporum f. sp. cubense (E. F. S.)
Snyder and Hansen. The fungal hyphae are present inter and intra cellularly in
the host tissues. The pathogen fills the cavities of vascular tissues and spread
systemically. The fungus produces numerous micro-conidia, macro-conidia and
chlamydospores. The sporodochium bears many conidiophores, is arises from
pseudo-parenchymatous tissues. The macro-conidia are sickle shaped, hyaline,
thin walled, 2-5 septate and measures 24-36 x 4-5 µm and micro-conidia are
ovate, single to non septate, hyaline and thin walled which measures 5-7 x 2-3
µm. The chlamydospores are oval or spherical, thick walled, may be paired,
measuring 7-12 x 7-8 µm. The pathogen has several races which are reported from
many countries.
Disease Cycle: - Light textured loam
and sandy loam soils which are acidic favours the disease development. The
pathogen is soil borne and invades the plant through injured roots and rhizomes.
The mycelium of the pathogen colonized the vascular bundles of host plant and
produces micro-conidia, macro-conidia and chlamydospores. The chlamydopores
survive in the soil for a long time. The pathogen can also survive in disease
rhizomes and other plant parts saprophytically and become active when conditions
are favourable and infection takes place. The pathogen spreads through suckers
from disease infested area to other areas. The pathogen can survive in the soil
more than twenty years.
Disease Management:
- Highly infected soil should not be replanted with banana at least for 4-5 years.
- Flooding of wilt affected areas for six months has been reported to give satisfactory results.
- Use the healthy planting material, removal of infected plants at first sight and avoidance of root injury through intercultural operations helps in reducing the disease incidence.
- Use of disease resistant cultivars is recommended.
- Growing of paddy followed by banana for 3-5 years once or twice, use of quick lime near the base of the plant and soaking with water and avoiding sunflower or sugarcane in crop rotation helps to reduce the disease incidence.
- Application of bioagents, such as, Trichoderma viride or Pseudomonas fluorescence in the soil is effective. Application of the capsule filled with P. fluorescence at 60 mg/capsule is recommended at 2, 4 and 6 months after planting.
- The modified Panchagavya mixture at 101 dilution should be applied (soil drenching) at 2-3 liters/plant.
- Soil drenching with 0.01% vapam or 0.15% thiram helps in managing the disease. Dipping of banana suckers in 0.1% carbendazim before plantation gives good control.
- Banana cultivars Giant Cavendish, Lacatan, Rajavazhai, Peyladen, Moongil, Poovan and Vamanakeli are reported to be resistant to wilt.
3. SIGATOKA LEAF SPOT
The disease mostly attacks leaves and has been reported to cause economic losses
to the banana crop. It has been reported to cause severe losses to banana crop
in Coasta Rica , Colombia ,
Fizi , Guatemala ,
Guyana , Haiti , Honduras ,
India , Jamaica , Java , Mexico , Panama ,
Surinam , Tanzania , Uganda
and Venezuela .
In India , the disease is
found in Andhra Pradesh , Assam , Bihar, Gujarat, Karnataka, Kerala, Maharashtra, Tamilnadu, and
West Bengal .
Symptoms: The initial symptoms seen
in the field are small lesions on leaves which are pale yellow or greenish
yellow streaks that appear on both sides of leaves parallel to the leaf veins.
The leaf spots on leaves are increases in size to form dark brown to black
linear oblong areas. Center of the spots eventually dry out, becoming light
gray, but a narrow, dark brown to black border persists giving a spindle shaped
appearance. Rapid drying and defoliation is the characteristic feature of this
disease. In severe cases, the petiole collapses and the leaf hangs down from the
pseudo stem. The infection may cause complete failure of maturity of the bunch.
In some cases, premature ripening of fruits is also reported. In a growing
plant, the leaf spots are seen mostly on the older leaves, the young leaves can
be free from the spots.
Epidemiology and Disease Cycle:
During rainy season, spread of the disease is very rapid. Both conidia and
ascospores can cause infection but conidia predominate for most of the period.
Conidia are produced in wet weather or in dew on the surface of lesions. The
conidia are dispersed by water droplets to other leaves, particularly to the
leaves of suckers. Ascospores are borne on older leaves in perithecia sunken
into the leaves tissue. The disease is favoured by warm temperature (23-25 °C),
rainy or humid weather, close planting, heavy weed or grass cover and failure to
remove the suckers.
Disease Management:
- Removal and destruction of infected leaves is necessary.
- Spraying 1 % Bordeaux mixture mixed with 2 % linseed oil, providing improved drainage, good weed control, removal of suckers and correct spacing helps in reducing the disease incidence.
- Spraying 0.1% Topsin M or prochloraz or 0.1 % carbendazim or 0.2 % chlorothalonil or 0.15% kitazin 3-4 times at fortnightly intervals was quite effective in field trials.
Crop Protection :: Pest of paddy
Crop Protection :: Pest of paddy |
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Crop Protection :: Pest of paddy
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