PAT 301 Diseases of Field and Horticultural crops and their management-I (1+1)

Theory
Etiology, symptoms, mode of spread, survival, epidemiology and integrated
management of important diseases

Unit-I Diseases of cereals and Millets

Cereals: rice and maize; Millets: sorghum, bajra, finger millet and small millets
Unit- II Diseases of Pulses and Oilseeds
Pulses: pigeon pea, urd bean, mung bean, soyabean, cowpea; Oilseeds: ground nut,
castor and Sesame
Unit- III Diseases of Cash crops: tobacco, jute and mulberry
Unit- IV Diseases of Fruits and vegetables crops
Fruits: banana, guava, papaya, pomegranate; Vegetables: tomato, brinjal, okra ,
cruciferous vegetables, beans, colacasia and sweet potato
Unit- V Diseases of Plantation crops
Plantation: coconut, arecanut, tea, coffee, rubber and cocoa

Practical
Study of symptoms and host parasite relationship of rice, maize, sorghum, bajra,
finger millet ,small millets, pigeon pea, urd bean, mung bean, soyabean, cowpea, ground
nut, castor Sesame, tobacco, jute , mulberry, banana, guava, papaya, pomegranate, tomato,
brinjal, okra , cruciferous vegetables, beans, colacasia , sweet potato, coconut, arecanut,
tea, coffee, rubber and cocoa
Theory
Etiology, symptoms, mode of spread, survival, epidemiology and integrated
management of
1. Diseases of rice
2. Diseases of maize and sorghum
3. Diseases of pearl millet, finger millet and small millets,
4. Diseases of pigeonpea, urdbean, mungbean, soybean and cowpea
5. Diseases of groundnu , sesame and castor
6. Diseases of tobacco, jute and mulberry
7. Diseases of banana
8. Diseases of guava, papaya and pomegranate
9. Mid semester examination
10. Diseases of tomato
11. Diseases of brinjal and okra
12. Diseases of crucifers
13. Diseases of sweet potato and beans
14. Diseases of coconut and arecanut
15. Diseases of tea
16. Diseases of coffee
17. Diseases of rubber and cocoa
Practical
Study of symptoms and host-parasite relationship of:
1. Diseases of rice
2. Diseases of maize and sorghum
3. Diseases of pearl millet, finger millet and small millets,
4. Diseases of pigeonpea, urdbean, mungbean, soybean and cowpea
5. Diseases of groundnut , sesame and castor
6. Diseases of tobacco, jute and mulberry
7. Diseases of banana
8. Diseases of guava, papaya and pomegranate
9. Diseases of crucifers
10. Field visit/ exposure visit to hilly fruits , vegetables and plantation crops
11. Diseases of tomato, brinjal and okra
12. Diseases of sweet potato and beans
13. Diseases of coconut and arecanut
14. Diseases of tea
15. Diseases of coffee
16. Diseases of rubber and cocoa
17. Final practical examination

Reference Books
1. Arjunan.G. Karthikeyan, G, Dinakaran ,D. Raguchander,T. 1999 Diseases of Horticultural
Crops, AE Publications, Coimbatore.
2. Rangasawmi ,G and Mahadevan, A. 1998. Diseases of crop Plants in India, Prentice Hall
of India Pvt. Ltd., New Delhi
3. Prakasam, V., Valluvaparidasan, V., Raguchander, T. and K.Prabakar. 1997. Field crop
diseases, AE Publication, Coimbatore.

E- Books
1. Agrios, G.N. 2008. Plant Pathology, Academic Press, New York.

2. Rangaswami, G. 2005. Diseases of Crop plants in India. Prentice Hall of India Pvt. Ltd.,
New Delhi.

Thakur, B.R. 2006. Diseases of field crops and their management

 DISEASES OF RICE

RICE (Oryza sativa)

1. Blast
Pyricularia oryzae (Syn : P. grisea)
(Sexual stage : Magnaporthe grisea)
Symptoms
The fungus attacks the crop at all stages from seedlings in nursery to heading in
main field. The typical symptoms appear on leaves, leaf sheath, rachis, nodes and even the
glumes are also attacked. On the leaves, the lesions start as small water soaked blusih
green flecks, soon enlarge and form characteristic spindle shaped spots with grey centre
and dark brown margin (Leaf blast). The spots join together as the disease progresses
and large areas of the leaves dry up and wither. Similar spots are also formed on the sheath.
Severely infected nursery and field show a burnt appearance. In infected nodes, irregular
black areas encircle the nodes can be noticed. The affected nodes may break up and all the
plant parts above the infected nodes may die (Node blast). At the flower emergence, the
fungus attacks the peduncle which is engirdled, and the lesion turns to brownish-black. This
stage of infection is commonly referred to as rotten neck/neck rot/neck blast/panicle blast. In
early neck infection, grain filling does not occur and the panicle remains erect like a dead
heart caused by a stem borer. In the late infection, partial grain filling occurs. Small brown to
black spots also may be observed on glumes of the heavily infected panicles. The pathogen
caused by yield losses ranged from 30-61 per cent depending upon the stages of infection.
Pathogen
Mycelium of the fungus, is hyaline to olivaceous, septate and highly branched.
Conidia are produced in clusters on long septate, olivaceous slender conidiophores.
Conidia are pyriform to ellipsoid, attached at the broader base by a hilum. Conidia are
hyaline to pale olive green, usually 3 celled. The perfect state of the fungus is M. grisea. It
produces perithecia. The ascospores are hyaline, fusiform, 4 celled and slightly curved.
Favourable Conditions
Application of excessive doses of nitrogenous fertilizers, intermittent drizzles,
cloudy weather, high relative humidity (93-99 per cent), low night temperature
(between 15-20°C or less than 26°C), more number of rainy days, longer duration of dew,
cloudy weather, slow wind movement and availability of collateral hosts.
Mode of Spread and Survival
The disease spreads primarily through airborne conidia since spores of the fungus
present throughout the year. Mycelium and conidia in the infected straw and seeds are
important sources of inoculum. Irrigation water may carry the conidia to different fields. The
fungus also survives on collateral hosts viz., Panicum repens, Digitaria magrginata,
Brachiaria mutica, Leersia hexandra, Dinebra retroflea, Echinochloa crusgalli and
Stenotaphrum secondatum.
Fore casting
Forecasting blast of rice can be made on the basis of minimum night temperature
range of 20-26OC in association with a high relative humidity range of 90 per cent and
above lasting for a period of a week or more during any of the three susceptible phases of
crop growth, viz., seedling stage, post transplanting tillering stage and neck emergence
stage. In Japan, the first leaf blast model was developed and named as BLAST. Later based
on different field experiments various models were developed namely, PYRICULARIA,
PYRIVIEW, BLASTAM, EPIBLA and P BLAST.
Management
Grow resistant varieties like Ponmani, ADT40, Co25 in Samba and Co37, Co43,
IR20, Co44, ADT36 and ADT39 in Thaladi seasons. The varieties viz. Co45, ADT37,
Vikas, Jaya, IR62, IR64 and ASD 18 also showed moderate resistance to blast. Avoid
cultivation of highly susceptible varieties viz., IR50 and TKM6 and susceptible varieties viz.,
Ponni, White Ponni and IR36 in disease favourable season. Remove and destory the weed
hosts in the field bunds and channels. Treat the seeds with Captan or Thiram or
Carbendazim or Carboxin or Tricyclazole at 2 g/kg. Seed treatment with biocontrol agent
Trichoderma viride@ 4g/kg or Pseudomonas fluorescens @ 10g/kg of seed. Avoid close
spacing of seedlings in the main field. Spray the nursery with Carbendazim 25 g or
Edifenphos 25 ml for 8 cent nursery. Spray the main field with Edifenphos 250 ml or
Iprobenphos 500 ml or Carbendazim 250 g or Tricyclazole 400 g or Thiophanate Methyl 500
g or Pyroquilon 500 g/ha.

2. Brown Spot or Sesame leaf spot

Helminthosporium oryzae (Syn : Drechslera oryzae)
(Sexual stage : Cochliobolus miyabeanus)
Symptoms
The fungus attacks the crop from seedling in nursery to milk stage in main field.
Symptoms appear as lesions (spots) on the coleoptile, leaf blade, leaf sheath, and glume,
being most prominent on the leaf blade and glumes. The disease appears first as minute
brown dots, later becoming cylindrical or oval to circular. The several spots coalesce
and the leaf dries up. The seedlings die and affected nurseries can be often recognised from
a distance by their brownish scorched appearance. Dark brown or black spots also appear
on glumes which contain large number of conidiophores and conidia of the fungus. It causes
failure of seed germination, seedling mortality and reduces the grain quality and weight.
Pathogen
H. oryzae produces greyish-brown to dark brown septate mycelium. Conidiophores
may arise singly or in small groups. They are straight, sometime geniculate, pale to brown in
colour. Conidia are usually curved with a bulge in the centre and tapering towards the
ends occasionally almost straight, pale olive green to golden brown colour and are 6-
14 septate. The perfect stage of the fungus is C. miyabeanus. It produces perithecia with
asci containing 6-15 septate, filamentous or long cylinderical, hyaline to pale olive green
ascospores. It produces C25 terpenoid phytotoxins called ophiobolin A, (or Cochliobolin
A), ophiobolin B (or cochliobolin B) and ophiobolin I. Ophiobolin A is most toxic.
These breakdown the protein fragment of cell wall resulting in partial disruption of integrity of
cell.
Favourable Conditions
Temperature of 25-30°C with relative humidity above 80 per cent are highly
favourable. Excess of nitrogen aggravates the disease incidence.
Mode of Spread and Survival
The infected seeds are the most common source of primary infection. The conidia
present on infected grain and mycelium in the infected tissue may viable for 2 to 3 years.
The fungus may survive in the soil for 28 months at 30°C and 5 months at 35°C. Airborne
conidia infect the plants both in nursery and in main field. Maximum flight of conidia takes
place at a wind velocity of 4.0 - 8.8 hr. Minimum temperature of 27 -28°C, Relative humidity
of 90-99% and rainfall of 0.4 -14.4 mm favoured the dispersal of the conidia to maximum
extent. The fungus also survives on collateral hosts like Leersia hexandra, Arundo donux,
and Echinochlora colonum.
Management
Field sanitation-removal of collateral hosts and infected debris in the field. Crop
rotation, adjustment of planting time and proper fertilization are suggested. Use of slow
release nitrogenous fertilizers is advisable. Grow disease tolerant varieties viz., Co44,
Cauvery, Bala Bhavani. Use disease free seeds. Treat the seeds with Thiram or Captan at
4 g/kg. Spray the nursery with Edifenphos 40 ml or Mancozeb 80 g or Captafol 40 g for 8
cents nursery. Spray the crop in the main field with Edifenphos 500 ml or Mancozeb 1 kg or
Captafol 625 g/ha.

3. Narrow brown leaf spot

Cercospora janseana
(Sexual stage : Sphaerulina oryzina)
Symptoms
The fungus produces short, linear brown spots mostly on leaves and also on
sheaths, pedicels and glumes. The spots appear in large numbers during later stages of
crop growth.
Pathogen
Conidiophores are produced in small groups and brown in colour. Conidia are hyaline
or sub hyaline, cylindrical and 3-5 septate.
Management
Spray Carbendazim 250 g or Mancozeb 1 kg/ha.

4. Sheath rot
Sarocladium oryzae
(Syn : Acrocylindrium oryzae)
Symptoms
Initial symptoms are noticed only on the upper most leaf sheath enclosing young
panicles. The flag leaf sheath show oblong or irregular greyish brown spots. They enlarge
and develop grey centre and brown margins covering major portions of the leaf
sheath. The young panicles may remain within the sheath or emerge partially. The panicles
rot and abundant whitish powdery fungal growth is formed inside the leaf sheath.
Pathogen
The fungus produces whitish, sparsely branched and septate mycelium. Condiophore
is slightly thicker than the vegetative hyphae. Conidia are hyaline, smooth, single celled and
cylindrical in shape.
Favourable Conditions
Closer planting, high doses of nitrogen, high humidity and temperature around 25-
30°C.Injuries made by leaf folder, brown plant hopper and mites increase infection.
Mode of Spread and Survival
Mainly through air-borne conidia and also seed-borne.

Management
Apply recommended doses of fertilizers. Adopt optimum spacing. Spray
Carbendazim 250g or Edifenphos 1 lit or mancozeb 1 kg or Chlorothalonil 1 kg/ha at boot
leaf stage and 15 days later. Soil application of gypsum in 2 equal splits (500 kg/ha) reduce
the sheath rot incidence.
5. Sheath blight
Rhizoctonia solani
(Sexual stage : Thanetophorus cucumeris)
Symptoms
The fungus affects the crop from tillering to heading stage. Initial symptoms are
noticed on leaf sheaths near water level. On the leaf sheath oval or elliptical or irregular
greenish grey spots are formed. As the spots enlarge, the centre becomes greyish white with
an irregular blackish brown or purple brown border. Lesions on the upper parts of plants
extend rapidly coalesing with each other to cover entire tillers from the water line to
the flag leaf. The presence of several large lesions on a leaf sheath usually causes death of
the whole leaf, and in severe cases all the leaves of a plant may be blighted in this way. The
infection extends to the inner sheaths resulting in death of the entire plant. Older plants are
highly susceptible. Five to six week old leaf sheaths are highly susceptible. Plants heavily
infected in the early heading and grain filling growth stages produce poorly filled grain,
especially in the lower part of the panicle.
Pathogen
The fungus produces usually long cells of septate mycelium which are hyaline when young,
yellowish brown when old. It produces large number of globoses sclerotia, which are initially
white, later turn to brown or purplish brown.
Favourable Conditions
High relative humidity (96-97 per cent), high temperature (30-32°C), closer planting
and heavy doses of nitrogenous fertilizers.
Mode of Spread and Survival
The pathogen can survive as sclerotia or mycelium in dry soil for about 20 months
but for 5-8 months in moist soil. It infects more than 188 crop species in 32 families.
Sclerotia spread through irrigation water.
Management
Avoid excess doses of fertilizers. Adopt optimum spacing. Eliminate weed hosts.
Apply organic amendments. Avoid flow of irrigation water from infected fields to healthy
fields. Deep ploughing in summer and burning of stubbles. Spray Carbendazim 250 g or
Chlorothalonil 1 kg or Edifenphos 1 lit/ha. Seed treatment with Pseudomonas fluorescens @
of 10g/kg of seed followed by seedling dip @ of 2.5 kg or products/ha dissolved in 100 litres
and dipping for 30 minutes. Soil application of P.fluorescens @ of 2.5 kg/ha after 30 days of
transplanting (This product should be mixed with 50 kg of FYM/Sand and then applied. Foliar
spray at 0.2% concentration commencing from 45 days after transplanting at 10 days
interval for 3 times depending upon the intensity of disease.
6. Grain discolouration
Drechslera oryzae, D. rostratum, D.tetramera, Curvularia lunata, Trichoconis
padwickii, Sarocladium oryzae, Alternaria tenuis, Fusarium moniliforme, Cladosporium
herbarum, Epicoccum purpurascens, Cephalosporium sp., Phoma sp., Nigrospora sp.
Symptoms
The grains may be infected by various organisms before or after harvesting causing
discolouration, the extend of which varies according to season and locality. The infection
may be external or internal causing discoloration of the glumes or kernels or both. Dark
brown or black spots appear on the grains. The discolouration may be red, yellow, orange,
pink or black, depending upon the organism involved and the degree of infection. This
disease is responsible for quantitative and qualitative losses of grains.
Favourable Conditions
High humidity and cloudy weather during heading stage.
Mode of Spread and Survival
The disease spreads mainly through air-borne conidia and the fungus survives as
parasite and saprophyte in the infected grains, plant debris and also on other crop debris.
Management
Pre and post-harvest measures should be taken into account for prevention of grain
discolouration. Spray the crop at bootleaf stage with Mancozeb 1 kg or Iprobenphos 500 ml
or Carbendazim 250 g/ha. Store the grains with 13.5-14% moisture content.

7. False smut
Ustilaginoidea virens
(Syn : Claviceps oryzae - sativa)
Symptoms
The fungus transforms individual grains into greenish spore balls of velvetty
appearance. Due to the development of the fructification of the pathogen, the ovaries are
transformed into large velvetty green masses. Usually only a few spikelets in a panicle are
affected.
Pathogen
Chlamydospores are formed on the sporeballs, they are spherical to elliptical, waxy
and olivaceous.
Favourable conditions
Rainfall and cloudy weather during the flowering and maturity periods are favourable.

8. Udbatta disease
Ephelis oryzae
(Sexual stage : Balansia oryzae-sativa)
Symptoms
The symptoms are evident at the time of panicle emergence. The infected panicle
inside the sheath is matted together by the mycelium. The entire ear head is converted
into a straight compact cylindrical dark spike like structure. The spikelets are cemented
to the central rachis and the size is remarkeably reduced. No grain is formed. The entire
spike is covered by greyish stroma and convex pycnidia are immersed in the stroma.
Pathogen
Pycnidiospores are hyaline, needle shaped and 4-5 celled.
Management
Hot water seed treatment at 45OC for 10 min. effectively controls the disease.
Removal of collateral hosts like Isachne elegans, Eragrostis tenuifolia and Cynadon
dactylon.

9. Stack burn disease

Trichoconis padwickii
(Syn : Alternaria padwickii)
Symptoms
Leaves and ripening grains are affected. In the leaves, circular to oval spots with dark
brown margins are formed. The central portion of the spot turns to light brown or almost
white and has numerous minute dots. On the glumes reddish brown or pale brown spots
appear. The kernels may shrivel and become brittle when severe spotting occurs.
Pathogen
Conidia are elongately fusoid, long beak at the tip, 3 to 5 septate, thick walled and
constricted at the septa.
Management
Treat the seeds with Thiram or Captan or Mancozeb at g/kg. Hot water treatment at
54°C for 15 minutes is also effective. Burn the stubbles and straw in the field.

10. Bunt or Kernel Smut or black smut

Tilletia barclayana
Minute black pustules or streaks are produced in the grains which burst open at the
time of ripening. The grains may be partially or entirely replaced by the fungal spores. The
sorus pushes the glumes apart exposing the black mass of spores. Only a few flowers are
infected in an inflorescence. The fungus survives as chlamydospores for one or more years
under normal condition and 3 years in stored grains.
11. Stem rot
Sclerotium oryzae
(Sexual stage : Magnaporthe salvinii)
Symptoms
Small black lesions are formed on the outer leaf sheath and they enlarge and reach
the inner leaf sheath also. The affected tissues rot and abundant sclerotia are seen in the
rotting tissues. The culm collapses and plants lodge. If the diseased tiller is opened, profuse
 mycelial growth and large number of sclerotia can be seen. The sclerotia may be seen in the
stubbles after harvest.
Pathogen
White to greyish hyphae produce smooth, spherical black and shiny sclerotia, visible
to naked eyes as black masses.
Favourable Conditions
Infestation of leaf hoppers and stem borer and high doses of nitrogenous fertilizers.
Mode of Spead of Survival
The sclerotia survive in stubbles and straw and are carried through irrigation water.
Management
Use of recommended doses of fertilizer. Deep ploughing in summer and burning of
stubbles. Avoid flow of irrigation water from infected fields to healthy fields.
12. Foot rot or Bakanae disease
Fusarium moniliforme
(Sexual stage : Gibberella fujikuroi)
Symptoms
The infected seedings in nursery are lean and lanky, much taller than healthy
seedlings and die after some time. In the main field, the affected plants have tall lanky tillers
and have longer internodes and aerial adventitious roots from the nodes above ground level.
The root system is fibrous and bushy. The plants are killed before earhead formation or they
produce only sterile spikelets. When the culm is split open white mycelial growth can be
seen.
Pathogen
Fungus produces both macro and micro conidia. Micro conidia are hyaline, single
celled and oval in shape. Macro conidia are slightly sickle shaped, narrow at both ends and
two to five celled. The fungus produces phytotoxin called fusaric acid, which is non-host
specific.
Mode of Spread and Survival
The fungus is externally seed-borne.
Management

Treat the seeds with Thiram or Captan or Carbendazim at 2 g/kg.

13 Bacterial leaf blight Xanthomonas oryzae p.v. oryzae

Symptoms
The disease is usually noticed at the time of heading but in severe cases occur
earlier also. Seedlings in the nursery show circular, yellow spots in the margin, later enlarge,
coalesce and cause drying of foliage. “Kresek” symptom is seen in seedlings, 1-2 weeks
after transplanting. The bacterium enters through the cut wounds in the leaf tips, becomes
systemic and cause death of entire seedling.
In grown up plants water soaked, translucent lesions appear usually near the leaf margin.
The lesions enlarge both in length and width with a wavy margin and turn straw yellow
within a few days, covering the entire leaf. As the disease progresses, the lesions cover
the entire leaf blade which may turn white or straw coloured. Lesions may also be seen on
leaf sheaths in susceptible varieties. Milky or opaque dew drops containing bacterial masses
are formed on young lesions in the early morning. They dry up on the surface leaving a white
encrustation. The affected grains have discoloured spots surrounded by water soaked areas.
If the cut end of leaf is dipped in water, bacterial ooze makes the water turbid.
Pathogen
The bacterium is strict aerobe, gram negative, non spore forming, rod shaped
with size ranging from 1-2 x 0.8-1.0um with monotrichous polar flagellum of 6-8 um.
The bacterial cells are capsulated and are joined to form an aggregate mass. Colonies are
circular, convex with entire margins, whitish yellow to straw yellow later and opaque.
Favourable Conditions
Clipping of tip of the seedling at the time of transplanting, heavy rain, heavy dew,
flooding, deep irrigation water, severe wind, temperature of 25-30OC and application of
excessive nitrogen, especially late top dressing.
Mode of Spread and Survival
The infected seeds as a source of inoculum may not be important since the bacteria
decrease rapidly and die in the course of seed soaking. The pathogen survives in soil and in
the infected stubbles and on collateral hosts like Leersia spp. Plantago najor, Paspalum
dictum, and Cyanodon dactylon. The pathogen spreads through irrigation water in dry
season and also through typhoons and rain storms.
Management
Burn the stubbles. Use optimum dose of fertilizers. Avoid clipping of tip of seedling at
the time of transplanting. Avoid flooded conditions. Remove weed hosts. Grow resistant
cultivars like IR 20 and TKM 6. Spray Streptomycin sulphate and tetracycline combination
300 g + Copper oxychloride 1.25 g/ha.

14. Bacterial leaf streak Xanthomonas campestris p.v. oryzicola

Symptoms
Fine translucent streaks are formed on the veins and the lesions enlarge lengthwise
and infect larger veins and turn brown. On the surface of the lesions, bacteria ooze out and
form small yellow band-like exudates under humid conditions. In severe cases the leaves
may dry up.
Management
Similar to bacterial leaf blight.
15. Tungro disease Virus
Symptoms
Infection occurs both in the nursery and in the main field. Plants are markedly
stunted. Leaves show yellow to orange discoloration and interveinal chlorosis. Yellow
discoloration is commonly seen in “Japonica” varieties, while “Indica” varieties show orange
discoloration. Young leaves are often mottled with pale green to whitish interveinal stripes.
The plants may be killed if infected early. Tillering is reduced with poor root system. The
infected plants have few spikelets and panicles are small with discoloured grains. Tungro
infected plants can be chemically identified by lodine Test. Ten cm long leaf tip is cut in the
early morning before 6 A.M. and dipped in a solution containing 2 g lodine and 6 g
Potassium lodide in 100 ml of water for 30 minutes. Tungro infected leaves show dark blue
streaks.
Pathogen
It is a composite disease caused by two morphologically unrelated viruses : rice
tungro bacilliform virus (RTBV) and rice tungro spherical virus (RTSV). RTBV has a
bacilliform capsid 130 x 30 nm made up of a single species of coat protein of MW 36 K and a
single molecule of circular double - standed DNA of 8.3 KbP. RTSV has a isomatric capsid,
30 nm in diameter comprising two to three polypeptide species and a single speices of
polyadenylated single - standed RNA of about 10 KbP.
Mode of Spread and Survival
Two types of virus particles are associated with the disease. Bacilliform particles
cause majority of the symptoms of the disease. Spherical particles help in the transmission
of bacilliform virus by the green leaf-hoppers. If the bacilliform virus particles are alone
present in the rice plant they will not be transmitted by the leafhopper vector. The
leafhoppers viz, Nephotettix virescens, N. nigropictus, N. parvus, N.malayanus and Recilia
dorsalis transmit the virus in a non-persistent manner. There is no latent period in the vector
and infectivity is retained for a maximum period of 6 days after acquisition of the virus.
Management
Summer deep ploughing and burning of stubbles. Destory weed hosts of the virus
and vectors. Grow disease tolerant cultivars like IR50 and Co45. Control the vectors in the
nursery by application of carbofuran 170 g/cent, 10 days after sowing. Spray Phosphamidan
500 ml or Fenthion 500 ml or Monocrotophos 1 lit/ha or Neem oil 3 per cent in the main field
15 and 30 days after transplanting to control leaf hoppers.
Grassy stunt Virus
The infected plants are markedly stunted and have excessive tillering and has an
erect growth habit. The leaves become short, narrow, pale green or pale yellow and have
numerous small dark brown spots. On older leaves these spots spreading give a bronze
colour to the plants. The plants may produce a few small panicles which bear dark brown
and unfilled grains.
Mode of Spread and Survival
The virus is transmitted in a persistent manner by the brown planthopper,
Nilaparvata lugens. It has a latent period of 5 to 28 days in the vector.
16. Rice dwarf Virus
Symptoms
The virus infected plants show marked stunted growth with chlorotic or whitish
specks on the leaves. The size of specks varies often and form interrupted streaks along the
veins and distal part of infected leaves show diffuse yellowing. The number of tillers may be
reduced with retarded growth. The diseased plants may survive until harvest time, remaining
more or less green. Plants which are infected at early stage produce no eartheads, if
produced, may have small unfilled grains.
Pathogen
The partially purified virus particle have a hexagonal outline and are 70 nm in
diameter with a surrounding envelope. The virus particle contains double stranded RNA or of
double helical in nature.
Favourable Conditions
High population of Nephotettix cincticeps, Recllia dorsalis and N. nigropictus. The
presence of gramineous weeds like Echinochloa crusgalli, Glyceria acutifolia and Panicum
miliaceaaum.
Mode of Spread and Survival
The virus is found to survive in the gramineous weeds. The virus is transmitted
through the egg masses of leafhoppers from one generation to another. (Trans ovarial
transmission).
Management
Destory the weed host which harbour the virus and the vectors. Spray
Phosphamidon or Fenthinon 500 ml or Monocrotophos 1 lit/ha.
Ragged stunt Virus
Symptoms
Formation of ragged leaves with irregularly edged portions, stunting of plants, vein
swelling, delay in flowering, production of nodal branches and incomplete emergence of
panicles are the main diagnostic symptoms.
Mode of Spread and Survival
The virus is transmitted in a persistent manner by the brown planthopper, Nilaparvata
lugens but not through seed. It has a latent period of 3 to 35 days in the vector.
17. Rice yellow dwarf
Mycoplasma Like Organism (MLO)
Symptoms
The infected plants are stunted and have yellowish green to whitish green leaves.
There is excessive tillering and leaves became soft and droop slightly. Plants are usually
sterile but some may produce small panicles with unfilled grains. If plants are infected early
they usually die before maturity, and even if they do survive no panicles are produced or
only a small number with no grains. With later infection there may be little sign that the plant
is diseased, but regrowth from stubble will show typical chlorosis.
Mode of Spread and Survival
The MLO is transmitted by Nephotettix virescens and N. nigropictus with a latent
period of 25-30 days. It survives on several grass weeds.
Management
Deep ploughing during summer and burning of stubbles. Rice varieties like IR62 and
IR64 are resistant to the disease. The management practices followed for Rice Tungro
disease may be adopted for this disease also.
 DISEASES OF MAIZE

(Zea mays)

1. Downy mildew/Crazy top

Peronosclerospora sorghi
Symptoms
The most characteristic symptom is the development of chlorotic streaks appear on
the leaves and the plants exhibit a stunted and bushy appearance due to the shortening of
the internodes. White downy growth can be seen not only on the lower surface of leaf but
also on the chlorotic streaks. The downy growth also occurs on bracts of green unopened
male flowers in the tassel. Sometimes miniature to large leaves has been noticed in the
tassel. These leaves bear well defined downy growth. Proliferation of auxillary buds on
the stalk of tassel as well as the cobs is very common (Crazy top).
Pathogen
The fungus grows as white downy growth on both surface of the leaves, consist of
sporangiophores and sporangia. Sporangiophores are quite short and stout, branch
profusely into series of pointed sterigmata which bear hyaline, oblong or ovoid sporangia
(conidia). Sporangia germinate directly and infect the plants. In advanced stages, oospores
are formed which are spherical, thick walled and deep brown.
Favourable Conditions
Low temperature (21-33OC), high relative humidity, (90 per cent), water logging
condition and light drizzling. Young plants are highly susceptible.
Mode of Spread and Survival
The primary source of infection is through the oospores present in the soil and also
the dormant mycelium present in the infected maize seeds. Secondary spread is through air-
borne conidia. The oospores survive in the soil as well as in the infected plant debris.
Management
Deep ploughing. Crop rotation with pulses. Adjust the time of sowing. Rogue out
infected plants. Treat the seeds with Metalaxyl compound (Apron 35SD) at 6g/kg. Spray the
crop with Metalaxyl + Mancozeb 2kg or Mancozeb 1.25 kg/ha on 20th day after sowing.
Grow resistant varieties and hybrids viz. Co1, CoH1 and CoH2.
2. Leaf blight
Helminthosporium maydis
(Syn : H. turcicum)
Symptoms
The fungus affects the maize plant at young stage. Small yellowish round to oval
spots are seen on the leaves. The spots gradually increase in area into bigger elliptical spots
and are straw to grayish brown colour in the centre with dark brown margins. The spots
coalesce to form bigger spots and gives blighted appearance. The surface is covered with
olive green velvetty masses of conidia and conidiophores.
Pathogen
Conidiophores are in group, geniculate, mid dark brown, pale near the apex and
smooth. Conidia are distinctly curved, fusiform, pale to mid dark golden brown with 5-11
pseudosepta.
Favourable Conditions
Optimum temperature for the germination of conidia is 8 to 27OC provided with free
water on the leaf. Infection takes place early in the wet season.
Mode of Spread and Survival
It is a seed-borne fungus. It also infects sorghum, wheat, barely, oats, sugarcane and
spores of the fungus are also found to associate with seeds of green gram, black gram,
cowpea, varagu, Sudan grass, Johnson grass and Teosinte.
Management
Treat the seeds with Captan or Thiram at 4 g/kg. Spray Mancozeb 1.25 kg or Captan
1 kg/ha.
3. Rust Puccinia sorghi
Symptoms
Circular to oval, elongated cinnamon-brown powdery pustules are scattered over
both surface of the leaves. As the plant matures, the pustules become brown to black owing
to the replacement of red uredospores by black teliospores.
Pathogen
Uredospores are globose or elliptical finely echinulate, yellowish brown with 4 germ
pores. Teliospores are brownish black, or dark brown, oblong to ellipsoidal, rounded to
flattened at the apex. They are two celled and slightly constricted at the septum and the
spore wall is thickened at the apex.
Favourable Conditions- Cool temperature and high relative humidity.
Mode of Spread and Survival
Presence of alternate hosts viz., Oxalis corniculata and Euchlaena mexicana.
Management
Remove the alternate hosts. Spray Mancozeb at 1.25 kg/ha.
4. Head smut- Sphacelotheca reiliana

Symptoms
Symptoms are usually noticed on the cob and tassel. Large smut sori replace the
tassel and the ear. Sometimes the tassel is partially or wholly converted into smut sorus.
Under such conditions the Individual spikelets on tassels may form shoot like growths, or the
entire tassel may develop into leaf like structures. The smutted plants are stunted in growth,
produce little yield and remain greener than that of the rest of the plants.

Pathogen
Smut spores (chlamydospores) are produced in large numbers which are reddish
brown to black, thick walled, finely spined, spherical or slightly irregular.
Favourable Conditions
Low temperature favours more infection and this fungus also infects the sorghum
crop and vice versa.
Mode of Spread and Survival
The smut spores retains its viability for two years. The fungus is externally seed-
borne and soil-borne. The major source of infection is through soil-borne chlamydospores.
Management
Field sanitation. Crop rotation with pulses. Treat the seeds with Captan or Thiram at
4 g/kg.
5. Charcoal rot Macrophomina phaseolina (Rhizoctonia bataticola)

Symptoms
The fungus attacks roots of seedlings and young plants. The affected plants first
exhibit the wilting symptoms. The stalk of the infected plants can be recognized by grayish
streaks and become weak. The pith become shredded and grayish black minute sclerotia
develop abundantly on the vascular bundles. Shreading of the interior of the stalk often
causes stalks to break in the region of the crown. The crown region of the infected plant
become dark in colour. Shreadding of root bark and disintergration of root system are the
common features.
Pathogen
The fungus produces large number of sclerotia which are round and black in colour.
Sometimes, it produces pycnidia on the stems or stalks.
Favourable Conditions- High temperature and low soil moisture (drought)

Mode of Spread and Survival

The fungus has a wide host range, attacking sorghum, cumbu, ragi and pulses. It
survives for more than 16 years in the infected plant debris. The primary source of infection
is through soil-borne sclerotia.

Management

Long crop rotation with crops that are not natural host of the fungus. Irrigate the
crops at the time of earhead emergence to maturity. Treat the seeds with Carbendazim or
Captan at 2 g/kg. Grow disease tolerant varieties viz., SN-65, SWS-8029, Diva and Zenit.
Minor diseases

Brown spot Physoderma maydis. Water soaked lesions, which are oval, later turn into light
green and finally brown.
Stalk rot Erwinia dissolvens. Dark brown lesion and rotting of stalk at crown level about 6”-
12” from ground level. Lodging of plants.
Mosaic Virus. Formation of mosaic symptoms. Plants produce smaller ear head and
immature seeds
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 DISEASES OF SORGHUM
(Sorghum bicolor)

1. Downy Mildew
Peronosclerospora sorghi
Symptoms
The fungus, Peronosclerospora sorghi is the cause of a systemic downy mildew of
sorghum. It invades the growing points of young plants, either through oospore or conidial
infection and as the leaves unfold they show various types of symptoms. The first few leaves
that show symptoms are only partially infected with green or yellow colouration of the
infected portion. Abundant downy white growth is produced on the lower surface of the
leaves, consists of conidiophores and conidia. Normally three or four leaves develop the
chlortic downygrowth type of symptoms. Subsequent leaves show progressively more of a
complete bleaching of the leaf tissue, sometimes in streaks or stripes. As the infected
bleached leaves mature they become necrotic and the interveinal tissues disintegrate,
releasing the resting spores (oospores) and leaving the vascular bundles loosely connected
to give the typical shredded leaf symptom.
Pathogen
P. sorghi is systemic in young host plant in the form of intercellular, non-septate
mycellium. It is an obligate parasite. Conidiophores emerge through the stomata in single or
in clusters which are stout and dichotomously branched. Conidia are single celled, hyaline,
globose and thinwalled. Oospores are typically produced abundantly in parallel bands
between fibro vascular strands of the shredded leaf tissue which are more or less round,
thickwalled and deep brown in colour.
Favourable Conditions
Maximum sporulation takes place at 100 per cent relative humidity. Optimum
temperature for sporulation is 21-23OC. Light drizzling accompanied by cool weather is
highly favourable.
Mode of Spread and Survival
The primary infection is by means of oospores present in the soil which germinate
and initiate the systemic infection. The oospores persist in the soil for several years.
Secondary spread is by means of air-borne conidia. Presence of mycelium of the fungus in
the seeds of systemically infected plants is also a source of infection.
Management
Crop rotation with other crops like pulses and oilseeds. Avoid the secondary spread
of the disease by roguing out the affected plants since the wind plays an important role in the
secondary spread of the disease from the infected plants. Grow moderately resistant
varieties like Co25 and Co26. Seed treatment with Metalaxyl (Apron 35 SD) at 6 g/kg of
seed. Spray Metalaxyl 500 g or Mancozeb 1 kg or Ziram 1 kg or Zineb 1 kg/ha.
2. Leaf blight
Exerohilum turcicum
(Syn : Helminthosporium turcicum)
Symptoms

The leaf blight pathogen also causes seed rot and seedling blight of sorghum. The
disease appears in the form of small narrow elongated spots in the initial stage. But in due
course they extend along with the length of the leaf becoming bigger. On older plants, the
typical symptoms are long elliptical necrotic lesions, straw coloured in the centre with dark
margins. The straw coloured centre become darker during sporulation. The lesions can be
several centimeters long and wide. Many lesions may develop and coalesce on the leaves,
destroying large areas of leaf tissue, giving the crop a distinctly burnt or blasted appearance.
Pathogen
The mycelium is localised in the infected lesion. Conidiophore emerges through
stomata and are simple, olivaceous, septate andgeniculate type. Conidia are olivaceous
brown, 3-8 septate and thick walled.
Favourable Conditions
Cool moist weather, high humidity (90 per cent) and high rainfall.
Mode of Spread and Survival
The fungus is found to persist in the infected plant debris. Seed borne conidia are
responsible for seedling infection. The secondary spread of the disease is through wind-
borne conidia.
Management
Use disease free seeds. Treat the seeds with Captan or Thiram at 4 g/kg. Spray
Mancozeb 1.25 kg or Captafol 1 kg/ha.
3. Rectangular Leaf spot
Cercospora sorghi
Symptoms
The symptoms appear as small leaf spots which enlarge to become rectangular
lesions (which can be 5-15 mm long by 2 to 5 mm wide) on the leaf and leaf sheath. Usually
the lower leaves are first attacked. The lesions are typical dark red to purplish with some
what lighter centres. The lesions are mostly isolated and limited by veins. Severe spotting
results in premature drying of leaves. The colour of the spots vary from red, purple, brown or
dark depending upon the variety.
Pathogen
 Mycelium of the fungus is hyaline and septate. Conidiophores emerge in clusters
through stomata, which are brown and simple, rarely branched. Conidia are hyaline, thin
walled, 2-13 celled and long obclavate.
Favourable Conditions
Cool mosit weather, high humidity (90 per cent) and high rainfall.

Mode of Spread and Survival

The conidia survive upto 5 months. The disease spreads through air-borne and seed-
borne conidia.

Management

Use disease free seeds. Treat the seed with Captan or Thiram at 4 g/kg. Spray
Mancozeb 1.25 kg or Captafol 1kg/ha.
4. Anthracnose and red rot
Colletotrichum graminicolum
Symptoms
The fungus causes both leaf spot (anthracnose) and stalk rot (red rot) in sorghum.
The disease appears as small red coloured spots on both surfaces of the leaf. The centre of
the spot is white in colour encircled by red, purple or brown margin. Numerous small black
dots are seen on the white surface of the lesions which are the fruiting bodies (acervuli). Red
rot can be characterized externally by the development of circular cankers, particularly in the
inflorescence. Infected stem when split open shows discoloration, which may be continuous
over a large area or more generally discontinuous giving the stem a marbeled appearance.
The stem lesion also show acervuli.
Pathogen
The mycelium of the fungus is localised in the spot. Acervuli with setae arise through
epidermis. Conidia are hyaline, single celled, vacuolate and falcate in shape.
Favourable Conditions
Continuous rain, temperature of 28-30OC and high humidity.
Mode of Spread and Survival
The disease spread by means of seed-borne and air-borne conidia and also through the
infected plant debris.
Management
Treat the seeds with Captan or Thiram at 4 g/kg. Spray the crop with Mancozeb 1.25
kg/ha.
 5. Rust
Puccinia purpurea

Symptoms
The fungus affects the crop at all stages of growth. The first symptoms are small
flecks on the lower leaves (purple, tan or red depending upon the cultivar). Pustules
(uredosori) appear on both surfaces of leaf as purplish spots which rupture to release
reddish powdery masses of uredospores. The pustules are elliptical and lie between and
parallel with the leaf veins. In highly susceptible cultivars, the pustules occur so densely that
almost the entire leaf is destroyed. Teliopores develop later sometimes in the old uredosori
or in telisori, which are darker and longer than the uredosori. The pustules may also occur
on the leaf sheaths and on the stalks of inflorescence.
Pathogen
The uredospores are pedicellate, elliptical or oval, thin walled, echinulated and dark
brown in colour. The teliospores are reddish or brown in colour and two celled, rounded at
the apex with one germ pore in each cell. The teliospores germinate and produce
promycelium and basidiospores. Basidiospores infect Oxalis corniculata (alternate host)
where pycnial and aecial stages arise after infection.
Favourable Conditions
Low temperature of 10 to 12OC favours teliospore germination and a spell of rainy
weather favours the onset of the disease.
Mode of Spread and Survival
The uredospores survive for a short time in soil and infected debris. Presence of
alternate host helps in perpetuation of the fungus.
Management
Remove the alternate host Oxalis comiculata. Spray the crop with Mancozeb at 1.25
kg/ha.
6. Grain smut/Kernel smut / Covered smut / Short smut
Sphacelotheca sorghi
Symptoms
The individual grains are replaced by smut sori which can be localized at a particular
part of the head or occur over the entire inflorescence. The sori are oval or cyclindrical and
are covered with a tough white cream to light brown skin (peridium) which often persists
unbroken upto threshing. The size, colour and degree of breakage of the sori varies
considerably with race of the fungus and the sorghum cultivar. Ratoon crops exhibit higher
incidence of disease.
 Loose smut/Loose kernel smut
Sphacelotheca cruenta
Symptoms
The affected plants can be detected before the ears come out. They are shorter
about a foot than the healthy plants with thinner stalks and marked tillering. The ears come
out much earlier than the healthy. The glumes are hypertrophied and the earhead gives a
loose appearance than healthy. The sorus is covered by a thin membrane which ruptures
very early, exposing the spores even as the head emerges from the sheath. The size of the
sorus varies with the variety of the host.
Long smut
Tolyposporium ehrenbergii
Symptoms
The presence of long smut can be discovered only by a close examination of the
ears in the field. This disease is normally restricted to a relatively a small proportion of the
florets which are scattered on a head. The sori are long, more or less cylindrical, elongated,
slightly curved with a relatively thick creamy-brown covering membrane (peridium). The
peridium splits at the apex to release black mass of spores among which are found several
darkbrown filaments which represent the vascular bundles of the infected ovary.
Head smut
Sphacelotheca reiliana
Symptoms
The head is completely replaced by a large gall (sorus). The galls are at first covered
by a whitish grey membrane of fungal tissue, which ruputres, often before the head emerges
from the boot leaf, to expose a mass of brown-black powder (smutspores) along which are
embedded long, thin, darkcoloured filaments which are the vascular bundles of the infected
head. Sometimes smaller sori develop on the leaves and lower part of the peduncle.
Management for all smuts
Treat the seed with Captan or Thiram at 4 g/kg. Use disease free seeds. Follow crop
rotation. Collect the smutted ear heads in cloth bags and dip in boiling water.
Ergot or Sugary disease
Sphacelia sorghi
Symptoms
The disease is confined to individual spikelets. The first symptom is the secretion of
honey dew (creamy stickly liquid) from infected florets. Under favourable conditions, long,
straight or curved, cream to light brown, hard sclerotia develop. At the base of the affected
plants white spots can be seen on the soil surface, denoting the drops of honey dew which
had fallen on the soil. Often the honey dew is colonised by Crerebella sorghivulgaris which
gives the head a blackened appearance.
Pathogen
The fungus produces septate mycelium. The honey dew is a concentrated
suspension of conidia, which are single celled, hyaline, elliptic or oblong in shape and
slightly constricted in the middle.
Favourable Conditions
A period of high rainfall and high humidity during flowering season. Cool night
temperature and cloudy weather aggravate the disease.
Mode of Spread and Survival
The primary source of infection is through the germination of sclerotia which produce
ascospores, which infect the ovary. The secondary spread takes place through air and
insect-borne conidia. Rain splashes also help in spreading the disease.
Management
Adjust the date of sowing so that the crop does not flower during September-October when
high rainfall and high humidity favour the disease. Spray any one of the following fungicides
at emergence of earhead (5-10 per cent flowering stage) followed by a spray at 50 per cent
flowering and repeat the spray after a week, if necessary. Ziram (or) Zineb (or) Mancozeb
(or) Carbendazim at 1 kg/ha.
7. Head mould/Grain mould/Head blight
More than thirty two genera of fungi were found to occur on the grains of sorghum.
Symptoms
If rains occur during the flowering and grain filling stages, severe grain moulding can
occur. Fungi from many genera have been isolated from the infected sorghum grains and
the most frequently occurring genera are Fusarium, Curvularia, Alternaria, Aspergillus and
Phoma. Fusarium semitectum and F.moniliforme develop a fluffy white or pinkish
colouration. C. lunata colours the grain black. Symptom varies depending upon the organism
involved and the degree of infection.
Favourable Conditions
Wet weather following the flowering favours grain mould development and the longer
the wet period the greater the mould development. Compact ear heads are highly
susceptible.
Mode of Spread and Survival
The fungi mainly spread through air-borne conidia. The fungi survive as parasites as
well as saprophytes in the infected plant debris.
Management
 Adjust the sowing time. Spray any one of the following fungicides in case of
intermittent rainfall during earhead emergence, a week later and during milky stage.
Mancozeb 1 kg/ha. or Captan 1 kg + Aureofungin-sol 100 g/ha.
8. Phanerogamic parasite
Witch Weed
Striga asiatica and Striga densiflora
It is a partial root parasite and occurs mainly in the rainfed sorghum. It is a small
plant with bright green leaves, grows upto a height of 15-30 cm. It always occurs in clusters
of 10-20/host plant. S. asiatica produces red to pink flowers while. S. densiflora produces
white flowers. Each fruit contains minute seeds in abundance which survive in the soil for
several years. The root exudates of sorghum stimulate the seeds of the parasite to
germinate. The parasite then slowly attach to the root of the host by haustoria and grow
below the soil surface and produce underground stems and roots for about 1-2 months. The
parasite grows faster and appears at the base of the plant. Severe infestation causes
yellowing and wilting of the host leaves. The infected plants are stunted in growth and may
die prior to seed setting.
Management
Regular weeding and interculture operation during early stages of parasite growth.
Spray Fernoxone (sodium salt of 2, 4-D) at 450g/500 litre of water.
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 DISEASES OF PEARL MILLET/CUMBU
(Pennisetum americanum)

1. Downy mildew
Sclerospora graminicola
Symptoms
Infection is mainly systemic and symptoms appear on the leaves and the
inflorescenses. The first symptoms can appear in seedlings at three to four leaf stage. The
affected leaves show patches of light green to light yellow colour on the upper surface of
leaves and the corresponding lower surface bears white downy growth of the fungus. The
yellow discolouration often turns to streaks along veins. The downy growth seen on infected
leaves consists of sporangiophores and sporangia. As a result of infection young plants dry
and die ultimately. Symptoms may appear first on the upper leaves of the main shoot or the
main shoot may be symptom free and symptoms appear on tillers or on the lateral
shoots.The inflorescences of infected plants can be completely or partially malformed with
florets converted into leafy structures, the ear head gives the typical symptom of green ear.
Infected leaves and inflorescences produce sporangia over a considerable period of time
under humid conditions and necrosis begins. The dry necrotic tissues from infected plant
contain masses of oospores.
Pathogen
The mycelium is systemic, nonseptae, intercellular in the parenchymatous tissues.
Short, stout, hyaline sporangeiophores arise through stomata and branch irregularly, ends
with characteristic stalks bearing the sporangia. Sporangia are hyaline, thin walled and
elliptical, bear prominent papilla. Oospores are round in shape, surrounded by a smooth,
thick and yellowish brown wall.
Favourable Conditions
Very high humidity (90 per cent), presence of water on the leaves and low
temperature of 15-25OC favour the formation of sporangiophore and sporangie. Under such
conditions, 35,000 sporangia are liberated from one sq. inch of leaf area.
Mode of Spread and Survival
The oospores remain viable in soil for 5 years or longer giving rise to the primary
infection on the host seedling. Secondary spread is through sporangia which are produced
during rainy season. It is also believed that the dormant mycelium is present in embryo of
infected seeds.
Management
Deep ploughing so as to bury the oospore deeply. Rogue out infected plants. Adopt
crop rotation. Use excess seed rate. Grow resistant varieties like X5, WCC-75 and Co7.
Treat the seeds with Metalaxyl (Apron 35SD) at 6g/kg. Spray Mancozeb 1kg or
Metalaxyl+Mancozeb (Ridomil MZ) at 2kg/ha on 20th day after sowing in the field.
2. Smut Tolyposporium penicillariae
Symptoms
The pathogen infects few florets and transforms them into plump sacs (sori)
containing black powder (smut spores). In the early stage, the sori are larger and greener
than normal healthy grains and when the sori mature they become dark brown and are
easily broken and release millions of black smut spore balls.
Pathogen
The fungus mostly confined to the sorus. The sori contains spores which are usually
in balls and are not easy to separate. Each spore is angular or round and light brown
coloured.
Favourable Conditions
High humidity and successive cropping with cumbu.
Mode of Spread and Survival
It survives spore balls in the soil and serve as primary source of inoculum. The
secondary spread is by air-borne conidia.
Management
The damage caused by the fungus is negligible. However, removal and destruction of
affected earhead will help in controlling the disease.
3. Rust
Puccinia penniseti
Symptoms
Symptoms first appear mostly on the distal half of the lamina. The leaf soon becomes
covered by uredosori which appear more on the upper surface. Sometimes, the necrotic
spots appear around the group of pustules. The pustules may be formed on leaf sheath.
stem and even on peduncles. Later, telial formation takes place on leaf blade, leaf sheath
and stem. While brownish uredinia get exposed at maturity, the black telia remain covered
by the epidermis for a longer duration.
Pathogen
Uredospores are oval, elliptic or pyriform with four germpores, sparsely echinulated
and pedicellate. Teliospores are dark brown in colour, 2 celled, cylindrical to club shaped,
apex flattered, broad at top and tapering towards base. The fungus has a long life cycle
producing uredial and telial stages on cumbu and aecial and pycnial stages on brinjal.
(Solanum melongena)
Favourable Conditions
Closer spacing. Presence of abundant brinjal plants and other species of Solanum viz.,
S.torvum, S. xanthocarpum and S. pubescents.
Mode of Spread and Survival
Air-borne uredospores are the primary sources. The uredial stages also occur on
several species of Pennisetum.
Management
 Spray with Wettable Sulphur 2.5 kg or Captafol 1 kg or Mancozeb 1.25 kg/ha.
4. Ergot or Sugary disease
Claviceps fusiformis
Symptoms
The symptom is seen by exudation of small droplets of light pinkish or brownish
sticky fluid (honey dew) from the infected spikelets. Under severe infection many such
spikelets exude plenty of honey dew which trickle along the earhead. This attracts several
insects. In the later stages, the infected ovary turns into small dark brown sclerotium which is
just projecting out of the spikelet.
Pathogen
The pathogen produces septate mycelium which produce conidiophores and are
closely arranged. Conidia are hyaline and one celled. The sclerotia are small and dark grey
but white inside. Sclerotia are 3-8 mm long and 0.3-15 mm broad.
Mode of Spread and Survival
Sclerotia are viable in soil for 6-8 months. The primary infection takes place by
germinating sclerotia present in the soil. Secondary spread is by insects or air-borne conidia.
The role of collateral hosts like Cenchrus ciliaris and C. setigerus in perpetuation of fungus is
significant. The fungus also infects other species of Pennisetum.
Management
Adjust the sowing date so that the crop does not flower during September when high
rainfall and high relative humidity favour the disease spread. Immerse the seeds in 10 per
cent common salt solution and remove the floating sclerotia. Remove collateral hosts. Spray
with Carbendazim 500g or Mancozeb 1.25 kg or Ziram 1kg/ha when 5-10 per cent flowers
have opened and again at 50 per cent flowering stage.
Minor diseases
Grain mould Fusarium and Curvularia spp. Complex of several fungi.
Grains covered with white, pink or black moulds.
Blast Pyricularia setariae. Diamond shaped to circular lesions with dark brown
margins and chlorotic haloes.
Zonate leaf spot Gloeocercospora sp. Rough circular lesions with alternating concentric
bands of straw and brown colour, often coalescing over the leaf surface.
Banded leaf Rhizoctonia spp. Patch work of light and dark and Sheath discoloured areas
often bearing fluffy to light Brown fungal mats
 DISEASES OF FINGER MILLETS AND SMALL MILLETS
RAGI (Eleusine coracana)

1. Blast
Pyricularia grisea
Symptoms
The pathogen attacks the crop from seedling stage to the time of grain formation.
The lesions are spindle shaped and are of different size. In the beginning, the spots have
yellow margin with grayish green centre. Under humid conditions, an olive grey overgrowth
of fungus can be seen on the centre of the spot. Later the centre become whitish grey and
disintegrate. The lesions on the seedlings are about 0.3 to 0.5 cm in breath and 1-2 cm in
length. Stem infection causes blackening of the nodal region. Maximum damage is caused
by the neck infection. The neck region turns black and shrink. Infection may also occur at the
basal portions of the panicle branches including the fingers. The affected portions turn brown
and ears become chaffy and only few shrivelled grains are formed.
Pathogen
Young hyphae are hyaline and septate and turns to brown when become old.
Numerous conidiophores and conidia are formed in the middle portion of the lesions.
Conidiophores are slender, thin walled, emerging singly or in groups, unbranched,
geniculate and pale brown in colour. Conidia are thin walled, sub-pyriform, hyaline 1-2
septate, mostly 3 celled with a prominent hilum.
Favourable Conditions
Optimum temperature is 25-30OC. High relative humidity (92-95 per cent) and
continuous drizzles. Presence of collateral hosts like Tenai, bajra, wheat, barley and oats.
Mode of Spread ans Survival
The fungus is seed-borne and the primary infection takes place through the seed-
borne conidia and also the other crops serve as source of inoculum. The secondary spread
is through air-borne conidia.
Management
Treat the seeds with Captan or Thiram at 4g or Carbendazim at 2 g/kg. Grow
moderately resistant varieties like Co10, Co11, Co12, Co13, PR202 and HR374. Spray with
Iprobenphos (IBP) or Edifenphos 500 ml or Carbendazim 250 g/ha, first spray immediately
after noticing the symptoms and second spray at flowering stage.
2. Seedling blight or Leaf blight
Helminthosporium nodulosum
(Sexual stage : Cochliobolus nodulosum)
Symptoms
The pathogen attacks all the parts of the plants including roots, base of the plants,
culms, leaf sheath, leaf blade, neck of the panicle and the fingers. Both pre-and post-
emergence rot may be seen. On young leaves the disease appears as minute, light brown
oval spots. The affected leaves wither prematurely and seedlings may be killed. The fungus
affect the base of the plants and cause root rot and foot rot. In grown up plants, spots are
oblong and dark brown. The spots on the leaf sheath and culms are irregular and are
generally found on the junction of blade and sheath. Infection on the neck causes
discoloration and sooty growth in the inflorescences.
Pathogen
Hypha of the fungus is light brown coloured and septate. Conidiophores are long,
septate, dark brown in colour, often branched and geniculate. Conidia are straight ovoid,

pale to dark golden brown, 5-7 pseudoseptate. C. nodulosum produces spherical perithecia
and asci contain 1 to 8 ascospores.
Favourable Conditions

Optimum temperature for infection is 30-32OC and 80-90% relative humidity. Rains
during earhead emergence is favourable.
Mode of Spread and Survival
The pathogen readily infects Setaria italica, Eleusine indica, Echinochlora sp,
Panicum miliaceum, Pennisetum typhoides, Sorghum bicolor and Zea mays. Primary spread
is through seed-borne inoculum and the secondary spread by air-borne conidia.
Management
Treat the seeds with Captan or Thiram at 4 g/kg. Spray with Mancozeb at 1.25 kg/ha.
3. Wilt
Sclerotium rolfsii
(Sexual stage : Corticium rolfsii)
Symptoms
The infected plants become pale, chlorotic and stunted. The fungus attacks basal
stem portion and later the leaf sheath and culm. The infected portion becomes soft and dark
brown in colour. A whitish mycelial mass can be seen on the basal stem and on the nodal
portions. On the surface of the lesions, small spherical, dark coloured sclerotia are formed.
Pathogen
The mycelium of the fungus is septate and white to tan coloured. Sclerotia are
minute, mustard seed like structures and black in colour.
Favourable Conditions
High soil moisture and high temperature (more than 30OC)
Mode of Spread and Survival
The fungus survives in the soil as sclerotia and spreads through irrigation water and
implements.
Management
Spot drench with Copper oxychloride at 0.25 per cent. Crop rotation with non host
plants.
4. Mottle streak and streak Virus
Symptoms

The virus affected plants are stunted and pale green in colour. Chlorotic streaks are
formed on the leaves and it is continuous in the case of streak and it is discontinous in mottle
streak. Early infection leads to reduction of tillers and grain formation.

Favourable Conditions
The disease is high in April-May sown crops due to high population of vectors viz.,
Cicadulina bipunctella and C. cinai.
Management
Rogue out the infected plants. Spray Monocrotophos or Methyl dementon 500 ml/ha.
Spray first on noticing symptoms and repeat twice at 20 days interval.
Minor diseases
Downy mildew Sclerospora macrospora Green ear symptom. Proliferation of spikeles.
Smut Melanopsicum eleusinis Grains are converted into enlarged greenish to dirty black sori
Bacterial disease Xanthomonas eleusineae Minute red leaf spots. Stunted
growth and ears are not formed.
Phanerogamic parasite Striga asiatica
TENAI (Setaria italica)

1. Blast -Pyricularia setariae

Symptoms
The spots are seen on the leaf blade. They are circular with light centre and are
surrounded by a dark brown margin. The spots are small and scattered. When the disease
appears in severe form the leaves wither and dry up. Neck infection is very rare.
Pathogen
The conidiophores emerge through epidermal cells or through stomata. Several
conidia are formed one after another from each conidiophore. They are sub-hyaline, three
celled and obpyriform. Thickwalled, olivebrown and globose chlamydospores are also
developed at the tips of the germ tube.
Favourable Conditions
The optimum temperature is 30OC. High relative humidity (90 per cent), low night
temperature and cloudy weather.
Mode of Spread and Survival
The primary source of infection is through seed-borne conidia and to some extent
soil-borne. The secondary spread is through air-borne conidia which are produced on ragi,
bajra, wheat and Dectylotacnium aegyptium.
Management
Treat the seeds with Captan or Thiram 4 g Carbendazim 2 g/kg. Spray the crop with
Iprobenphos (IBP) or Edifenphos 500 ml/ha.
 2. Leaf spot or Leaf blotch
Helminthosporium setariae
(Sexual stage : Cochliobolus setariae)
Symptoms
Leaf spots are brown in colour and small. Some times lesions also appear as
blotches and the rotting of the secondary roots may also occur.
Pathogen
The conidiophores are simple, erect, cylindrical, brown, slightly swollon at the base
and geniculate at the apex. Conidia are ellipsoid, straight or slightly curved and pale to
moderately dark brown.
Favourable Conditions
Optimum temperature for growth and sporulation is 30OC
Mode of Spread and Survival

Externally seed borne.

Management

Treat the seeds with Captan or Thiram at 4 g/kg.

3. Smut
Ustilago crameri
Symptoms

The fungus grows systemically inside the host and express the symptom at the time
of flowering. The sori are seen in the flowers and the basal parts of the palea. The fungus
affects most of the grains in an ear but sometimes the terminal portion of ear may escape.
The sori are pale grey in colour and measures 2 to 4 mm in diameter. When the crop
matures the sori rupture and liberate dark powdery mass of spores.
Pathogen
The chlamydospores are dark brown in mass but lighter singly, irregular or angular in
shape and smooth walled. The chlamydospores are inter calary in hyphal strands.
Mode of Spread and Survival
The fungus is externally seed-borne and secondary spread by air-borne
chlamydospores.
Management
Treat the seeds with Captan or Thiram at 4 g/kg.
4. Rust
Uromyces setariae italicae
Symptoms
Numerous minute, brown uredosori appear on both surface of the leaf and are
covered by the epidermis for very long time. The pustules are small, oblong and cinnamon
brown in colour. The telia are smaller but covered by epidermis for quite a longer period and
are grayish black in colour. Severe incidence of disease reduces the yield.
Pathogen
The uredospores are round, spiny, yellowish brown with 3 or 4 germpores. The
teliospores are one celled, smooth, oblong globose and thick walled especially at the apex.
Mode of Spread and Survival
The fungus can also attack other species of Setaria viz., S. glauca, S. viridis and S.
verticillata. The air-borne uredospores cause primary infection.
Management
No control measure is generally taken against this disease.
5. Downy mildew or Green ear
Sclerospora graminicola
Symptoms

Primary infection causes chlorosis of the plant and the leaves turn whitish. The
terminal spindle fails to unroll, becomes chlorotic and later turn brown and get shredded.
Whitish bloom of sporangiophores and sporangia develop on the surface of the affected
leaves under humid conditions. The affected plants rarely comes to flowering. If the infection
is mild, the plants may develop ears but the floral parts are proliferated into green leafy
structures called green ear.
Pathogen
The sporangiophores are quite and branch heavily. The sporangia are hyaline,
broadly fusiform or ovate in shape. Oospores are also produced in the infected host tissue.
They are spherical with smooth well and dark brown in colour.
Mode of Spread and Survival
Primary infection is mainly from soil-borne oospores or from oospores on the grains.
The oospores are able to survive upto 8-10 years.
Favourable Conditions
Rainy weather, low temperature (15-25OC), high humidity (90 per cent) and high soil
moisture.
Management
Treat the seeds with Captan or Thiram at 4 g/kg.
 KUTHIRAIVALI (Echinochloa frumentacea)

1. Smut
Ustilago crus-galli
Symptoms

The infected ear heads are completely destroyed. The fungus also produces gall-like
swellings on the stem, the nodes of young shoots and in the axils of older leaves. The gall-
like swellings are covered by a hairy tough membrane of host tissue.

Pathogen

The smut spores are mikado-brown, spherical and echinulated.

Mode of Spread

Externally seed-borne.

Management

Treat the seeds with Captan or Thiram at 4 g/kg.

VARUGU (Paspalum scrobiculatum)

1. Head smut Sorosporium paspali-thunbergii

Symptoms
The entire panicle is transformed into a long sorus and cream coloured thin
membrane covers the sorus. In some cases it is enclosed in the flag leaf and may not
emerge fully. The membrane bursts open and exposes the black mass of spores.
Pathogen
Spores are globose to angular and dark brown with a thick smooth epispore.
Mode of Spread and Survival
Mainly seed-borne. The spores stick to surface of the grains and infect the next crop.
Management
Treat the seeds with Thiram or Captan at 4 g/kg.
PANIVARAGU (Panicum miliare)

1. Rust
Uromyces linearis
Symptoms
Numerous, narrow, minute, brown pustules arranged in linear rows appear on the
upper surface of the leaves.
Pathogen
Uredia are erumpent and brown in colour. The fungus also attacks the other hosts
like Panicum ripens and P. antidotale. The fungus is spread through air-borne uredospores.
Leaf spot
Helminthosporium oryzaeThe fungus which attacks the rice also attacks this crop and
produce brown rectangular spots.
 SAMAI (Panicum miliaceum)
1. Smut Sphacelotheca destruens
Symptoms
The entire inflorescence is converted into a sorus containing spores
(Chlamydospores) and fibrous vascular bundles. The sorus is covered by a white or grey
membrane. Abnormal development of hairs is evident on the leaf sheaths of infected plants.
The smut spores are round or angular and yellowish brown.
Mode of Spread and Survival
Externally seed-borne and survive for more than 8 years.
 DISEASES OF PIGEON PEA/REDGRAM
(Cajanus cajan)

1. Wilt
Fusarium oxysporum f. sp. udum
Symptoms
The diseases may appear from early stages of plant growth (4-6 week old plant) upto
flowering and podding. The disease appears as gradual withering and drying of plants, as if
they were suffering from drought. In the beginning, yellowing of leaves and blackening of
portion of stem appear, starting from collar to branches which gradually result in drooping
and premature drying of leaves, stems, branches and finally death of plant. Vascular tissues
exhibit brown discolouration. Often only one side of the stem and root system is affected
resulting in partial wilting.
Pathogen
The fungus produces hyaline, septate mycelium. Microconidia are hyaline, small,
elliptical or curved, single celled or two celled. Macroconidia are also hyaline, thin walled,
linear, curved or fusoid, pointed at both ends with 3-4 septa. The fungus also poduce thick
walled, spherical or oval, terminal or intercalary chlamydospores singly or in chains of 2 to 3.
Favourable Conditions
Soil temperature of 17-25OC. Continuous cultivation of redgram in the same field.
Mode of Spread and Survival
The fungus survives in the infected stubbles in the field. The primary spread is by
soil-borne chlamydospores and also by seed contaminant. Chlamydospores remain viable in
soil for 8-20 years. The secondary spread in the field is through irrigation water and
implements.

Management
Treat the seeds with Trichoderma viride at 4 g/kg. Avoid successive cultivation of
redgram in the same field. Follow long crop rotation with tobacco. Adopt mixed cropping of

sorghum in the field. Grow resistant lines like ICP 8862, ICPL 88046, ICPL 227, BWR 254,
DPPA 85-14, DPPA 85-15 and GPS 52.
2. Dry root rot
Macrophomina phaseolina
(Sclerotial stage : Rhizoctonia bataticola)
Symptoms
The disease occurs both in young seedlings and grown up plants. Infected seedlings
can show reddish brown discoloration at collar region. The lower leaves show yellowing,
drooping and premature defoliation. The discolored area later turns to black and sudden
death of the plants occur in patches. The bark near the collar region shows shredding. The
plant can be easily pulled off leaving dark rotten root in the ground. Minute dark sclerotia are
seen in the shredded bark and root tissues. The fungus also produce dark discoloration of
sub-epidermal tissue in lower part stem. Large number of brown dots seen on the stem
portion represent the pycnidial stage of the fungus.
Pathogen
The fungus produces dark, brown, filamentous hyphae and constrictions are seen in
hyphal branches at the junction with main hyphae. Sclerotia are jet black, smooth, hard,
minute, globose and 110-130u in diameter. The pycnidia are dark brown and ostiolated.
Conidiophores (phialides) are hyaline, short, obpyriform to cylindrical, develop from the inner
walls of the pycnidium. The conidia (Pycnidiospores) are hyaline, single celled and ellipsoid
to ovoid.
Favourable Conditions
Prolonged drought followed by irrigation. High temperature of 28-35OC.

Mode of Spread and Survival

The primary spread of the disease is by seed borne sclerotia. Secondary spread is
by soil-borne sclerotia and air-borne conidia. The pathogen survives as sclerotia in the soil
as facultative parasite and in dead host debris.

Management

Treat the seeds with Carbendazim or Thiram at 4 g/kg or pellet the seeds with
Trichoderma viride at 4 g/kg. Apply heavy doses of farm yard manure or green leaf manure
like Gliricidia maculata at 10 t/ha or Apply Neemcake at 250 kg/ha. Grow resistant varieties
like Co4.

3. Powdery mildew Leveillula taurica

Symptoms
White powdery growth of the fungus can be seen on the lower surface of leaves. The
corresponding areas in upper surface show pale yellow discoloration. The white powdery
mass consists conidiophores and conidia of the fungus. In severe cases, the white growth
can be seen on the upper surface also. The severe infection of the fungus leads to
premature shedding of leaves and plant remains barren.
Pathogen
The fungus is intercellular and absorbs nutrition through haustoria. The
conidiophores, which arise through stomata, are hyaline, long, non septate, slender and
rarely branched and bear single conidium at the tip. The conidia are hyaline, single celled
and elliptical or clavate. The fungus also produce black, globose cleistothecia with simple
myceloid appendages. They contain 9-20 cylindrical asci. Each ascus contains 3-5
ascospores which are also hyaline and unicellular.
Favourable Conditions
Dry humid weather following rain fall.
Mode of Spread and Survival
The fungus survives in the soil as cleistothecia and ascospores from asci infect the
first lower most leaves near the soil level. Secondary spread is by air-borne conidia.
Management

Spray Carbendazim 500g or Wettable sulphur 1.5 kg/ha at the initiation of the
disease and repeat after 15 days.
4. Stem blight - Phytophthora drechsleri f. sp. cajani
Symptoms
Initially purple to dark brown necrotic lesions girdle the basal portion of the stem and
later may occur an aerial parts of the seedlings. Initially lesions are small and smooth, later
enlarging and slightly depressed. Infected tissue become soft and whole plant wilts. In the
adult plants, infection is mostly confined to basal portions of the stem. The infected bark
become brown and the tissue softening causing the plant to collapse. The infected branches
may break off in wind. The upper portions of the infected twigs eventually wilt and dry. In
leaf, localized yellowing starts from the tip and margin and gradually extends towards the
mid-rib. The centre of the spots later turn brown and hard. The spots increase in size and
cover a major portion of the lamina, leading to drying.
Pathogen
Fungus produces hyaline, coenocytic mycelium. The sporangiophores are hypha-like
with a swelling on the tip bearing hyaline, ovate or pyriform, non-papillate sporangia. Each

sporangium produces 8-20 zoospores. Oospores are globose, light brown, smooth and thick
walled.
Favourable Conditions
Soils with poor drainage, low lying areas, heavy rain during the months of July-
September and high temperature (28-30OC).
Mode of Spread and Survival
The fungus survives in the soil and plant debris in the form of oospores. Primary
infection is from oospores and secondary spread by zoospores from sporangia. Rain splash
and irrigation water help for the movement of zoospores.
Management
Treat the seeds with Metalaxyl at 7 g/kg. Spray Metalaxyl at 500 g/ha. Adjust the
sowing time so that crop growth should not coincides with heavy rainfall.
5. Leaf spot Cercospora indica
Symptoms
Small, light brown coloured spots appear on leaves. The spots later become dark
brown and the infected portions drop off leaving shot hole symptoms. When several spots
join together, irregular necrotic blotches develop and premature defoliation occurs. In severe
cases, black lesions develop on petioles and stem.
Pathogen
The fungus produces large number of whip-like, hyaline, 7-9 septate conidia in
groups on the conidiophores which are light to dark brown in colour.
Mode of Spread and Survival
 The fungus survives in the infected plant tissues. The disease is spread by air-borne
conidia.
Management
Remove the infected plant debris and destroy. Spray Mancozeb 1 kg or Carbendazim
500 g/ha soon after the appearance of symptom and repeat after a fortnight.
6. Sterility Mosaic Virus
Symptoms
The disease attack can be seen in all stages of crop growth. Leaves show typical
mosaic mottling symptoms. Yellow patches intermingle with green colour of leaf. The green
portions exhibit puckering symptom. In severe cases, leaves become smaller and cluster
near tip because of shortened internodes and stimulation of auxillary buds. The plants are
generally stunted and do not produce pod. Plants infected at early stages (upto 45 days) of
crop growth show near complete sterility and yield loss upto 95 per cent. As plants become
older (after 45 days), their susceptibility to the disease decreases and such plants show

partial sterility. If pods develop, the seeds may be small, shrivelled and immature. Because
the infected plants show sterility and the leaves show the ‘mosaic’ symptom, the name of the
disease is sterility mosaic.
Mode of Spread and Survival
The disease is transmitted by an Eriophyid mite Aceria cajani. The self-sown
redgram plants and perennial types of redgram serve as sources of infection.
Management
Rogue out infected plants upto 40 days after sowing. Spray Monocrotophos at 500
ml/ha soon after appearance of the disease and if necessary, repeat after 15 days. Grow
resistant genotypes/cultivars like ICP 7035, VR3, Purple 1, DA11, DA32, ICP 6997, Bahar,
BSMR 235, ICP 7198, PR 5149, ICP 8861 and Bhavanisagar 1.
7. Yellow Mosaic Virus
Symptoms
Small yellow patches or spots appear on young leaves. The area of yellow
discoloration slowly increases and newly formed leaves may completely turn yellow. Infected
plants are stunted and mature later and produce very few flowers and pods. The pods are
small and distorted. The early infection of virus leads to heavy yield loss.
Mode of Spread and Survival
The virus survives in weed hosts and perennial redgram plants. The disease is
transmitted by white flies (Bemisia tabaci).
Management
Rogue out the diseased plants upto 45 days after sowing. Remove weed hosts
periodically. Spray Monocrotophos or Methyldemeton at 500 ml/ha immediately on noticing
the disease and repeat after 15 days, if necessary.
---------------------------------------------------------------------------------
 DISEASES OF BLACK GRAM AND GREEN GRAM
1. Powdery mildew
Erysiphe polygoni
Symptoms
Small, irregular powdery spots appear on the upper surface of the leaves, sometimes
on both the surfaces. The disease becomes severe during flowering and pod development
stage. The white powdery spots completely cover the leaves, petioles, stem and even the
pods. The plant assumes greyish white appearance, leaves turn yellow and finally shed.
Often pods are malformed and small with few ill-filled seeds.
Pathogen
The fungus is ectophytic, spreading on the surface of the leaf, sending haustoria into
the epidermal cells. Conidiophores arise vertically from the leaf surface, bearing conidia in
short chains. Conidia are hyaline, thinwalled, elliptical or barrel shaped or cylindrical and
single celled. Later in the season, cleistothecia appear as minute, black, globose structures
with myceloid appendages. Each cleistothecium contains 4-8 asci and each ascus contains
3-8 ascospores which are elliptical, hyaline and single celled.
Favourable Conditions
Warm humid weather. The disease is severe generally during late kharif and rabi
seasons.
Mode of Spread and Survival
The fungus is an obligate parasite and survives as cleistothecia in the infected plant
debris. Primary infection is usually from ascospores from perennating cleistothecia. The
secondary spread is carried out by the air-borne conidia. Rain splash also helps in the
spread of the disease.
Management
Remove and destory infected plant debris. Spray Carbendazim 500g or Wettable
sulphur 1.5 kg or Tridemorph 500 ml/ha at the initiation of disease and repeat 15 days later.
Grow resistant varieties like LBG17, PDU10, ICI12/2 and PLU 322.
2. Anthracnose
Colletotrichum lindemuthianum
(Sexual stage : Glomerella lindemuthianum)
Symptoms
The symptom can be odserved in all aerial parts of the plants and at any stage of
crop growth. The fungus produces dark brown to black sunken lesions on the hypocotyl area
and cause death of the seedlings. Small angular brown lesions appear on leaves, mostly
adjacent to veins, which later become greyish white centre with dark brown or reddish
margin. The lesions may be seen on the petioles and stem. The prominent symptom is seen
on the pods. Minute water soaked lesion appears on the pods initially and becomes brown
and enlarges to form circular, depressed spot with dark centre with bright red or yellow
margin. Several spots join to cause necrotic areas with black dots (Acervuli). The infected
pods have discolored seeds.
Pathogen
The fungus mycelium is septate, hyaline and branched. Conidia are produced in
acervuli, arise from the stroma beneath the epidermis and later rupture to become erumpent.
A few dark coloured, septate setae are seen in the acervulus. The conidiophores are hyaline
and short and bear oblong or cylindrical, hyaline, thinwalled, single celled conidia with oil
globules. The perfect stage of the fungus produces perithecia with limited number of asci,
which contain typically 8 ascospores which are one or two celled with a central oil globule.
Favourable Conditions
High relative humidity (Above 90 per cent), low temperature (15-20OC) and cool
rainy days.
Mode of Spread and Survival
The fungus is seed-borne and cause primary infection. It also lives in the infected
plant tissues in soil. The secondary spread by air borne conidia produced on infected plant
parts. Rain splash also helps in dissemination.
Management
Remove and destroy infected plant debris in soil. Treat the seeds with Carbendazim
at 2 g/kg. Spray Carbendazim 500g or Mancozeb 1 kg/ha soon after the appearance of
disease and repeat after 15 days.
3. Leaf spot
Cercospora canescens
Symptoms
Small, circular spots develop on the leaves with grey centre and brown margin. The
several spots coalesce to form brown irregular lesions. In severe cases defoliation occurs.
The brown lesions may be seen on petioles and stem in severe cases. Powdery growth of
the fungus may be seen on the centre of the spots.
Pathogen
The fungus produces clusters of dark brown septate conidiophores. The conidia are
linear, hyaline, thin walled and 5-6 septate.
Favourable Conditions
Humid weather and dense plant population.
Mode of Spread and Survival
The fungus survives on diseased plant debris and on seeds. The secondary spread
by air-borne conidia.
Management
Remove and burn infected plant debris. Spray Mancozeb at 1 kg/ha or Carbendazim
250 g/ha.
4. Rust
Uromyces phaseoli typica
(Syn: U.appendiculatus)
Symptoms

The disease is mostly seen on leaves, rarely on petioles, stem and pods. The fungus
produces small, round, reddish brown uredosori mostly on lower surface. They may appear
in groups and several sori coalesce to cover a large area of the lamina. In the late season,
teliosori appear on the leaves which are linear and dark brown in colour. Intense pustule
formation causes drying and shedding of leaves.
Pathogen
It is an autoecious, long cycle rust and all the spore stages occur on the same host.
The uredospores are unicellular, globose or ellipsoid, yellowish brown with echinulations.
The teliospores are globose or elliptical, unicellular, pedicellate, chestnut brown in colour
with warty papillae at the top. Yellow coloured pycnia appear on the upper surface of leaves.
Orange coloured cupulate aecia develop later on the lower surface of leaves. The
aeciospores are unicellular and elliptical.
Favourable Conditions
Cloudy humid weather, temperature of 21-26OC and nights with heavy dews.
Mode of Spread and Survival
The pathogen survives in the soil as teliospores and as uredospores in crop debris.
Primary infection is by the sporidia developed from teliospores. Secondary spread is by
wind-borne uredospores. The fungus also survives on other legume hosts.
Management
Remove the infected plant debris and destory. Spray Mancozeb 1 kg or Carbendazim
500 g or Wettable sulfur 1 kg/ha, immediately on the set of disease and repeat after 15 days.
5. Dry root rot
Rhizoctonia bataticola
(Pycnidial stage : Macrophomina phaseolina)
Symptoms
The disease symptom starts initially with yellowing and drooping of the leaves. The
leaves later fall off and the plant dies with in week. Dark brown lesions are seen on the stem
at ground level and bark shows shredding symptom. The affected plants can be easily pulled
out leaving dried, rotten root portions in the ground. The rotten tissues of stem and root
contain a large number of black minute sclerotia.
Pathogen
The fungus produces dark brown, septate mycelium with constrictions at hyphal
branches. Minute, dark, round sclerotia of size 110-130u are produced in abundance. The
fungus also produces dark brown, globose ostiolated pycnidia on the host tissues. They
pycnidiospores (conidia) are thin walled, hyaline, single celled, elliptical and measure 10-
42X6-10u.
Favourable Conditions
Day temperature of 30OC and above and prolonged dry season followed by
irrigation.
Mode of Spread and Survival
The fungus survives in the infected debris and also as facultative parasite in soil. The
primary spread is through seed-borne and soil-borne sclerotia. The secondary spread is
through seed-borne and soil-borne sclerotia. The secondary spreads is through
pycnidiospores which are air-borne.
Management
Treat the seeds with Carbendazim or Thiram at 4 g/kg or pellet the seeds with
Trichoderma viride at 4 g/kg or Pseudonomas fluorescens @ 10g/kg of seed. Apply farm
yard manure or green leaf manure (Gliricidia maculate) at 10 t/ha or neemcake at 250 kg/ha.
6. Yellow mosaic Virus
Symptoms
Initially small yellow patches or spots appear on green lamina. The young leaves are
the first to show the symptoms. The yellow discoloration slowly increases and newly formed
leaves may completely turn yellow. The infected plants normally mature later and bear a
very few flowers and pods. The pods are small and distorted. The early infection causes
death of the plant before seed set.
Favourable Conditions
Summer sown crops are highly susceptible. The presence of weed hosts viz., Croton
sparsiflorus, Acalypha indica, Eclipta alba and Cosmos pinnatus and legume hosts.
Mode of Spread and Survival
The virus survives in the weed hosts and other legume crops. The disease spreads
through wind-borne viruliferous white fly, Bemisia tabaci.
Management
Rogue out the diseased plants upto 40 days after sowing. Remove the weed hosts
peiodically. Increase the seed rate (25 kg/ha). Grow resistant black gram variety like VBN-1,
PDU 10, IC12/2 and PLU 322. Cultivate the crop during rabi season. Follow mixed cropping
by growing two rows of maize (60 x 30 cm) or sorghum (45 x 15 cm) or cumbu (45 x 15 cm)
for every 15 rows of black gram or green gram.
7. Leaf crinkle Virus
Symptoms

The symptom appears initially in young leaves. The enlargement of 4th or 5th leaf is
seen four or five weeks after sowing. Later crinkling and curling of the tips of leaflets are
seen. The petioles as well as internodes are shortened. The infected plant gives a stunted
and bushy appearance. Flowering is delayed, infloresence, if formed, are malformed with
small size flower buds and fail to open. The age of the plant is prolonged with dark green
leaves till harvest.
Favourable Conditions
The presence of weed hosts like Aristolochia bracteata and Digera arvensis. Closs
planting. Kharif season crop is highly susceptible. Continuous cropping of other legumes
which also harbour the virus.
Mode of Spread and Survival
The virus is seed-borne and primary infection occurs through infected seeds. White
fly, Bemisia tabaci, is the vector, helps in the secondary spread. The virus is also
transmissible.
Management
Use increased seed rate (25 kg/ha). Rogue out the diseased plants at weekly interval
upto 45 days after sowing. Cultivate seed crop during rabi season. Remove weed hosts
periodically. Spray Monocrotophos or Methyl demeton on 30 and 40 days after sowing at
500 ml/ha.
8. Leaf curl
(Tomato Spotted Wilt Virus)
Symptoms
The infection starts as chlorosis of lateral veins near the leaf margins and margins
slowly curl downwards. The infected leaves are brittle and sometimes show vein necrosis on
the under surface of the leaves, extends to the petiole. Plants affected in the early stages of
growth develop top necrosis and die. The plant may produce a few small and malformed
pods.
Favourable Conditions
Rainy days during kharif season show high incidence of disease. The presence of
the weed hosts viz., Acanthospermum hispidum,Ageratum conyzoides, Amaranthus viridis,
Calotropis gigantea, Lagasca mollis, Trianthema portulacastrum, Cassia tora, Cleome
gynandra, Solanum nigrum and Datura metal and other legume hosts.
Mode of Spread and Survival
The virus is transmitted by thrips viz., Frankliniella schultzii, Thrips tabaci and
Scirtothrips dorsalis. The virus survives in weed hosts, tomato, petunia and Chilli.
Management
Rogue out infected plants upto 30 days after sowing. Remove the weed hosts which
harbour virus and thrips. Spray Monocrotophos or Methyl demeton at 500 ml/ha on 30 and
45 days after sowing.
 DISEASES OF COWPEA (Vigna unguiculata)

1. Wilt
Fusarium oxysporum f. sp. tracheiphilum
Symptoms
Symptoms do not appear until the plants are about six weeks old. Initially a few
plants are noticed with pale green flaccid leaves which soon turn yellow. Growth is stunted,
Chlorosis, drooping, premature shedding or withering of leaves with veinal necrosis often
occurs and finally plant dies within 5 days. Brownish, purple discoloration of the cortical area
is seen, often extends throughout the plant.
The fungus produces falcate shaped macroconidia which are 4-5 septate, thin walled and
hyaline. The microconidia are single celled. hyaline and oblong or oval. The chlamydospores
are also produced in abundance.
Favourable Conditions
Temperature of 20-25OC and moist humid weather.
Mode of Spread and Survival
The fungus survives in the infected stubbles in the field. The primary spread is
through chlamy dospores and seed contamination. The secondary spread is through conidia
by irrigation water.
Management
Treat the seeds with Carbendazim or Thiram at 2 g/kg or treat the seeds with
Trichoderma viride at 4 g/kg. Spot drench with Carbendazim at 0.5 g/litre.
2. Bacterial leaf spot
Xanthomonas vignicola
Symptoms
The disease attacks at any stage of plant growth. The seedling infection starts as red
lesion at cotyledon leads to withering. In adult plants yellow circular spots appear on leaves,
enlarge and become angular and encircled by a yellow halo. The infection can be seen on

the petiole, stem and pods as brown linear lesions. The affected twigs show twig blight and
infected pods contain shrivelled seeds.
Favourable Conditions Heavy rainfall, high relative humidity (above 80 per cent) and
temperature of 20-25OC.
Mode of Spread and Survival
The bacterium is seed-borne and cause primary infection in the field. The wind, rain
splash and insects help in the secondary spread.
Management
Collect the seeds from healthy plants and use disease free seeds.
3. Aphid-borne mosaic Virus
Symptoms
The affected plants are stunted and the leaves show variable amounts of dark green
vein banding, leaf distortion and blistering. The affected leaves are leathery. The infected
plants produce a few pods which are small and distorted.
Favourable Conditions
The presence of weed hosts and other legume hosts.
Mode of Spread and Survival
The virus is transmitted aphid vectors viz., Aphis craccivora, A. fabae, A. gossypii,
Macrosphum euphorbiae and Myzus persicae. The virus survives in weed hosts and other
legume crops.
Management
Remove the infected plants upto 30 days after sowing. Rogue out the weed hosts
periodically. Grow resistant varieties like Co.6. Spray thrice with Monocrotophos or Methyl
demeton at 500 ml/ha at 15 days intervals.
-

DISEASES OF SOYBEAN
SOYA BEAN (Glycine max)
Dry root rot Macrophomina phaseolina Refer Black gram
Yellow mosaic Virus Refer Black gram
Wilt Fusarium oxysporum Refer Cowpea
Leaf spot Cercospora sojana Well defined spots often bound by veins
 DISEASES OF GROUNDNUT
(Arachis hypogaea)
1. Tikka leaf spots
Early leaf spot : Cercopora arachidicola
(Sexual Stage) : Mycosphaerella arachidis)
Late leaf spot : Phaeoisariopsis personata
Syn : cercospora personata
(Sexual stage) : Mycosphaerella berkeleyii)
Symptoms

The disease occurs on all above ground parts of the plant, more severely on the
leaves. The leaf symptoms produced by the two pathogens can be easily distinguished by
the following characters.Both the fungi produce lesions also on petiole, stem and pegs. The
lesions caused by both species coalesce as infection develops and severely spotted leaves
shed prematurely. The quality and yield of nuts are drastically reduced in severe infections.

Pathogen C. arachidicola (Sexual stage : M. arachidis)

The fungus is intercellular and do not produce haustoria and become intracellular
when host cells die. The fungus produces abundant sporulation on the upper surface of the
leaves. Conidiophores are olivaceous brown or yellowish brown in colour, short, 1 or 2
septate, unbranched and geniculate and arise in clusters. Conidia are sub hyaline or pale
yellow, obclavate, often curved 3-12 septate, 35-110 x 2.5 - 5.4 um in size with rounded to
distinctly truncate base and sub-acute tip. The perfect stage of the fungus produces
perithecia as ascostromata. They are globose with papillate ostiole. Asci are cylindrical to
clavate and contain 8 ascospores. Ascospores are hyaline, slightly curved and two celled,
apical cell larger than the lower cell.
P. personata (C. personata) (Sexual stage : M. berkeleyii)
The fungus produces internal and intercellular mycelium with the production of
haustoria. The conidiphores are long, continuous, 1-2 septate, geniculate, arise in clusters
and olive brown in colour. The conidia are cylindrical or obclavate, short, measure 18-60 x 6-
10um, hyaline to olive brown, usually straight or curved slightly with 1-9 septa, not
constricted but mostly 3-4 septate. The fungus in its perfect stage produces perithecia as
ascostromata which are globose or brodly ovate with papillate ostiole. Asci are cylindrical to
ovate, contain 8 ascospores. Ascospores are 2 celled and constricted at septum and
hyaline.
Favourable Conditions
 Prolonged high relative humidity for 3 days, low temperature (20OC) with dew on leaf
surface, heavy doses of nitrogen and phosporus fertilizers and deficiency of magesium in
soil.
Mode of Spread and Survival
The fungi survives for a long period in the infected plant debris as conidia, dormant
mycelium and perithecia in soil. The volunteer groundnut plants also harbour the pathogens.
The fungi also survives on contaminated pods and seeds. The primary infection is by
ascospores or conidia liberated from infected plant debris. The secondary spread is by wind
blown conidia. Rain splash also helps in the spread of conidia.
Management
Remove and destory the infected plant debris. Eradicate the volunteer groundnut
plants. Keep weeds under control. Treat the seeds with Carbendazim or Thiram at 2g/kg.
Spray Carbendazim 250g or Mancozeb 1 kg or Chlorothalonil 1 kg/ha and if necessary,
repeat after 15 days. Grow moderately resistant varieties like ALR.1.
2. Rust
Puccinia arachidis
Symptoms
The disease attacks all aerial parts of the plant. The disease is usually found when
the plants are about 6 weeks old. Small brown to chestnut dusty pustules (uredosori) appear
on the lower surface of leaves. The epidermis rupture and exposes a powdery mass of
uredospores. Corresponding to the sori, small, necrotic, brown spots appear on the upper
surface of leaves. The rust pustules may be seen on petioles and stem. Late in the season,
brown teliosori, as dark pustules, appear among the necrotic patches. In severe infection
lower leaves dry and drop prematurely. The severe infection leads to production of small and
shriveled seeds.
Pathogen
The fungus produces both uredial and telial stages. Uredial stages are produced
abundant in groundnut and production of telia is limited. Uredospores are pedicellate,
unicellular, yellow, oval or round and echinulated with 2 or 3 germpores. Teliospores are
dark brown with two cells. Pycnial and aecial stages have not been recorded and there is no
information available about the role of alternate host.
Favourable Conditions
High relative humidity (above 85 per cent), heavy rainfall and low temperature (20-
25OC).
Mode of Spread and Survival
The pathogen survives as uredospores on volunter groundnut plants. The fungus
also survives in infected plant debris in soil. The spread is mainly through wind-borne
inoculum of uredospores. The uredospores also spread as contamination of seeds and
pods. Rainsplash and implements also help in dissemination. The fungus also survives on
the collateral hosts like Arachis marginata, A. nambyquarae and A. prostrate.
Management
Avoid monoculturing of groundnut. Remove volunteer groundnut plants and reservoir
hosts. Spray Mancozeb 1 kg or Wettable sulphur 2.5 kg or Tridemorph 500 ml or
Chlorothalonil 1 kg/ha. Grow moderately resistant varieties like ALR.1
3. Collar rot or seedling blight or crown rot
Aspergillus niger and A. pulverulentum
Symptoms
The fungus is both seed-borne and soil-borne and so the infection can be seen at
any stage from sowing onwards. The disease usually appears in three phases.
i. Pre-emergence rot : Seeds are attacked by soil-borne conidia and rotten of seeds prevents
the seeds to germinate. The seed are covered with black masses of spores and internal
tissues of seed become soft and watery.
ii. Post-emergence rot : The pathogen attacks the emerging young seedling and cause
circular brown spots on the cotyledons. The symptom spreads later to the hypocotyl and
stem. Brown discoloured spots appear on collar region. The affected portion become soft
and rotten, resulting in the collapse of the seedling. The collar region is covered by profuse
growth of fungus and conidia and affected stem also show shredding symptom.
iii. Crown rot : The infection when occurs in adult plants show crown rot symptoms. Large
lesions develop on the stem below the soil and spread upwards along the branches causing
drooping of leaves and wilting of plant.
Pathogen
The mycelium of the fungus is hyaline to sub-hyaline. Conidiophores arise directly
from the substrate and are septate, thick walled, hyaline or olive brown in colour. The
vesicles are mostly globose and have two rows of hyaline phialides viz., primary and
secondary phialides. The conidial head are dark brown to black. The conidia are globose,
dark brown in colour and produce in long chains.
Favourable Conditions
Deep sowing of seeds, high soil temperature (30-35OC) and low soil moisture.
Mode of Spread and Survival
The pathogen survive in plant debris in the soil, not necessarily from a groundnut
crop. Soil-borne conidia cause disease carry over from season to season. The other primary
source is the contaminated seeds. The fungi are carried on the seed surface or under the
testa.
Management
 Select good quality seeds. Treat the seeds with Carbendazim 2 g or Thiram 4g/kg.
Avoid deep sowing of seeds. Destroy the crop debris by burning.
4. Root rot
Macrophomina phaseolina
Symptoms
In the early stages of infection, reddish brown lesion appears on the stem just above
the soil level. The leaves and branches show drooping, leading to death of the whole plant.
The decaying stems are covered by whitish mycelial growth. The death of the plant results in
shredding of bark. The rotten tissues contain large number of black or dark brown, thick
walled sclerotia. When infection spreads to underground roots, the sclerotia are formed
externally as well as internally in the rotten tissue. Pod infection leads to blackening of the
shells and sclerotia can be seen inside the shells.
Pathogen
The fungus produces hyaline to dull brown mycelium. The sclerotia are thick walled
and dark brown in colour.
Favourable Conditions
Prolonged rainy season at seedling stage and low lying areas.
Mode of Spread and Survival
The fungus remains dormant as sclerotia for a long period in the soil and in infected
plant debris. The primary infection is through soil-borne and seed-borne sclerotia. The
secondary spread of sclerotia is aided by irrigation water, human agency, implements, cattle
etc.
Management
Treat the seeds with Thiram 4g or Carbendazim 2g/kg or treat the seeds with
Trichoderma viride at 4g/kg. Spot drench with Carbendazim at 0.5 g/lit.
5. Rossetts VirusSymptoms
The affected plants are characterized by the appearance of dense clump or dwarf
shoots with tuft of small leaves forming in a rossette fashion. The plant exhibits chlorosis and
mosaic mottling. The infected plants remain stunted and produce flowers, but only a few of
the pegs may develop further to nuts but none bear seeds.
Mode of Spread and Survival
The virus can survive on the volunteer plants of groundnut and other hosts. The virus
is transmitted by Aphis craccivora in a persistent manner.
Management
Use heavy seed rate and rogue out periodically the infected plants. Spray
Monocrotophos or Methyl demeton at 500 ml/ha.
 6. Peanut spotted wilt or bud necrosis or groundnut ring mosaic
Tomato spotted wilt virus (TSWV)
Symptoms

First symptoms are visible 2-6 weeks after infection as ring spots on leaves. The
newly emerging leaves are small, rounded or pinched inwards and rugose with varying
patterns of mottling and minute ring spots. Necrotic spots and irregularly shaped lesions
develop on leaves and petioles. Stem also exhibits necrotic streaks. As the plant matures, it
becomes generally stunted with short internodes and short auxillary shoots. Leaf lets formed
on these auxillary shoots show a wide range of symptoms including reduction in size,
distortion of the lamina, mosaic mottling and general chlorosis. In advanced conditions, the
necrosis of buds occurs. Drastic reduction in flowering is noticed and seeds produced are
abnormally small and wrinkled with the dark black lesions on the testa
Mode of Spread and Survival

The virus perpetuates in the weed hosts viz., Bidens pilosa, Erigon bonariensis,
Tagetes minuta and Trifolium subterraneum. The virus is transmitted by thrips viz., Thrips
tabaci and Frankliniella sp..

Management

Adopt spacing of 15x15 cm. Remove and destory infected plants upto 6 weeks after
sowing. Monocrotophos 500 ml/ha, 30 days after sowing either alone or in combination with
AVP (Anti-Viral Principle) extracted from sorghum or coconut leaves. Spray the crop with 10
per cent AVP at 500 lit/ha, ten and twenty days after sowing.

EXTRACTION OF 10 PER CENT AVP

Dried sorghum or coconut leaves are cut and powdered. To one kg of leaf powder, two litres
of water is added and heated to 600C for one hour. It is then filtered through muslin cloth
and diluted to 10 litres and sprayed. Five hundred litres of extract is required to cover one
hectare.
------------------------------------------------------------------------------
 DISEASES OF SESAME
(Sesamum indicum)
1. Root rot or stem rot or charcoal rot
Macrophomina phaseolina
Syn : cercospora personata
(Sclerotial stage : Rhizoctonia bataticola)
Symptoms
The disease symptom starts as yellowing of lower leaves, followed by drooping and
defoliation. The stem portion near the ground level shows dark brown lesions and bark at the
collar region shows shredding. The sudden death of plants is seen in patches. In the grown-
up plants, the stem portion near the soil level shows large number of black pycnidia. The
stem portion can be easily pulled out leaving the rotten root portion in the soil. The infection
when spreads to pods, they open prematurely and immature seeds become shrivelled and
black in colour. Minute pycnidia are also seen on the infected capsules and seeds. The
rotten root as well as stem tissues contain a large number of minute black sclerotia. The
sclerotia may also present on the infected pods and seeds.
Pathogen
The fungus produces dark brown, septate mycelium showing constrictions at the
hyphal junctions. The sclerotia are minute, dark black and 110-130um in diameter. The
pycnidia are dark brown with a prominent ostiole. The conidia are hyaline, elliptical and
single celled.
Favourable Conditions
Day temperature of 30OC and above and prolonged drought followed by copious
irrigation.
Mode of Spread and Survival
The fungus remains dormant as sclerotia in soil as well as in infected plant debris in
soil. The infected plant debris also carry pycnidia. The fungus primarily spreads through
infected seeds which carry sclerotia and pycnidia. The fungus also spreads through soil-
borne sclerotia. The secondary spread is through the conidia transmitted by wind and rain
water.
Management
Treat the seeds with Trichoderma viride at 4g/kg or Pseudomonas fluorescens 10
g/kg or treat the seeds with carbendazim of Thiram at 4g/kg. Apply farm yard manure or
green leaf manure at 10t/ha or neem cake 250 kg/ha. Spot drench with Carbendazim at 0.5
g/litre.
2. Leaf blight
Alternaria sesami
Symptoms
Initially small, circular, reddish brown spots (1-8mm) appear on leaves which enlarge
later and cover large area with concentric rings. The lower surface of the spots are greyish
brown in colour. In severe blighting defoliation occurs. Dark brown lesions can also be seen
on petioles, stem and capsules. Infection of capsules results in premature splitting with
shriveled seeds.
Pathogen
The mycelium of the fungus is dull brown and septate and produce large number of
pale grey-yellow conidiophores which are straight or curved. The conidia are light olive
coloured with transverse and longitudinal septa. There are around 3-5 septate and conidia
are borne in chain over short conidiophore.
Favourable Conditions
Low temperature (20-25OC), high relative humidity and cloudy weather.
Mode of Spread and Survival
The fungus is seed-borne and also soil-borne as it remains dormant in the infected
plant debris.
Management
Treat the seeds with Thiram or Carbendazim at 2g/kg. Spray Mancozeb at 1kg/ha.
3. Leaf spot
Cercospora sesami
Symptoms
The disease first appears on the leaves as minute water-soaked lesions, which
enlarge to form round to irregular spots of 5-15 mm diameter on both the leaf surface. The
spots coalesce to form irregular patches of varying size leading to premature defoliation. The
infection is also seen on stem and petiole forming spots of varying lengths. Dark linear spots
also occur on pods causing drying shedding.
Pathogen
The hypha of the fungus is irregularly septate, light brown and thick walled.
Conidiophores are produced in cluster and are 1-3 septate, hyaline at the tip and light brown
coloured at base. Conidia are elongated, 7-10 septate, hyaline to light yellow, broad at the
base and tapering towards the apex.
Mode of Spread and Survival
The fungus is externally and internally seed-borne. The fungus also survives in plant
debris. Primary infection may be from the seed and infected debris. The secondary spread is
through wind-borne conidia.
Management
Treat the seeds with carbendazin or Thiram at 2g/kg. Spray with Mancozeb at
1Kg/ha.
4. Wilt
Fusarium oxysporum f.sp. sesami
Symptoms
The disease appears as yellowing, drooping and withering of leaves. The plants
gradually wither, show wilting symptom leading to drying. The infected portions of root and
stem show long, dark black streaks of vascular necrosis.
Pathogen
The fungus produces macroconidia, microconidia and chlamydospores.
Macroconidia are falcate shape, hyaline and 5-9 celled. Microconidia are hyaline, thin
walled, unicellular and ovoid. The dark walled chlamydospores are also produced.
Mode of Spread and Survival
The fungus survives in the soil in the infected plant debris. It is also seed-borne and
primary infection occurs through infected seeds or through chlamydospores in soil. The
secondary infection may be caused by conidia disseminated by rain splash and irrigation
water.
Management
Treat the seeds with Thiram or Carbendazim at 2g/kg or pellet the seeds with
Trichoderma viride at 4g/kg. Apply heavy doses of green leaf manure or farm yard manure.
5. Stem blight
Phytophthora parasitica var. sesami
Symptoms
Black coloured lesions appear on the stem near the soil level. The disease spreads
further and affects branches and may girdle the stem, resulting in the death of the plant.
Leaves may also show water-soaked patches and spread till the leaves wither. Infection may
be seen on flowers and capsules. Infected capsules are poorly developed with shrivelled
seeds.
Pathogen
The fungus produces non-septate, hyaline mycelium. The sporangiophores are
hyaline and branched sympodially and bear sporangia. The sporangia are hyaline and
spherical with a prominent apical papilla. The oospores are smooth, spherical and thick
walled.
Favourable Conditions
Prolonged rainfall, low temperature (25OC) and high relative humidity (above 90 per
cent)
Mode of Spread and Survival
The fungus can survive in the soil as dormant mycelium and oospores. The seeds
also carry the fungus as dormant mycelium, which causes the primary infection. Secondary
spread of the disease is through wind-borne sporangia.
Management
Treat the seeds with Captan or Thiram at 2g/kg. Avoid continuous cropping of
sesamum in the same field. Remove and destroy infected plant debris.
6. Powdery mildew
Erysipha cichoracearum
(Syn : Oidium acanthosperml)
Symptoms
 Initially greyish-white powdery growth appears on the upper surface of leaves. When
several spots coalesce, the entire leaf surface may be covered with powdery coating. In
severe cases, the infection, the infection may be seen on the flowers and young capsules,
leading to premature shedding. The severaly affected leaves may be twisted and malformed.
In the advanced stages of infection, the mycelial growth changes to dark or black because of
development of cleistothecia.
Pathogen
The fungus produces hyaline, septate mycelium which are extophytic and send
haustoria into the host epidermis. Conidiophores arise from the primary mycelium and are
short and non septate bearing conidia in long chains. The conidia are ellipsoid or barrel-
shaped, single celled and hyaline. The cleistothecia are dark, globose with the hyaline or
pale brown myceloid appendages. The asci are ovate and each ascus produces 2-3
ascospores, which are thin walled, elliptical and pale brown in colour.
Favourable Conditions
Dry humid weather and low relative humidity.
Mode of Spread and Survival
The fungus is an obligate parasite and disease perennates through cleistothecia in
the infected plant debris in soil. The ascospores from the cleistothecia cause primary
infection. The secondary spread is through wind-borne conidia.
Management
Remove the infected plant debris and destroy. Spray Wettable sulphur at 2.5 kg/ha or
dust Sulphur at 25 kg/ha and repeat after 15 days.
7. Bacterial leaf spot
Xanthomonas campestris p.v. sesami
Symptoms
Initially water-soaked spots appear on the undersurface of the leaf and then on the
upper surface. They increase in size, become angular and restricted by veins and dark

brown in colour. Several spots coalesce together froming irregular brown patches and cause
drying of leaves. The reddish brown lesions may also occur on petioles and stem.
Pathogen
The bacterium is bacilliform with a monotrichous flagellum. It is gram negative and
non-spore forming.
Mode of Spread and Survival
The bacterium survives in the infected plant debris and is seed-borne. The secondary
spread is by rain water.
Management
Remove and burn infected plant debris. Spray Streptomycin sulphate or
Oxytetracycline hydrochloride at 100g/ha.
8. Bacterial leaf spot
Pseudomonas sasami
Symptoms
The disease appears as water-soaked yellow specks on the upper surface of the
leaves. They enlarge and become angular as resticted by veins and veinlets. The colour of
spot may be dark brown with shiny oozes of bacterial masses.
Pathogen
The bacterium is gram negative and rod shaped. It is an aerobic bacterium with one
or more polar flagella.
Mode of Spread and Survival
The bacterium remains viable in the infected plant tissues. It is internally seed-borne
and secondary spread through rainsplash and storms.
Management
Keep the field free of infected plant debris. Spray with Streptomycin sulphate or
Oxytetracycline hydrochloride at 100g/ha.
9. Phyllody
Mycoplasma Like Organism
Symptoms
The disease manifests itself mostly during flowering stage, when the floral parts are
transformed into green leafy structures, which grow profusely. The plants bear cluster of
leaves and malformed flowers at the tip. The flower is rendered sterile. The veins of phylloid
structure is thick and prominent. Stamens also become leaf like to certain extent. Anthers
become green and do not dehisce. Ovary is transformed into a elongated out growth
resembling a shoot. The plant is stunted with reduced internodes and abnormal branching
gives a bushy appearance.
Mode of Spread and Survival
The pathogen has a wide host range and survives on hosts like Brassica campestris
var. toria, B. rapa, Cicer arietinum, Crotalaria sp., Trifolium sp., Arachis hypogaea and some
weed hosts. The disease is transmitted by jassid, Orosius albicinctus. Optimum acquisition
period of vector is 3-4 days and inoculation feeding period is 30 minutes. The incubation
period of the pathogen in leaf hoppers may be 15-63 days and 13-61 days in sesamum.
Nymphs are incapable of transmitting the MLO. Vector population is more during summer
and less during winter months.
Management
Remove all the reservoir and weed hosts. Avoid growing sesaumu near cotton,
groundnut and grain legumes. Rogue out the infected plants periodically. Spray
Monocrotophos or Dimethoate at 500ml/ha to control the jassids.
-
Seedling blight DISEASES OF CASTOR
Phytophthora parasitica (Ricinus communis)
Symptoms
The disease appears circular, dull green patch on both the surface of the
cotyledonary leaves. It later spreads and causes rotting. The infection moves to stem and
causes withering and death of seedling. In mature plants, the infection initially appears on
the young leaves and spreads to petiole and stem causing black discoloration and severe
defoliation.
Pathogen
The fungus produces non-septate and hyaline mycelium. Sporangiophores emerge
through the stomata on the lower surface singly or in groups. They are unbranched and bear
single celled, hyaline, round or oval sporangia at the tip singly. The sporangia germinate to
produce abundant zoospores. The fungus also produces oospores and chlamydospores in
adverse seasons.
Favourable Conditions
Continuous rainy weather, low temperature (20-25OC), low lying and ill drained soils.
Management
Remove and destroy infected plant residues. Avoid low-lying and ill drained fields for
sowing. Treat the seeds with Thiram or Captan at 4g/kg.
1. Rust
Melampsora ricini
Symptoms
Minute, orange-yellow coloured, raised pustules appear with powdery masses on the
lower surface of the leaves and the corresponding areas on the upper surface of the leaves
are yellow. Often the pustules are grouped in concentric rings and coalesce together to for
drying of leaves.
Pathogen
The fungus produces only uredosori in castor plants and other stages of the fungus
are unknown. Uredospores are two kinds, one is thick walled and other is thin walled. They
are elliptical to round, orange-yellow coloured and finely warty.
Mode of Spread and Survival
The fungus survives in the self sown castor crops in the off season. It can also
survive on other species of Ricinus. The fungus also attacks Euphorbia obtusifolia,
E.geniculata, and E.marginata. The infection spreads through air-borne uredospores.
Management
Rogue out the self-sown castor crops and other weed hosts. Spray Mancozeb at
1kg/ha or dust Sulphur at 25kg/ha.
2. Leaf blight
Alternaria ricini
Symptoms
All the aerial parts of plants viz., leaves, stem, inflorescences and capsules are liable
to be attacked by the fungus. Irregular brown spots with concentric rings form initially on the
leaves and covered with fungal growth. When the spots coaleasce to form big patches, The
fungus remains in the soil as chlamydospores and oospores which act as primary source of
infection. The fungus also survives on other hosts like potato, tomato, brinjal, sesamum etc.
The secondary spread takes place through wind-borne sporangia. premature defoliation
occurs. The stem, inflorescence and capsules are also show dark brown lesions with
concentric rings. On the capsules, initially brown sunken spots appear, enlarge rapidly and
cover the whole pod. The capsules crack and seeds are also get infected.
Pathogen
The pathogen produces erect or slightly curved, light grey to brown conidiophores,
which are occasionally in groups. Conidia are produced in long chains. Conidia are
obclavate, light olive in colour with 5-16 cells having transverse and longitudinal septa with a
beak at the tip.
Favourable Conditions
High atmospheric humidity (85-90 per cent) and low temperature (16-20OC)
Mode of Spread and Survival
 The fungus also survives on hosts like Jatropha pandurifolia and Bridelia
hamiltoniana. The pathogen is externally and internally seed-borne and causes primary
infection. The secondary infection is through air-borne conidia.
Management
Treat the seeds with Captan or Thiram at 4g/kg. Remove the reservoir hosts periodically.
Spray Mancozeb at 1kg/ha.
3. Brown leaf spot
Cercospora ricinella
Symptoms
The disease appears as minute brown specks surrounded by a pale green halo. The
spots enlarge to greyish white centre portion with deep brown margin. The spots may be 2-4
mm in diameter and when several spots coalesce, large brown patches appear but restricted
by veins. Infected tissues often drop off leaving shot-hole symptoms. In severe infections,
the older leaves may be blighted and withered.
Pathogen
The fungal hyphae collect beneath the epidermis and form a hymenial layer. Clusters
of conidiophores emerge through stomata or epidermis. They are septate and unbranched
with deep brown base and light brown tip. The conidia are elongated, colourless, straight or
slightly curved, truncate at the base and narrow at the tip with 2-7 septa.
Mode of Spread and Survival
The fungus remains as dormant mycelium in the plant debris. The fungus mainly
spreads through wind borne conidia.
Management
Remove the infected plant debris. Spray Mancozeb at 1kg/ha.
Minor diseases
Powdery mildew Leveillula taurica White cottony growth on the lower surface of leaves
with yellow discolouration on upper surface.
 DISEASES OF TOBACCO
(Nicotiana tabacum)

1. Damping off
Pythium aphanidermatum
Symptoms
The fungus may attack the seedling at any stage in the nursery. Sprouting seedlings
are infected and wither before emergence from the soil (Pre-emergence damping off). Water
soaked minute lesions appear on the stems near the soil surface, soon girdling the stem,
spreading up and down in the stems and with in one or two days stem may rot leading to
toppling over of the seedlings (Post-emergence damping off). The young seedlings in the
nursery are killed in patches and infection spreads quickly. Under the favourable conditions,
the entire seedlings in the nursery are killed within 3 to 4 days. A thick weft of mycelium may
be seen on the surface of the soil.
Pathogen
The fungus produces thick, hyaline, thinwalled, non-septate mycelium. It produces
irregularly lobed sporangia which germinate toproduce vesicle containing zoopores. The
zoospores are kidney shaped and biflagellate. Oospores spherical, light to deep yellow or
yellowish brown coloured, measuring 17-19um in diameter.
Favourable Conditions
Over crowding of seedling, ill drained nursery beds, heavy shade in nursery, high
atmospheric humidity (90-100 per cent), high soil moisture, low temperature (below 24OC)
and low soil temperature of about 20OC.
Mode of Spread and Survival
The fungus survives in the soil as oospores and chlamydospores. The primary
infection is from the soil-borne fungal spores and secondary spread through sporangia and
zoospores transmitted by wind and irrigation water.

Management
Prepare raised seed beds with adequate drainage facility. Burn the seed beds with
paddy husk before sowing. Drench the seed bed with 1 per cent Bordeaux mixture or 0.2 per
cent Copper oxychloride, two days before sowing. Avoid over crowding of seedlings by using
recommended seed rate (1 to 1.5g/2.5m2).
Avoid excess watering of the seedlings. Spray the nursery beds two weeks after sowing with
1 per cent Bordeaux mixture or 0.2 per cent Copper oxychloride or 0.2 per cent Mancozeb
and repeat subsequently at 4 days interval under dry weather and at 2 days interval under
wet cloudy weather or spray 0.2 per cent Metalaxyl compound (Ridomil MZ) at 10 days
interval commencing from 20 days after germination.
 2. Black shank
Phytophthora parasitica var. nicotianae
Symptoms
The pathogen may affect the crop at any stage of its growth. Eventhough all parts are
affected, the disease infects chiefly the roots and base of the stem. Seedlings in the nursery
show black discolor of the stem near the soil level and blackening of roots, leading the wet
rot in humid condition and seedling blight in dry weather with withering and drying of tips.
The pathogen also spreads to the leaves and causes blighting and drying of the bottom
leaves. In the transplanted crop, the disease appears as minute black spot on the stem,
spreads along the stem to produce irregular black patches and often girdling occurs. The
upward movement leads to development of necrotic patches on the stems. The infected
tissues shrink, leaving a depression and in advanced condition the stem shrivels and plant
wilts. When the affected stem is split open, the pith region is found to be dried up in disc-like
plates showing black discolouration. On the leaves large brown concentrically zonate
patches appear during humid weather, leading to blackening and rotting of the leaves.
Pathogen
The fungus produces hyaline and non-septate mycelium. The sporangia, which are
hyaline, thin walled, ovate or pyriform with papillae, develop on the sporangiophores in a
sympodial fashion. Sporangia germinate to release zoospores which are usually kidney
shaped, biciliate and measure 11-13 x 8-9um. The fungus also produces globoose and thick
walled chlamydospores, measuring 27-42um in diameter. Oospores are thickwalled,
globose, smooth and light yellow coloured, measuring 15-20um in diameter.
Favourable Conditions
Frequent rainfall, high soil moisture and high population of rootknot nematodes
Meloidogyne incognita var. acrita.
Mode of Spread and Survival
The fungus lives as a saprophyte on organic wastes and infected crop residues in
soil. The fungus also presents in the soil as dormant mycelium, oospores and
chlamydospores for morethan 2 years. The primary infection is by means of oospores and
chlamydospores in the soil. Secondary spread is by wind-borne sporangia. The pathogen in
the soil spreads through irrigation water, transport of soil, farm implements and animals.
Management
Burn the seed beds with paddy husk or groundnut shell at 15-20 cm thick layer.
Provide adequate drainage in the nursery. Drench the nursery beds with 1 per cent
Bordeaux mixture or 0.2 per cent Copper oxychloride, two days before sowing. Spray the
beds two weeks after sowing with 0.2 per cent Metalaxyl or 0.2 per cent Captafol or 0.2 per
cent Copper oxychloride or 1 per cent Boreaux mixture and repeat after 10 days. Select
healthy, disease free seedlings for transplanting. Remove and destroy the affected plants in
the field. Spray Mancozeb 1 kg or Copper oxychloride 1 kg or Ziram 1 lit/ha. Spot drench
with 0.4 per cent Bordeaux mixture or 0.2 per cent Copper oxychloride.
3. Frog eye spot
Cercospora nicotianae
Symptoms
The disease appears mostly on matured, lower leaves as small ashy grey spots with
brown border. The typical spots has a white centre, surrounded in succession by grey and
brown portions, surrounded by a dark brown to black margin, resembling the eyes of a frog.
Under favourable conditions, several spots coalesce to form large necrotic areas, causing
the leaf to dry up from the margin and wither prematurely. Both yield and quality are reduced
greatly. The disease may occur in the seedlings also, leading to withering of leaves and
death of the seedlings.
Pathogen
The mycelium is intercellular and collects beneath the epidermis and clusters of
conidiophores emerge through stomata. The conidiophores are septate, dark brown at the
base and lighter towards the top bearing 2-3 conidia. The conidia are hyaline, slender,
slightly curved, thinwalled and 2-12 septate.
Favourable Conditions
Temperature of 20-30OC, high humidity (80-90 per cent), close spacing, frequent
irrigation and excess application of nitrogenous fertilizers.
Mode of Spread and Survival
The fungus is seed-borne. The fungus also persists on crop residues in the soil. The
primary infection is from the seed and soil-borne inoculum. The secondary spread is through
wind-borne conidia.
Management
Remove and burn plant debris in the soil. Avoid excess nitrogenous fertilization.
Adopt optimum spacing. Regulate irrigation frequency. Spray the crop with 0.4 per cent
Bordeaux mixture or Thiophanate Methyl 750g/ha or Carbendazim 750 g/ha and repeat after
15 days.

4. Powdery mildew

Erysiphe cichoracearum var. nicotianae

Symptoms
Initially the disease appears as small, white isolated patches on the upper surface of
the leaves. Later, it spreads fast and cover the entire lamina. The disease initially appears
on the lower leaves and as disease advances, the rest of the leaves are also infected and
sometimes powdery growth can be seen on the stem also. The affected leaves turn to brown
and wither and show scorched appearance. The severe infection leads to defoliation and
reduction in quantity and quality of the curable leaves.
Pathogen
The fungus is ecotophytic and produce hyaline, septate and highly branched
mycelium. Short, stout and hyaline conidiophores arise from the mycelium and bear conidia
in chains. The conidia are barrel shaped or cylindrical, hyaline and thin walled. Cleistothecia
are black, spherical with no ostiole, with numerous densely-woven septate, brown-coloured
appendages. They contain 10-15 asci which are ovate with a short stalk. Each ascus
contains two ascospores which are oval to elliptical, thinwalled, hyaline and single celled.
Favourable Conditions
Humid cloudy weather, low temperature (16-23OC), close planting and excess doses
of nitrogenous fertilizers.
Mode of Spread and Survival
The fungus remains dormant as mycelium and cleistothecia in the infected plant
debris in soil. The primary infection is mainly from soil-borne inoculum. The secondary
spread is aided by wind blown conidia.
Management
Apply balanced ferilizers. Avoid overcrowding of plants. Remove and destroy the
affected leaves. Plant early in the season so that crop escapes the cool temperature at
maturity phase. Apply Sulphur dust to the soil at 40kg/ha. (Mix 1 part of Sulphur with 3 parts
of fine sand or ash and apply). Spray Dinocap at 375 ml or Carbendazim at 500g/ha.
5. Wild fire
Pseudomonas tabaci
Symptoms
The leaf spots may occur at any stage of plant growth including the nursery
seedlings. Dark brown to black spots with a yellow halo spreads quickly causing withering
and drying of leaves. In advanced cases, lesions develop on the young stem tissues leading
to withering and drying of the seedlings. In the fields, initially numerous water soaked black
spots appear and latter become angular when restricted by the veins and veinlets. Several
spots may coalesce to cause necrotic patches on the leaves. In advanced conditions, the
entire leaf is fully covered with enlarged spots with yellow haloes. The leaves slowly wither
and dry. Under humid weather condition, the disease spreads very fast and cover all the
leaves and the entire plant gives a blighted appearance.
Pathogen
The bacterium is a rod, motile with a single polar flagellum, non-capsulated, non-
spore forming and Gram negative.
Favourable Conditions
Close planting, humid wet weather and strong winds.
Mode of Spread and Survival
The bacterium survives in the infected crop residues in the soil, which is the primary
source of infection. The secondary spread of the pathogen in the field is through wind
splashed rain water and implements.
Management
Remove and burn the infected crop residues in the soil. Avoid very close planting.
6. Mosaic
Tobacco Mosaic Virus (TMV)
Symptoms
The disease appears as light discoloration along the veins of the youngest leaves.
Soon the leaves develop a characteristic light and dark green pattern, the dark green areas
are usually associated with the veins. The dark green areas later develop into irregular
crumpled swellings or blisters due to more rapid growth. The plants that become infected
early in the season are usually very much stunted with small, chlorotic, mottled and curled
leaves. In severe infections, the leaves are narrowed, puckered, thin and malformed beyond
recognition, Later, dark brown necrotic spots develop under hot weather and this symptom is
called “Mosaic burn” or “Mosaic scorching”.
Pathogen
Tobacco mosaic is caused by Nicotiana virus I (Marmor tabaci var. vulgare). It is a
rod shaped particle measuring 300 X 150-180um with a central hollow tube of about 4um
diameter. It is madeup of centrally placed Ribo Nucleic Acid molecules (RNA) covered with a
protein coat. It is capable of remaining infective when stored dry for over 50 years.
Mode of Spread and Survival
The virus remains viable in the plant debris in the soil. The virus has a wide host
range, affecting nearly 50 plant species belonging to nine different families. The virus is sap -
transmissible and enters the host through wounds. The virus is not seed-transmitted in
tobacco but tomato seeds transmit the virus. In the field, the virus is transmitted by contact.
The farm workers engaged in topping and clipping operations transmit it through their
dresses. The implements used in the field also transmit the virus.
Management
Remove and destroy infected plants. Keep the field free of weeds which harbour the
virus. Wash hands with soap and running water before or after handling the plants or after
weeding. Prohibit smoking, chewing and snuffing during field operations. Spray the nursery
and main field with leaf extracts of Bougainvillea or Basella alba at 1 litre of extract in 150
litres of water, two to three times at weekly intervals. Adopt crop rotation by growing non-
host plants for two seasons. Grow resistant varieties like TMV RR2, TMV RR 2a and TMV
RR3.
7. Leaf curl
Niccotiana Virus 10 (Ruga tabaci)
Symptoms
The virus may attack the plant at any stage. When young plants are infected the
entire plant remains very much dwarfed. Three forms of leaf curl expression are observed.
The leaf margins curl downward towards the dorsal side and show thickening of veins with
enation on the lower surface. Crinkle form shows curling of whole leaf edge towards dorsal
side with enation on the veins and the lamina arching towards the ventral side between the
veinlets. The transparent symptom shows the curling of leaves towards the ventral side with
clearing of the veins and enations are absent.
Pathogen
The virus is spherical and measuring 35um in diameter. The virus is Nicotiana virus
10 or Ruga tabaci.
Mode of Spread and Survival
The virus has wide host range of 63 crops species belonging to fourteen families.
The virus is not transmissible through sap or seed. It is graft-transmissible. The whitefly,
Bemisia tabaci is the vector responsible for transmission in the field.
Management
Remove and destroy the infected plants. Rogue out the reservoir weed hosts which
harbour the virus and whiteflies. Avoid growing solanaceous crops like tomato near tobacco
fields. Spray Methyldemeton at 0.1 to 0.2 per cent to control the vectors.
8. Phaneroganic parasite
Broom rape
Orobanche cernua var. desertorum
Symptoms
The affected tobacco plants are stunted and show withering and drooping of leaves
to wilting. These are the indicates of underground parasitism of the tobacco roots by the
parasite. The young shoot of the parasite emerges from the soil at the base of the plants 5 -6
weeks after transplanting. Normally, it appears on clusters of 50-100 shoots around the base
of a single tobacco plant. The plants which are attacked very late exhibit no external
symptoms but the quality and yield of leaves are reduced.
Parasite
It is a total root parasite. It is an annual, fleshy flowering plant with a short, stout
stem, 10-15 inches long. The stem is pale yellow or brownish red in colour and covered by
small, thin, brown scaly leaves and the base of the stem is thickened. White-coloured
flowers appear in the leaf axils. The floral parts are well developed with a lobed calyx,
tubular corolla, superior ovary, numerous ovules and a large four-lobed stigma. The fruits
are capsules containing small, black, reticulate and ovoid seeds.
Mode of Spread and Survival
The seeds of the parasite remain dormant in the soil for several years. Primary
infection occurs from the seeds in the soil. The seeds spread from field to field by irrigation
water, animals, human beings and implements. The dormant seeds are stimulated to
germinate by the root exudates of tobacco and attaches itself to the roots by forming
haustoria. Later, it grows rapidly to produce shoot and flowers. Orobanche also attacks the
crops like brinjal, tomato, cauliflower, turnip and other cruciferous crops.
Management
Rogue out the tender shoots of the parasite before flowering and seed set. Spray the
soil with 25 per cent Copper sulphate. Spray 0.1 per cent Allyl alcohol. Apply few drops of
kerosene directly on the shoot. Grow decoy or trap crops like chilli, motherbean, sorghum or
cowpea to stimulate seed germination and kill the parasite.

DISEASES OF BANANA
1. Fusarium wilt/Panama disease – Fusarium exysporum f.sp.cubense
2. Sigatoka leaf spot – Yellow Sigatoka - Mycosphaerella musicola
– Black Sigatoka - Mycosphaerella fijiensis

3. Moko disease / Bacterial wilt – Ralstonia solanaceaum (Burkholderia solanaceaum)

4. Tip over / Rhizome rot / top rot – Erwinia carotovora carotovora
5. Bunchy top – Banana bunchy top virus (BBTV)
6. Banana Mosaic / Infectious chlorosis – Cucumber Mosaic Virus (CMV)
7. Banana bract mosaic – BBMV
8. Post Harvest Disease
1. Cigar end rot – Verticillium thoebromae
2. Anthracnose – Colletotrichum musae
3. Deightoniella leaf spot / Black spot / fruit spot – Deightoniella torulosa
4. Crown / Stem end rot – Botryodiplodia theobromae (Lasiodiplodia theobromae)
5. Main stalk rot – Ceratostomella paradoxa
6. Pitting disease – Pyricularia grisea
Minor Diseases

1. Freckle leaf spot – Physlostictinia musarum

2. Bacterial leaf spot – Xanthomonas musicola
 3. Cordana leaf spot – Cordana musae
1. Fusarium wilt/Panama disease – Fusarium exysporum f.sp.cubense
 It is the most destructive and wide spread disease of banana.
 First recorded from Australia in 1874 (Bancroft 1876).
 The disease had attained alarming proportion in Panama and Costa Rica in 1904.
 In 1917, the cultivation of Gros Michel banana in Panama was completely abandoned
because of the disease which was later replaced by red banana.
 Now the disease has been reported in all the banana growing countries.
 In India the disease was first reported from Chinsurah in 1911
 It is presently prevalent in Tamil Nadu, Kerala, Karnataka, Bihar, Assam, Andhra
Pradesh, West Bengal and Maharashtra.
Symptoms:

 Plants will not exhibit any external symptoms initially up to 4-6 month even though 2-3
months old seedlings are also affected.
 The infected plants show characteristic yellowing of older leaves.
 The yellowing develops along the margin as a band and spreads towards the midrib.
 Yellowing of leaves spreads upwards and finally heart leaf alone remains green.
 Leaves wilt, dry and break at the base of the petiole and hang around the pseudostem
 This forms a skirt of dead leaves around the plants.
 Often all the leaves collapse except the heart leaf which alone remains upright.
 After 4-6 weeks, the pseudostem remains with dead leaves hanging around it.
 More number of daughter suckers are produced from the infected plants.
 The pseudostem shows longitudinal splitting at the base above the soil level.
 The internal symptoms are more reliable for diagnosis.
 When the infected pseudostem cut transversely, dark brown or black discoloration of water
conducting tissues are seen.
 Gum pockets are also seen in water conducting tissues due the accumulation of gel in
response to infection by the host.
 When the infected corm cut transversely, central portion of the affected corm is dark brown
 In the corm yellow, red, brown black or purplish dots or streaks run in all directions through
the strands radiating from the centre of the corm.
 The corm smells like rotten fish.
 Roots of diseased rhizomes are black in colour.
 The affected plants may show dwarfing.
 The bunch may show various abnormal developments.
 It ripens prematurely or irregularly.
 The fingers become bottle necked.
 The flesh becomes pithy, acrid and yellow.
Mechanism of Wilt infection

 The pathogen gains entry into the water – conducting xylem vessels and proliferate
causing water blockage.
 The blockage of xylem vessel is also caused by the gel-like materials produced by the host
in response to invasion of the pathogen.
 Yellowing and loss of control of stomatal function in leaves are caused by the upward
translocation of toxins (Propionic aldehyde, fusaric acid, dopamine etc) produced by the
pathogen.
 The closing of xylem vessels by tyloses and destruction of roots contribute significantly
towards wilting.

Casual Organism: Fusarium oxysporum f.sp cubense.

The causal agent of Fusarium wilt or Panama disease of banana is the fungus Fusarium
oxysporum f. sp. cubense (E.F. Sm.) W.C. Snyder & H.N. Hansen (Foc). Foc is an
anamorphic fungus without a known sexual stage (teleomorph). Sexual stage (teleomorph)
has not been found even in isolates carrying genes Mat 1 and Mat 2 (Fourie et al., 2011).
Its taxonomic position is as follows:
Domain: Eukaryota
Kingdom: Fungi
Phylum: Ascomycota
Class: Ascomycetes
Subclass: Sordariomycetidae
Order: Hypocreales

Morphology

Mycelium – Intracellular in xylem vessels – Mycelium is white or tinted rose or violet

There are three types of asexual spores formed; macroconidia, microconidia and
chlamydospores (Nelson, 1991).

Macroconidia are formed from monophialides on branched conidiophores in

sporodochia, and to a lesser extent from monophialides on hyphae (Leslie and Summerell
2006). Macroconidia are four to eight celled, falcate to erect to almost straight, sickle-
shaped, thin-walled and delicate, with foot-shaped basal attenuated apical cells (Jones
2000). 27-55μm x 3.3-5.5μm
 Microconidia abundantly borne on false heads on short monophialides in
sporodochia, are one or two celled, hyaline, oval- to kidney shaped. The dimensions of the
microconidia are 5-16μm x 5-16 × 2.4-3.5 μm.

Chlamydospores are thick-walled, asexual, globose 7-11μm, usually formed

singularly or in pairs, but may also be found in clusters or short chains (Jones 2000; Leslie
and Summerell 2006). Oval or globose

Pathogenic races of Fusarium oxysporum f. sp. cubense

Four physiological races exist based on the pathogenicity on different genotypes of

banana and related hosts.

Race: 1 attacks Gros Michel (AAA), Manzano/Apple/Latundan (Silk, AAB), Pisang awak
(Karpooravalli (ABB) and Pome (Pachanadan, Ney Poovan, Virupakshi (AAB) and Rasthali
(Silk) (AAB) Worldwide (Central America)
Race: 2 attacks Bluggoe (Monthan, Sakkia (AAB)

Race: 3 attacks only Heliconia sp

Race: 4 not exist in India. Attacks Cavendish varieties – resistant to race 1 - and
mildly resistant to race 2

Mode of survival and spread of the pathogen:

 The pathogen is soil borne. It is able to survive as chlamydospores in previously

colonized tissues and in soil where it can persist for long periods, latent or as an
endophyte of host weeds (Hennessey et al. 2005).
 It survives in soil as chlamydospores for more than 30 years.
 The primary spread of the disease is through infected planting material, rhizomes and
suckers.
 The infected trash is an important source of infection.
 Secondary spread is also through the movement of soil, running water, farm machinery
and implements and root to root contact.
 There is also the possibility of dissemination by insect vectors, especially the banana
weevil borer Cosmopolites sordidus (Coleoptera: Curculionidae).
Epidemiology:

 The infection entry is facilitated by mechanical wounds and root damage caused by
burrowing nematode Radopholus similis
 Survival is influenced by soil moisture, soil texture and soil Ph etc.
 Survival and growth is more in acidic, light textured loam and sandy loam soils than in
clayey and alkaline soil with high calcium content.
 Depth of penetration is more in sandy loan than in silt loam soil.
 Clay minerals retard the spread of the disease.
 Survival of the pathogen in the field soil is best at 25% saturation, while increase in soil
moisture the survival ability is decreased.
 Growth of the pathogen and disease development in the roots occurs at 21-270C but not
at 340C
 Symptom development declines during winter months.
 Saturated, poorly drained soils have been correlated with greater disease incidence.
 Low levels of Zinc and high Ca: Mg and K: Mg ratios are associated with more severe
disease.
 In soils submerged under 5cm depth of water, the survival was reduced to only one
month.
 There is a positive correlation between the amount of inoculum present in the proximity
of the roots and extent of root infection.
 During drought period there is considerable reduction in the number of newly diseased
plants but soon after heavy rains there is rapid increase in the disease incidence.
 Mechanical wounds caused by tillage operations also help in dispersal of the pathogen.
 The disease is severe in stiff, acid clay and alluvial soils with poor drainage and
aeration.
Management:

 Selection and use of resistant varieties Res. Var: Raja bale, Red banana, Walha, Dwarf
Cavendish, Robusta, Grand Nain, Nendran.
 Sus Var: Gros Michel, Monthan, Karpooravalli, Rasthali.
 Use of planting materials collected from disease free fields.
 Use of disease free planting materials
 Infected plants should be completely removed and destroyed.
 The pits have to be treated with lime @1-2kg/pit.
 Crop rotation with paddy or Sugarcane for 3-4 years in infected fields.
 Proper drainage facilities.
 Flood fallowing for 6-24 months.
 Dipping of suckers in carbendazim 0.1% for ½ h before planting
 Soil drenching with carbendazim 0.1% at 5, 7 and 9 months after planting.
 Paring and prolinage with carbofuran 3G @40g per suckers for the control of burrowing
nematodes.
  Avoidance of root injury through tillage.
 Regular optimum irrigation.
 Plant quarantine. Avoidance of transport of infected planting materials to areas where
the disease is not present.
 Deep tillage before planting – the heavily infected upper (20-30cm) soil could be buried
to a depth of 60-90 cm and the pathogen could be destroyed by biological and other soil
factors.
 Soil organic amendments with crops like legumes, sorghum or sugarcane trash reduce
the disease incidence.
 The tissue culture plants are more susceptible hence the Tissue Culture banana should
be planted only in pathogen free soils.
 Application of lime reduced the survival of the pathogen to 2 months.
 Capsule application with Carbendazim 50 WP @ 60 mg per capsule on 5,7 and 9
months after planting .
Biological Control:

 Sucker treatment with commercial formulation of Pseudomonas fluorescens @10g per

sucker.
 Soil application @2.5 kg /ha
 Capsule application@50mg per sucker at 3, 5 and 7th month after planting.
2. Sigatoka Leaf Spots: 1. Yellow Sigatoka: Mycosphaerella musicola,
2. Black leaf streak or Black Sigatoka: Mycosphaerella fijiensis

The most important leaf spot disease of banana is caused by three species of
the ascomycete genus Mycosphaerella.

Yellow Sigatoka, or banana leaf spot, was first recorded in Java in 1902 and the first
major epidemic in commercial plantations occurred in the Sigatoka in the Fiji Islands in 1913
and hence the name was given. The disease now occurs in all major banana-producing
countries.

In 1963, a more severe Sigatoka-like leaf spot was detected in Sigatoka Valley of
Vita Levu in the Fiji Islands and was named 'black leaf streak' because of the dark brown to
black spots and streaks formed on affected leaves. Black leaf streak is caused by
Mycosphaerella fijiensis

A third serious disease of banana is black Sigatoka caused by Mycosphaerella

fijiensis var. difformis. It was first recorded in Honduras in I972 and reached epidemic levels
in commercial plantations in 1973-74. Recent studies of the fungi causing black leaf streak
and black Sigatoka indicate that there is no consistent morphological difference between
Mycosphaerella fijiensis and Mycosphaerella fijiensis var. difformis which are now regarded
as synonyms. Thus, the disease caused by what is now called Mycosphaerella fijiensis is
commonly known as black Sigatoka

 The disease occurs throughout the world.

 Defoliation by Mycosphaerella diseases reduces the quantity and quality of bananas
 It is also one of the most destruction diseases of banana.
 In the absence of control measures, the disease can reduce bunch weight by up to
50% and cause a 100% loss of production due to deterioration in the quality of the
fruit (length and thickness).
 In India the disease is prevalent in all the major banana growing states.
 In India the leaf spot is caused by the yellow Sigatoka pathogen
Symptoms:

 Starts with pale yellow or greenish yellow streaks parallel to veins on the leaves.
 These enlarge to become linear oblong, muddy brown to black spots (up to 1-2cm).
 The centre of the spots become light grey and necrotic surrounded by dark brown or
black border with yellow halo.
 The matured spots are elliptical giving eye – spot appearance.
 On the upper surface of the spots fructification of the fungus appears as black
specks.
 The spots often coalesce to form large irregular patches of dried tissues.
 In severe conditions the whole leaf dries up from the tip.
 The petiole collapses and the leaf hangs down from the pseudostem.
 Rapid drying and defoliation also seen.
 In case of Dwarf Cavendish except 2 or 3 leaves all the leaves dry out.
 In severe cases, the quality of fruits is drastically reduced.
 Small angular fingers premature ripening peels splitting are commonly seen.
 The bunch starts ripening during the transit affecting the export quality.
Casual Organism: Mycospharella musicola, Mycosphaerella fijiensis

Conidia – narrow, elongated, multi septate, hyaline

Perithecia – Dark brown to black globose, ostiolate, amphigenous, erumpent,

Asci- Oblong, clavate,

Ascospores – Hyaline, 2- celled obtuse – ellipsoid with slightly broader upper cell.

YELLOW SIGATOKA BLACK SIGATOKA

 More common in cooler environments More common in warmer
environments

Inoculum consists of both conidia Windborne ascospores are the major

(water-dispersed) and ascospores (wind- inoculum
dispersed)

Conidia first appear in the matured Conidia first appear in early streak
spot stage stage

Produce more than 30,000 condia Produce about 1200 condia per spot
per spot

conidia not dislodged by wind Conidia both water- and wind-

dispersed

Matured ascospores are produced 4 Matured ascospores are produced 2

weeks after the appearance of streaks weeks after the appearance of streaks

Mode of spread and survival:

The pathogen survives on dry infected leaves on the field soil.

The conidia and ascospores spread through rain water and wind.

Epidemiology:

 The dissemination of conidia takes place only by the action of rain or dew.
 A film of water is required for conidia formation.
 Conidia collection takes place early in the morning when leaves are covered with
dew.
 Perithecia are produced during warm, humid weather.
 The disease spread is favoured by warm (23-250C) and rainy humid weather.
 Below 210C reduction in the infection even if other conditions are favourable.
 The disease is common on poor, badly, drained soils and in shaded areas.
 Closer spacing heavy weed population or grass cover, failure to remove the suckers
enhances the disease spread.
 Banana grown in partially shade especially under coconut tends to be less affected.
 Rainy days favour disease development and spread.
 RH (morning) and minimum temperature positively correlated on disease incidence.
  RH (evening) and max temperature negatively correlated on disease incidence.
 For every 1% increase in RH 5 points increases in disease severity index in
Coimbatore.
Management:

 Removal and destruction of infected leaves.

 Improved drainage.
 Field sanitation i.e. efficient weed control.
 Regular removal of suckers.
 Proper spacing and fertilizer application.
 Spraying of any one of the fungicides like mancozeb (0.2%), Tridemorph (0.2%)
Carbendazim (0.1%) Chlorothalonil (0.2%), Thiophanate. Methyl (0.1%)
Propiconazole (0.1%), Hexaconazole (0.1%) along with spreading agents like teepol
or sandovit or Triton, AE Continuous use of same systemic fungicides will cause
resistance or tolerance in pathogenic population. Hence alternate spray of contact
and systemic fungicides at 10-15 days interval should be preferred.
3. Moko disease / Bacterial Wilt: Burkholderia solanacearum
 The disease was first noticed in British Guyana in 1840.
 The disease is widely distributed and occurs in most banana growing regions.
 In India the disease was first reported in west Bengal in 1968 and then in southern
states of Tamil Nadu and Kerala in 1979.
 It is reported to occur on cv. Robusta and Poovan in TN causing 75-100% loss.
Symptoms:

 The affected plants show rapid wilting and collapse of the leaves.
 The newly emerged three leaves turn pale green or yellow and collapse near the
point of lamia and petiole.
 Most leaves collapse within 3-7 days.
 In Cavendish banana the lower leaves become yellow.
 This spreads to upwards.
 Later the leaves acquire a white tinge – yellow and become dry and flaccid and
readily droop.
 The petiole breaks at its junction with pseudostem and droop around the
pseudostem.
 If the diseased suckers planted, the terminal leaf become necrotic and the plants die.
 The suckers in infected plants also affected.
 The affected suckers are blackened get twisted and remain stunted.
  The internal symptoms indicate that moko is a typical vacular infection or vascular
disease.
 When the pseudostem, corm and peduncle cut transversely all the vascular strands
are pale yellow to dark brown or bluish black.
 In some advanced condition, a reddish brown ring of vascular tissue may be seen.
 The vascular discoloration tends to be central.
 Opaque greyish brown or dirty white, slimy bacterial ooze comes out from the cut
opened pseudostem.
 The fingers of the infected plants become distorted or turn yellow.
 The pulp turns into a very characteristic dark brown colour with dry rot symptoms.
The distinguishing symptoms between moko and Panama

Panama Moko

No external symptoms upto 4-6 Suckers are blackened get twisted

months and stunted.

No symptoms on newly emerged Newly emerged leaves turn pale

leaves and are not collapsed green or yellow and collapse

Leaves turn yellow Leaves turn white tinge yellow

Wilting of leaves starts from older Wilting of leaves starts from youngest
leaves leaves

More number of suckers are A few suckers are affected

produced and all the suckers are affected

Longitudinal splitting of psedostem No longitudinal splitting of

seen above soil level pseudostem

Dark brown or black discoloration of Pale yellow to dark brown or bluish

water conducting tissues in pseudostem black discoloration of water conducting
tissues in pseudostem

Reddish tinge is present in Absent

pseudostem

Reddish brown ring of Vascular Present

tissues in the corm is absent

Central portion of the affected corm Central portion of the affected corm is
is dark brown. Yellowish brown

In the corm purplish streaks run In the corm no purplish streaks run
radiating from the centre in all direction. radiating from the centre in all direction.
 The vascular discoloration in the The vascular discoloration in the corm
corm is peripheral tends to central.

No bacterial ooze comes out from Opaque grayish brown or dirty white
pseudostem slimy bacterial ooze comes out from
pseudostem

No soft rot of corm or pseudostem Soft patches of bacterial rot is seen in

the corm and pseudostem

The flesh become pithy acrid and The flesh turns into a very
yellow in colour characteristic dark brown with dry tor
symptoms.

Causal organism: Ralstonia solanacearum (Burkholderia solanacearum)

Moko disease is caused by the bacterium Ralstonia solanacearum (Yabuuchi,

Kosako et al. 1995). Initially when it was identified by Rorer in 1911 he named the causal
agent Bacillus musae however after the bacterium was shown to cause symptoms on
solanaceous plants it was reclassified as B. solanacearum (Ashby 1926). Then
Pseudomonas solanacearum then Burkholderia solanacearum. This group has now been
renamed Ralstonia solanacearum. The bacterium is described as an aerobic, gram-negative,
non-fluorescent rod belonging to the rRNA homology group II and single polar flagellate
(Palleroni 1984).

Ralstonia solanacearum is a species complex and is traditionally classified into five

races based on differences in host range and into biovars based on biochemical properties.

Moko disease, a bacterial wilt of banana, is recognised as Ralstonia solanacearum

race 2, biovar 1.

Mode of spread and survival:

 The bacterium survives through infected suckers and in soil for 12-24 months.
 Other host plants include ornamentals e.g. Heliconia, red ginger, cocoa, dasheen,
tomato, potato, castor bean (”Oil nut”) and several weeds.
 The disease is spread through infected rhizome cutting machetes, insects, soil, and
irrigation water.
Management:

 Strict plant quarantine and phytosanitary measures against movement of infected

suckers from one place to other.
 The suckers should be collected from disease free fields.
  Use of disease free suckers.
 Removal and destruction of weed hosts like Heliconia
 Disinfection of pruning machetes using formalin diluted with water at 1:3 ratio.
 Early detection and rapid destruction of infected plants.
 Removal of male flowers after the emergence of female hand.
 Better drainage should be provided in the field.
 Avoidance of irrigation water passing from infected field to healthy fields.
 Keeping the soil fallow and weed free for 6-12 months.
 Crop rotation with non hosts like sorghum sugarcane and rice. (In TN 3 year rotation
of banana, Sugarcane and rice (two crops) effective.
 Soil and planting materials can be fumigated with methyl bromide.
 Bacterization of planting materials, soil and capsule application of P. fluorescens.

4. Erwinia Head Rot / Tip Over / Rhizome Rot: Erwinia carotovora sub sp. carotovora
The disease is wide spread in banana growing areas of the world. In India it is
present in Tamil Nadu, Kerala and Andhra Pradesh. The disease was first noticed in cv,
Monthan and Pachanadan in 1985 in Coimbatore, Tamil Nadu. It is most commonly
observed during hot summer and monsoon season. The disease is predominantly observed
in tissue culture plants at 3-5 months after planting.

Symptoms:

 The affected plants show discoloration and soft rot of rhizome and suckers.
 Rotting of collar region followed by epinasty of leaves which dry out suddenly.
 The pseudostem tips over breaking across the rotted stem at the ground level.
 Infected plants can be pushed over easily and it comes out from collar region leaving
the corm in the soil.
 Severe splitting of pseudostem is common in late stage of infection and being locally
called vedivazhai (Split banana) in Kerala
 Yellowish to reddish bacterial ooze is seen when collar region is cut open.
 Bunch fails to develop.
 In severely infected soil newly planted rhizome rots
 Dark water soaked areas develop in the rhizome.
 Cavities are formed in Rhizomes and the rotten corm emits foul smell.
Casual Organism: Erwinia carotovora sub sp. carotovora

 Gram negative bacteria with peritrichous flagella.

Mode of spread and survival:
  The pathogen is soil borne enters through wounds.
 The disease also spread through infected suckers.
Management:

 Selection of disease free suckers for planting.

 Use of bigger sized suckers (>500g)
 Avoid planting during rainy season.
 Provide adequate drainage system.
 Banana should not be grown along with onion. Soft rot pathogen increases.
 Soil drenching with 0.2% Bleaching powder at planting and 3rd month of planting.
5. Bunchy top – Banana Bunchy top virus
 The disease is also called as strangles, or curly top or cabbage top.
 It is one of the threatening diseases of banana occurring throughout the world.
 It was first reported in Musa sp. in 1879 in Fiji and thereafter from almost all the
banana growing countries of the world.
 In India it was first reported from Bengal in 1925, Bihar in 1940, Assam in 1941 and
Kerala in 1943.
 Now the disease is prevalent throughout the country.
 It was reported as an introduced disease to our country from Sri Lanka.
 ICAR has categorized bunchy top as one of the diseases of national importance due
to drastic and non bearing of fruits.
 Bunchy top disease almost wiped out many precious varieties like Hill banana
(Virupakshi) in TN, Nendran and Planthodan of Kerala, Harissal and Lal Velchi of
Maharashtra.
Symptoms:

 The disease initially shows series of dark green dots or streaks along the secondary
veins on the underside of the lamia, mid rib, petiole and leaf sheath. This symptom is
referred to as “Morse code streaking” because the streaks are irregular and
resemble a series of “dots” and “dashes.”
 Dark green, hook-like extensions of veins can be seen in the narrow, light-green
zone between the midrib and the lamina
 A powdery bloom covers the mid rib and petiole.
 The leaves are very small, narrow, erect and brittle in texture
 Leaves show marginal chlorosis and upward rolling.
 Petiole incompletely elongated.
 The leaf margin become wavy
 Transverse of wrinkling occurs along the length of lamia.
  The affected plants become very dwarf.
 The internodes get shorten.
 Bunching of leaves occurs at the apex of the pseudostem forming a rosette or
bunchy top.
 Opening of young leaves is earlier than older leaves giving a funnel – shape at the
top.
 Pale whitish streaks may be seen along the length of lamia.
 Mottling on petiole, pseudostem and flower.
 In early infection no bunches are produced.
 In late infection, bunches are very small and malformed.
 The emergence of bunches are chocked by pseudostem and may split it.
 The rhizomes show decaying.
 The affected plants do not die for at least 1or 2 years.
Casual organism: Banana Bunchy Top Virus (BBTV) OR Banana Virus 1 (or) Musa
Virus 1

The virus is isometric, non – enveloped, circular, single stranded DNA virus, 18-20
nm in dia.

Classified in the genus Babuvirus, within the family Nanoviridae

Mode of spread and survival:

 The virus survives in infected plants and perennial hosts.

 Infected suckers are primary source of spread.
 The virus is not sap transmissible.
 ‘Transmission by banana aphid Pentalonia nigronervosa
 Non persistant virus.
 All the stages of aphid can acquire and transmit the virus.
 Nymphs are most efficient than adults.
 Single aphid can transmit the virus. The minimum no of aphids required for maximum
infection is 20.
 Acquisition feeding period is 3h.
 The transmission feeding period in 30min.
 The aphids remain infective up to 13 days.
6. Banana Mosaic / Infectious chlorosis – Cucumber Mosaic Virus (CMV)
 It is also called as Heart rot or Mosaic disease or virus sheath rot.
 The disease was first recorded in NSW of Australia in 1930.
 In India it was first observed in 1949 in Maharashtra and Gujarat.
  Now it occurs in almost all banana growing states of the country.
Symptoms:

 The disease is characterized by the presence of typical mosaic like or discontinuous

linear chlorotic streaks in bands extending from margin to mid rib along the veins.
 Raised veins, rolling of leaf margin, twisting and bunching of leaves at the crown
 Newly emerged leaves are rigid and erect.
 The leaves are narrow and small.
 Plants remain stunted.
 Plants seldom produce bunches.
 Early infection leads to sheath rot and heart rot phase especially in Cavendish and
robusta clones.
Casual Organism: Cucumber Mosaic Virus (CMV)

 The virus is isometric and 26nm in dia possess tripartite ssRNA genome. Non persistent
virus.
 The host range of the virus exceeds 800 spices.
Transmission:

 Not sap transmissible.

 Primary spread through infected daughter suckers.
 Sec. spread through aphids like Aphids gossypi. A. craccivora, Rhophalosiphum
maidis, Myzus persicae etc.
 Cucumis sativus var. khira serves as a reservoir of the virus.
7. Banana Bract Mosaic virus: Banana Bract Mosaic Virus (BBMV)
 The disease is also considered as a disease of economic importance.
 This is commonly known as Kokkan disease since 1966.
 Presently the virus is a major constraint in southern states of India.
 Nendran, Robusta, Poovan, Ney Poovan, Rasthali, Karpooravalli, Monthan and Red
banana are highly susceptible.
Symptoms:

 Spindle shaped pinkish to reddish streaks are seen on pseudostem, midrib,

peduncle.
 In Nendran variety, the orientation of leaf changes giving the appearance of
traveler’s palm.
 Spindle shaped waxy coating appears on lower side of the leaves corresponding with
spindled shaped mosaic pattern on the upper surface.
  In Nendran variety, very short or long peduncle, abortion of bunches and raised corky
growth on the peduncle also observed.
 In Ney Poovan and Nendran varieties, necrotic streaks are seen on leaf,
pseudostem, petiole mid rib and fingers.
 In Red banana and Robusta leaf stripping symptom is common.
 In Robusta, fingers stop to develop and become pencil shaped and locally called as
pencil kai (Pencil sized fruit).
 In Kerala farmers named the disease as Pola roga means disease of pseudostem
in cv. Nendran.
Casual Organism: Banana Bract Mosaic Virus (BBMV)

 The virus is flexuous rod – shaped measuring 750 nm x 15 nm in size.

 Belongs to PVY group.
Transmission:

 Transmission by Pentalonia nigronervosa, Aphis gossypii, A. craccivora

 Non persistent virus
Banana streak Virus

The disease was first noticed on Poyo belong to Cavendish sub group (AAA) and
was first reported in1986 in Dwarf Cavendish and Giant Cavendish. The yield loss was 48%.

Symptoms:

 Initially small, golden yellow dots appear on the leaves.

 Later they extend to form long chlorotic streaks.
 The chlorotic streaks become necrotic giving a blackish appearance on lamia.
 Necrotic streaks are also seen on mid rib pseudostem and petiole.
 Fruits get distorted, plant vigour reduced.
 Virus particles are bacilliform 119 x 30 nm.
 Transmitted by the citrus mealy bug Planococcus citri as non persistent manner.
 The disease is controlled by planting virus free suckers and control of vector.
Management of virus diseases of banana:

 Selection of suckers from healthy garden.

 Use of disease free suckers for planting.
 Plant quarantine. Prohibition of movement of infected suckers to healthy areas.
 Periodical Removal and destruction of infected plants.
 Use of fernoxone 80WP (2,4-D) or Gramaxone 20 EC applied through capsule
applicator or psedostem injection 5 ml (125 mg/lit)
  Control of insect vector using systemic insecticides like carbofuran 3G @ 40g/
Phosphamideon 1ml/lit / Methyl dematon 1ml / li
 Heat treatment of suckers at 400C for one day for banana mosaic.
 Avoidance of cucurbitaceous and leguminous intercrops for banana mosaic.
 Eradication of weed hosts for banana mosaic.
Post Harvest diseases

1. Cigar end rot – Verticilluim theobromae

Wide spread in banana growing areas. In India it has been reported from Andhra
Pradesh and Madhya Pradesh. It can cause serious loss of fruits.

Symptoms:

 It attacks even the immature fingers.

 Sometimes few fingers or all the fingers in the bunch are affected.
 Infection starts from the tip of the fingers.
 The disease causes blackening and shrinkage of the skin and folding of tissues in the
fingers.
 The corrugated necrotic portion is covered with powdery mass of conidiophores and
conidia
 This gives the appearance of grey ash of a cigar end. Hence it is called as Cigar end
rot.
 There is a clear demarcation between infected tissues and healthy tissues.
 Normally less than 2cm length to one third of fruit is affected.
 The internal pulp is reduced to dry fibrous condition known as dry rot.
Casual organism: Verticilluim theobromae

Conidia are hyaline, oblong to cylindrical.

2. Anthracnose/ Black rot/ Fruit rot – Gloeosporium musarum (Collectorichum

musae)
It is a serious disease in all banana growing areas especially in Bihar, Karnataka and
Tamil Nadu. All the varieties are susceptible. Causes severe infection on table varieties.

Symptoms:

 The pathogen attacks the plants at all stages of their growth.

 There are two types of anthracnose infection.
 They are latent and non latent.
 The latent infection originates in the field on uninjured green fruits, when the fruit
reaches maturity typical lesions develop on the fruit.
  Non latent infection starts during or after harvest and develops without dormant
period.
 The disease starts as small, black circular specks on flowers and fruits.
 These specks increase in size and become sunken dark-brown spots with diffused
edges
 Spots coalesce forming larger lesions with bright moist salmon – pink coloured spore
masses.
 The skin of the fruit turns to black, shrivels and covered with pink acervali.
 The latent infected fruits ripe prematurely
 This causes discoloration and rotting of the pulp.
Casual organism: Gloeosporium musarum (Collectorichum musae)

 Mycelium is septate and coloured

 Acervali – round or elongated, erumpent, setae absent
 Conidiophores – Cylindrical, tapered towards apex hyaline, septate, branched
 Conidia – small, hyaline, single celled, aseptate, oval to elliptical, guttulate,
Mode of spread:

 Air – borne conidia

Epidemiology:

 The opt. temperature for disease development is 30- 350C.

 Conidia germinate at 85.7 – 100% RH.
 The disease is more abundant during rainy season.
 The disease is more severe in June – September when the temperature is high
accompanied by showers for number of days.
3. Crown / Stem end rot – Botryodiplodia theobromae (Lasiodiplodia theobromae)
 The fungus invades the fruit through wounds.
 The pulp turns rapidly into black watery mass.
 Greyish black mycelial growth is seen on the fruit surface.
 The skin becomes black, soft and wrinkled.
 The skin later gets encrusted with pycnidia
 Maximum damage to fruits occur at 25 – 300C and 70C
4. Deightoniella leaf and fruit spot / Black spot/ Black tip/ Fruit speckle: Deightoniella
torulosa (Syn. Helminthosporium torulosum)
 The disease is noticed in many places of TN on Robusta variety.
 The disease occurs in three forms namely Black spot on leaves, black tip or black
end on fruits and speckle (fruit spot) on fruits.
  The disease first appears as round pin point black spots on the main veins of lamina
close to the leaf margin.
 These increase in size.
 The spots are separated from healthy tissue by a narrow bright yellow peripheral
band.
 The centre of the spots dry and the pale brown areas extend to the edge of the leaf
margin.
 The infected fruits show a black tip below the perianth advancing along the fruit.
 The diseased areas are surrounded by a narrow grey or yellowish margin.
 The diseased areas may crack when the fruits develop.
 At later stage pale brown mycelial wefts of the fungus is seen on the surface of the
fruit.
Casual Organism: Deightoniella torulosa

Conidiophores arising singly or in small groups, brown, 40–170 × 6–10 µm, straight
or slightly flexuous, occasionally branched, thick-walled, with up to 6 successive percurrent
proliferations near apex, swollen at apex and at point of proliferation to 13–16 µm giving a
‘beaded’ appearance.

Conidia single, distoseptate, olivaceous, smooth, obpyriform to obclavate, straight or

slightly curved, tip rounded, basal cell with a dark protruding scar.

 Conidia spread by air

 Infection requires dew or rain water and is more severe during wet weather.
5. Main stalk rot / Black head – Ceratostomella paradoxa
 The main stalk decay rapidly.
 The affected tissues become soft and black.
 Emit a characteristic sweet smell.
 Black mycelial growth is seen on the rotting area.
 Infection spreads to hands, fruit stalk and to stem end of the fruits causing black
lesions.
 The affected fingers drop off
 The disease spreads to fruit causing uneven black discoloration on the skin.
 The disease causes premature ripening of fruit.
 The pulp is changed to dark brown soft wet mass
6. Pitting disease – Pyricularia grisea
 Round sunken pits appears on the finger stalk, crown pads and fruits.
  The sunken centre is surrounded by reddish brown zone with greenish, narrow water
– soaked halo.
 The finger stalk infection leads to fruit drop.
 The disease causes serious post harvest loss of quality.
Management of post harvest diseases:

 Eradication alternate hosts like Heliconia bihal, H. brasiliensis, Bambusa sp, Musa
spp for the control of cigar end rot
 Young bunches should be opened up to light and air by removing the bract.
 Avoiding of closer spacing.
 Removal of distal floral remnants perianth and male buds regularly bud after all the
hands are opened.
 Removal of infected materials.
 Covering the bunch with polythene sleeves having 4-6% ventilation immediately after
all the hands is opened.
 Harvesting of bunches at correct stage of maturity
 Handling of fruits without causing any wounds, bruise or scratch on fruit skin.
 Preharvest spray with Prochloroz 0.2% (or) Carbendazim (0.1%) Chlorothalonil 0.2%
four times at fortnightly intervals.
 Dehanding, delatexing and dipping in fungicidal solution (TBZ, Benomyl,
Carbendazim),
 Vacuum packing or irradiation can also be followed.
Minor Diseases

Cordana leaf spot – Cordana musae

 The spots are oval pale brown or yellow in colour.

 The centre of the spots is necrotic with delicate concentric zonation.
 The spots are surrounded by yellow halo.
 The spots coalesce to form larger infected zones.
 The underneath of such spots become grayish brown without clear border.
 As the spots grow light fawn coloured lesions with deeply coloured zonation become
prominent.
 The underside of the spots becomes smoky grey due to large number of
conidiophores.
Freckle Leaf spot: Phyllostictinia musarum

 Common in many districts of Tamil Nadu.

 Numerous minute dark brown raised spots are formed on the lower surface of leaf.
  Similar spots are also seen on the fruits giving unsightly appearance.
Bacterial leaf spot – Xanthomonas musicola

 First reported in TN.

 Widespread on Monthan, Peyan, Poovan and Rasthali varieties.
 Chlorotic linear streaks appear along the veins.
 Streaks coalesce to form large chlorotic patches.
-----------------------------------------------------------------------------------------------------
DISEASES OF GUAVA

1. Wilt – Fusarium oxysporum f.sp psidii; Fusarium solani; Macrophomina phaseolina;

Cephalosporium sp
2. Anthracnose – Gloeosporuim psidii
3. Fruit canker – Pestalotiopsis psidii
4. Red rust – Cephaleuros virescens
5. Sooty mould -
6. Post Harvest Diseases
1. Phytophthora fruit rot – Phytophthora nicotinae var. parasitica
2. Dry rot – Diplodia natalensis
3. Phomopsis fruit rot/ Stylar end rot – Phomopsis psidii
4. Anthracnose – Gloeosporium psidii
5. Fruit canker / Scab – Pestalotiopsis psidii
6. Soft watery rot: Botryodiplodia theobromae Pat
7. Botryosphaeria rot: Botryosphaeria ribis Gross. & Duggar
1. Wilt – many fungi
Wilt is the most important disease of guava.
Causes serious loss in guava production
First reported in Allahabad, UP in 1935
Occurs in almost all the guava growing states
More severe in UP and WB
Wilted guava plants have also been reported from Florida, U.S.A. (Webber, 1928),
Taiwan (Leu and Kao, 1979), Cuba (Rodrigvez and Landa, 1977), South Africa (Vos et al.,
2000), Brazil (Junqueira et al., 2001), Pakistan (Ansar et al., 1994), Bangladesh
(Hamiduzzamanet al., 1997), and Canberra, Australia (Lim and Manicom, 2003)
In general, losses due to wilt in guava around Lucknow area vary from 5-60 per cent
(Misra and Shukla, 2002). In West Bengal, the disease reduced the yield by 80 percent
Symptoms:
  First external symptom of the disease is yellowing with slight curling of leaves at the
terminal branches
 Later drowsiness of plants with yellow to reddish discolouration of the leaves
 Premature defoliation
 Twigs become bare and fail to put forth new flushes and eventually dry up.
 Small sized fruits
 Fruits remain under developed, hard and stony
 Later, the entire plant becomes defoliated and eventually dies.
 Finer roots show black streaks on removing the bark.
 The cortical regions of the stem and roots show discolouration and rotting.
 Vascular tissue becomes light brown in colour.
 Partial wilting is also very common
 Wilted plants later show bark splitting.
Casual organism:
The exact causal agent of the disease is still not fully understood. Various pathogens
were involved with the affected plants viz. Fusarium oxysporum f. sp. psidii, F. solani,
Macrophomina phaeseolina, Cephlosporium sp., Gliocladium roseum and Verticillium albo-
atrum etc. have been reported by different workers.
Mode of Spread and survival:
 The disease is soil-borne
 The pathogens survive on dead root bits in soil.
 Spread through movement of plants containing sick soil in virgin areas.
 Short distance spread is by irrigation water
Epidemiology:
 Severity of the disease is more in rainy season.
 Highest incidence is noticed during September- October
 Trees of 6 years of age and above are generally affected.
 More disease in clay loam and sandy loam compared to heavy soil types.
Management:
 Field sanitation
 Removal and destruction of wilted plants
 Forming trenches around the wilted plants
 Avoiding injuries to roots while transplanting
 Maintaining tree vigour with adequate irrigation, manuring, interculture etc.,
 Incorporation of organic maures or green manures
 Use of resistant root stocks like jamun, Psidium cattleianum var. lucidum and a cross
of Psidium malle x P. guajava
  The pits may be treated with formalin and kept covered for about 3 days and
transplanting after two weeks.
 Biological control by Aspergillus niger strain AN-17 is found effective. Aspergillus
niger multiplied in FYM @ 5 kg/pit, applied in the pits while planting new plants.
 In older plants Aspergillus niger enriched FYM can be applied @ 10 kg plant1.
 Partially wilted plants recovered fully after rejuvenation / heavy pruning of the tree
 Trunk injection of 0.1% 8 Quinolonol sulphate
 Soil application of lime or Gypsum @ 4lb / trees
 Severe pruning of affected branches followed by soil drenching with 0.2% Benlate or
Carbendazim 4 times in a year and foliar spraying with Methyl dematon and Zinc
sulphate in a balanced manner.
2. Anthracnose: Gloeosporuim psidii
Common in all the guava growing regions of India
Causes die back, twig blight, wither tip and fruit rot
Symptoms:
Die back phase:
 Young shoots, leaves and fruits are readily attacked, while they are still tender.
 The growing tips turn dark brown
 The black necrotic areas extend backward causing dieback of the plant.
 The plant begins to die backwards form the tip of a branch.
 The fungus develops from the infected twigs and then petiole and young leaves.
 These droop down or fall leaving the dried twigs without leaves.
 The disease appears in epidemic form, during August to September.
Fruit and leaf infection phase:
 Pin-head spots are first seen on unripe fruits, which gradually enlarge.
 They gradually enlarge to form sunken circular, dark brown to black spots or rough
blisters with acervuli in concentric rings.
 Creamy spores are produced in masses in moist weather.
 Several spots coalesce to form bigger lesions.
 The infected area on unripe fruits become corky and hardy, and often develops
cracks.
 Unopened buds and flowers are also affected which causes their shedding.
 On leaves, the fungus causes necrotic lesions at the tip or on the margin.
 These lesions are usually ashy grey and bear fruiting bodies.
Casual Organism: Gloeosporuim psidii
 Acervuli - irregular in shape and approximately 500 µm in diameter. Setae are one to four
septate, brown, slightly swollen at the base, and tapered at the apex.
Conidiophores - hyaline to faintly brown
Conidia - hyaline, unicellular, and either cylindrical with obscure ends or ellipsoidal with a
rounded apex and a narrow, truncate base. They form on in
Mode of spread and survival:
 Survive on mummified fruits and infected tissues of twigs and branches on the tree.
 The conidia are disseminated by wind or rain
Epidemiology:
 The disease develops more rapidly at 300C and 96.1% RH on both ripe and unripe
fruits.
 Closer planting without canopy management
 Lack of timely harvesting
 Availability of free water in the farm of dew or rains encourages spore production and
its dispersal around canopy.
Managements:
 Orchard sanitation
 Pruning and burning of infected twigs.
 Spraying captafol or Zineb or Benomyl
 Pre and post harvest spray with Benlate 0.1%
 Post harvest dip in Benlate or TBZ is also helpfull
3. Fruit canker/ grey blight / leaf spots / scab: Pestalotiopsis psidii
Symptoms:
 The disease generally occurs on green fruits and rarely on leaves.
 Small rusty brown angular spots appear on the leaves.
 Spots enlarge with dark brown margin and grey or ashy centre with acervuli.
 On fruits minute brown or rust coloured, circular necrotic areas develop.
 Later the infection tears open the epidermis in a circinate manner.
 The margin of the lesion is elevated with depressed centre showing crater –like
appearance.
 In older cankers, white mycelium consisting of numerous spores is noticeable.
 In severe cases the fruits break open to expose seeds.
 The fruits become under developed hard malformed and mummified which drop off.
Casual Organism: Pestalotiopsis psidii
Spread and survival
 Survive on infected leaves, twigs and fruits
  Conidia air borne
Management:
 Orchard sanitation
 Pruning and burning of infected twigs.
 Spraying captafol or Zineb or Benomyl
 Pre and post harvest spray with Benlate 0.1%
 Post harvest dip in Benlate or TBZ is also helpfull
4. Algal leaf and Fruit Spot: Cephaleuros virescens
 Orange, rust- coloured, dense, silky tufts appear on both surfaces of leaves
 They turn reddish-purple in colour as they mature
 If tufts are scraped away, a thin gray-white or dark-coloured necrotic spot remains
 Bark on twigs and branches may be cracked
 Young stems and fruit may also be attacked
 Lesions are usually smaller than leaf spots.
 As fruits enlarge, lesions get sunken.
 They are darkish green to brown or black to colour.
 Cracks develop on older blemishes as a result of enlargement of fruits
 The pathogen sporulates readily during the period of high rainfall (July-September)
 The disease incidence is greatest during September.
 Spray Copper oxychloride (0.3%) 3-4 times at an interval of 15 days when initial
symptoms noticed
5. Cercospora Leaf Spot: Cercospora sawadae Yamamoto
 Water soaked, brown irregular patches on the lower surface
 Yellowing on the upper surface of the leaf.
 Older leaves are mostly affected.
 Severely affected leaves curl and subsequently drop off
 Spray mancozeb 0.2% at monthly interval
6. Sooty mould Phragmocapnias betle, Scorias philippensis, Tichomerium grandisporum,
Limacinula musicola, Aithaloderma clavatisporum, Tripospermum sp., Polychaeton sp.,
Leptoxyphium sp. and Conidiocarpus sp.
 Sooty mould proliferates in abundance on the foliage
 Blackish brown velvety thin membranous covering on the leaves
 In severe infection, the foliage appears black due to heavy infection.
 The affected leaves curl and shrivel under dry conditions
 The disease is controlled by controlling the insects by suitable insecticides.
 Foliar spraying of wettable sulphur + chlorpyriphos + Gum Acacia (0.2 + 0.1 +0.3%)
at 15 days interval has been found very effective.
7. Damping off of Seedlings: Rhizoctonia solani Kuhn
 Both pre emergence and post emergence phases are observed.
Pre emergence phase
 The infected seeds and seedlings show water soaked discoloration
 The seed becomes soft and ultimately rots.
 The affected young seedlings are killed before they reach the soil surface.
Post emergence phase
 Hypocotyle at ground level or upper leaves are discolored into yellowish to brown
colour
 It spreads downwards and later turn soft and finally rot and constrict.
 The affected seedlings ultimately topple down and die.
 Strands of mycelium may appear on the surface of the plants under humid
conditions.
Management:
 Diseased seedlings should be removed and burnt.
 Excessive use of water and close planting should be avoided
 Seedbeds should be prepared with proper drainage arrangement.
 Dipping of guava seeds in captan / thiram (0.2%) is advocated
 Drenching of soil with Copper oxychloride (0.3%) helps in reducing the diseases
intensity in nursery.
8. Guava rust: Puccinia psidii G. Wint.
Symptoms
 Orange to red pustules appear on leaves young shoots, flowers and/or fruit
 Leaves distorted
 Defoliation
 Reduced growth
9. Post Harvest Diseases
1. Phytophthora fruit rot – Phytophthora nicotinae var. parasitica
Occurs in Tamil Nadu, AP, Rajasthan, Punjab, Maharashtra and KK
The disease incidence varies from 8-30%, depending upon the weather and foliage
conditions
Symptoms:
 The symptom starts at calyx disc (stylar) end of the fruit during rainy season
 Whitish cottony growth develops and covers almost entire surface rapidly during
humid weather.
 The skin becomes little soft turns light brown to dark brown.
  Affected fruits emit a characteristic unpleasant smell.
 Affected fruits either remain intact on tree or drop off.
 The young or half matured fruits become shrunken, dirty brown, hard and either
remain intact as mummified fruit or drop off.
Epidemiology
 Rain and the wind are important for spread.
 Sporangial production is more on the surface of diseased tissues when the
temperature is near 250 C
 This is an important source of inoculum in the development of epidemics.
 Drops of rain are necessary for the liberation of sporangia from the infected plant
material or soil.
 Under high relative humidity, the fruits near the soil level covered with dense foliage
are most severely affected.
 The fallen fruits are badly affected.
 Cool, wet environmental conditions with high soil moisture favour disease
development.
 High humidity, temperature from 28-320C, poorly drained soils and injuries are
important for initiation of disease.
 Close plantation.
Management:
 Spraying Dithane Z-78 (0.2%) or Ridomil or Aliette (0.2%) or Copper oxychloride
(0.3%) are found effective to control foliar infection.
 Soil drenching with Copper oxychloride (0.3%) or Ridomil or Aliette (0.2%)
 Avoiding unnecessarily dense plant canopy
2. Anthracnose: Gloeosporuim psidii
Symptoms:
 Pin-head spots are first seen on unripe fruits, which gradually enlarge.
 They gradually enlarge to form sunken circular, dark brown to black spots or rough
blisters with acervuli in concentric rings.
 Creamy spores are produced in masses in moist weather.
 Several spots coalesce to form bigger lesions.
 The infected area on unripe fruits become corky and hardy, and often develops
cracks.
Managements:
 Orchard sanitation
 Pruning and burning of infected twigs.
 Spraying captafol or Zineb or Benomyl
  Pre and post harvest spray with Benlate 0.1%
 Post harvest dip in Benlate or TBZ is also helpfull
3. Fruit canker / scab: Pestalotiopsis psidii
Symptoms:
 The disease generally occurs on green fruits.
 On fruits minute brown or rust coloured, circular necrotic areas develop.
 Later the infection tears open the epidermis in a circinate manner.
 The margin of the lesion is elevated with depressed centre showing crater –like
appearance.
 In older cankers, white mycelium consisting of numerous spores is noticeable.
 In severe cases the fruits break open to expose seeds.
 The fruits become under developed hard malformed and mummified which drop off.
Management:
 Orchard sanitation
 Pruning and burning of infected twigs.
 Spraying captafol or Zineb or Benomyl
 Pre and post harvest spray with Benlate 0.1%
 Post harvest dip in Benlate or TBZ is also helpfull
4. Dry fruit rot: Diplodia natalensis
 The disease initially appears as light brown spots at stalk end.
 The infection spreads very quickly covering the entire surface.
 The affected young and mature fruits become dark brown to almost black and
ultimately dry up.
 Numerous pycnidia appear as pin head like structure on the rind of dried fruits.
 Spraying Ziride 0.3% Controls.
5. Phomopsis fruit rot /Stylar end rot: Phomopsis psidii De camara and P. destructim
 Serious losses up to 10% occur
 The disease affects the unripe fruits at the stylar end.
 Discoloration appears in the region lying just below and adjoining the persistent
calyx.
 Small circular white or light brown water soaked lesions are produced.
 Such area gradually increases in size and turn dark brown
 Later the affected area becomes soft
 Covers the entire surface quickly.
 The pulp becomes soft.
 The skin gets wrinkled and loose.
 Diseased area is pulpy and light brown in colour
  Later mycelial growth and pycnidia can be seen on the fruit surface.
 Spray Copper oxychloride (0.3%) or carbendazim or Thiophonate methyl (0.1%)
before onset of winter fruiting.
 Post harvest dip in carbendazim 0.1% controls the disease.
6. Soft watery rot: Botryodiplodia theobromae Pat
Symptoms
The infection starts as a brownish discoloration mostly at the stem end
It gradually proceeds downwards in an irregular wavy manner.
Finally the whole fruit may get involved.
The decay takes in the form of a soft, watery break down
In advanced cases, numerous small pycnidia are produced over the entire surface of the fruit
Avoidance of wounding
Captan found effective against the fungus
Applications of Bacillus subtilis and Streptosporangium pseudovulgare on guava fruits have
been found effective.
7. Botryosphaeria rot: Botryosphaeria ribis Gross. & Duggar
Symptoms
 The infection usually occurs at or near the distal end in the region of persistent calyx.
 The rot begins with a translucent zone around the distal end
 It becomes brown in colour.
 With the progress of the disease, the lesion becomes dark black and wrinkled with
dry skin with translucent margins
 Spraying with copper oxychloride (0.3%)/ dithane M 45 (0.2%) at 15 days interval
controls
Phanerogamic Parasites: Loranthus sp.
Symptoms:
 Guava trees are commonly affected in the neglected orchards.
 They are commonly present on trunk or branches of the tree
 Makes the tree weak.
 The foliage of the infected host plant is sparse and reduced in size
 Its bearing capacity and quality of fruit is considerably lowered.
 The point at which the guava host is penetrated is usually characterized by swollen
growths called “burrs”.
 The burrs help in the identification of sites at which the parasite has entered the host
Management
  The affected branches should be cut sufficiently to completely eradicate the
haustoria.
 Cuttings out affected portion of tree for enough below burrs to remove haustoria
 Cut surface is treated with wound dresser viz. Copper oxychloride (0.39%)
paste/spray to prevent the secondary pathogens infecting through wounds.
 Spraying of emulsion of diesel (30-40%) in soap water is recommended found
affective.
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DISEASES OF POMEGRANATE
1. Cercospora leaf and fruit spot – Pseudocercospora punicae (Cercospora punicae)
 Leaf spots are subcircular to irregular, 1– 4 mm diam
 Initially brown, dingy gray to pale tan and eventually brown to dark brown at the
margin.
 Black elliptic spots appear on the twigs.
 The affected areas in the twigs become flattened and depressed with raised edge.
 The affected fruits show small irregular black spots, which later coalesce into large
spots.
 Conidiophores olive brown, short, fasciculate sparingly septate.
 Conidia hyaline to pale olivaceous cylindric, sub fusoid to sub – clavate septate.
 Primary source of inoculums is infected leaves, diseased plant debris.
 The pathogen spreads through wind borne conidia.
 The disease is serious during September to November.
 The diseased fruits should be collected and destroyed.
 Controlled by thiophanate – Methyl 0.1% or Chlorothalonil 0.2% or Mancozeb 0.2%
2. Bacterial blight – Xanthomonas axonopodis pv. punicae
Bacterial blight has been of wide occurrence in India, resulting in economic losses in
all major pomegranate growing areas of Maharashtra, Karnataka, Andhra Pradesh, Tamil
Nadu, Himachal Pradesh and Rajasthan. Outside India it is reported from Pakistan and
South Africa. The disease affects all plant parts, but is most destructive on fruits.
Symptoms
 The disease initially appears as irregular to circular, translucent, small, dark water
soaked spots on leaves.
 Spots turn to dark brown to black oily and glistering are surrounded by prominent
yellow hallo or water soaked margins.
 Later they become necrotic at the centre.
 Spots coalesce to form large patches.
  Severely infected leaves turn yellow and drop off prematurely.
 Stem infection seen around the nodes which leads to girdling and cracking of nodes.
 On fruits disease starts with water soaked lesions on the skin surface
 Lesions turn dark brown to black, irregular, slightly raised with oily appearance
 Spots enlarge and merge with each other to cover large area
 Fruits split open with L or Y-shaped cracks under severe stages of disease.
 The spots may be covered with thin shining white encrustation consisting of bacteria.

Casual Organism: Xanthomonas axonopodis pv. punicae

Gram-negative, aerobic, rod – shaped, with single polar flagellum
Mode of spread and survival
 This bacterium can survive on infected plant debris lying in and around the orchards
for more than 8 months
 It can also survive for several years on stem cankers on plants or in dormant buds;
these are major sources of primary inoculum
 Survives on fallen leaves and on the trees (120 days)
 Wind splashed rain, insects and contaminated pruning tools help in spreading the
disease locally
 Long distance spread via infected plants, twigs, and fruits
Epidemiology
 Warm and humid condition favours the disease
 Disease build up is rapid during rainy season.
 High disease severity is observed from July to October.
 Temperatures between 25 to 35oC coupled with humidity above 50%, rains and wind
favour rapid disease development.
Management
 Orchard sanitation
 Removal and destruction of infected plant parts by pruning
 Use disease free planting materials
 Spray Bordeaux mixture (0.5% except 1% just after pruning and rest period), altered
with spray of streptocycline (5g/10 l) or 2-bromo, 2-nitro propane-1, 3-diol (5g/10 l)
mixed with copper based formulations like copper oxychloride or copper hydroxide
(20-25g/ 10 l) and spreader sticker (0.5ml/l) at 10-15 days interval depending on
weather conditions.
3. Wilt: (Ceratocystis fimbriata, Xyleborus fornicates and X. perforans Fusarium
oxysporum, Rhizoctonia solani and Meloidogyne incognita)
 Wilt is the second most important disease of pomegranate, adversely affecting
pomegranate cultivation in India. The disease has been reported from Maharashtra,
Karnataka, Andhra Pradesh and Himachal Pradesh. Pomegranate vascular wilt is mainly
caused due to a fungus Ceratocystis fimbriata occasionally by other agents like Fusarium
solani and F. oxysporum. Root rot organisms viz. Macrophomina phaseolina, Phytophthora
nicotianae, Rhizoctonia bataticola; root-knot nematode Meloidogyne incognita and shot hole
borer –Xyleborus fornicates and X. perforans - are the other agents which, alone or in
association with C. fimbriata result in drying and wilting of plants.

Symptoms
 Initially yellowing of leaves is observed in some twigs or branches, followed by
drooping and drying of leaves, finally the entire tree dies.
 Dark bluish-black/grey/brown discolouration of the wood is seen if the pathogen is
Ceratocystis, in Fusarium browning of only xylem is observed.
 Pin holes are observed in the bark and wood when shot hole borers are associated
with wilt.
 Macrophomina sp. destroy the feeder roots and result in root rots
 Rhizoctonia sp. cause girdling of stems in nursery or young plants-resulting in wilting
 In nematode infestations infected plants form knots on the roots
Mode of Spread survival
 Survive as conidia of C. fimbriata, in soil, and plant debris which are primary source
of inoculum.
 C. fimbriata, can also be carried on through air, irrigation /rain water.
Management
 Use disease free planting materials
 Avoid water stagnation and create proper drainage.
 Follow recommended spacing of 4.5 m × 3.0 m in the orchard
 On observing first symptoms of wilt due to fungal pathogens immediately soil drench
with chlorpyriphos 20EC (2.5-4ml/l) + carbendazim 50WP (2g/l) or propiconazole
25EC (2g/l). Use 5-8 l solution/tree. Also drench at least 2-3 healthy plants on all the
four sides around the infected plant/s, repeat the drenching 3-4 times at 20 days
interval.
 For root knot nematodes apply carbofuran 3G @ 40g/plant or phorate 10G @ 25g/
plant in wet soil. Drenching with azadirachtin 1% @ 2ml/l.
 Plant Tagetes erecta (African marigold) between plants in a row, or in a ring, on the
border of plant basin, for more than 4-5 month.
  For shot hole borer (Xyleborus spp.), 10 litres preparation containing red soil (4kg) +
Methyl parathion 4% dust (25g) + Chlorpyriphos 20EC (20ml) + Copper oxychloride
(25 g) needs to be applied on plant base up to 1-2 ft. from second year onwards
4. Collectotrichum Leaf and Fruit Spot – Collectotrichum gloeosporioides
 The disease appears as small regular to irregular dull violet or black spots on the
leaves.
 The spots are surrounded by yellow margin.
 Infected leaves turn yellow and fall off.
 The pathogen spreads wind borne conidia.
 High humidity and temperature of 20 – 270C prevailing during August – September
favours for severe infection.
 Controlled by carbendazim 0.1% or Topsin M 0.1% or Mancozeb 0.2% at fortnightly
interval.
5. Fruit spot – Pestalotiopsis versicolor
 Brown or rust – coloured spots develop on fruits.
 Spots coalesce and cause necrotic patches.
 Centre of the lesions depressed inward with raised margin.
 Severe infections tear open the rind and course discoloration of seeds.
6. Cladosporium fruit rots: Cladosporium oxysporum
 Olive brown spots develop on the fruits later the entire fruit rots.
7. Aspergillus fruit rots – Aspergillus niger; A.flavus; A.niveus; A.versicolor
 Starts as brown discoloration and become blackish brown and slimy and depressed.
 Rotten fruits emit fermented odour.
 Rotten area is covered with fungal growth.
8. Soft Rot – Rhizopus arrhizus
 ‘First small spots appear on the fruits.
 They increase and coalesce.
 Infection restricted to rind.
 The internal content decay into a pulpy mass
 Under dry condition crackings develops at the point of infection
9. Collectotrichum Fruit rot – Collectotrichum gloeosporioides
10. Black heart: Alternaria alternate
11. Phytophthora fruit rot: Phytophthora spp.
12. Botrytis grey mould: Botrytis cineria
-----------------------------------------------------------------------------------------------------------------------
 DISEASES OF PAPAYA
1. Stem rot / Collar rot / Foot rot / Fruit rot / Root rot – Pythium aphanidermatum,
Rhizoctonia solani
2. Anthracnose – Colletotrichum gloeosporioides
3. Powdery mildew – Oidium caricae
4. Phytophthora blight / Fruit rot / Stem rot – Phytophthora nicotianae var. parasitica
5. Asperisporium Black spot - Asperisporium caricae
6. Cornyspora Brown spot - Corynespora cassiicola
7. Papaya Mosaic - Papaya Mosaic Virus
8. Papaya Ring Spot – Papaya Ring Spot Virus
9. Papaya leaf curl – Tobacco leaf curl virus
10. Fruit rots – Many fungi
1. Foot rot / Stem rot – Pythium aphanidermatum and Rhizoctonia solani
The diseases is most serious all over the tropical and sub tropical region of the world.
In India, the disease appears during rainy season and is prevalent throughout the country.
The disease is able to annihilate the entire plantation within a season under favourable
conditions and makes the soil unfit for papaya planting.
Symptoms:
 The disease occurs in both young and old plants and young seedlings in the nursery.
 Foot rot or collar rot or root rot is common in 2-3year old trees.
 Water soaked patches appear on the stem at collar region.
 The patches enlarge and girdle the base of the stem.
 The affected tissues turn dark brown or black and rot.
 The terminal leaves turn yellow wilt and drop.
 Fruits become shriveled and drop off.
 The entire plant topples down and dies due to disintegration of parenchymatous
tissues.
 The internal tissues of the bark become dry brown and honey comb appearance.
 The rotting may extend upward and downward upto the roots.
 The roots also rot and are destroyed.
Casual Organism: Pythium aphanidermatum and Rhizoctonia solani
Pythium aphanidermatum
Mycelium – intracellular, branched, thick, hyaline Coenocytic,
Sporangia – Lobed toruloid vesicles formed, encysted zoospores
Oogonia – Spherical, Smooth walled borne in terminal hyphae
Antheridia – Broadly clavate, terminal or intercalary monoclinous
Oospores – Apleurotic, single
 Mode of spread and survival:
 The pathogen is soil inhabitant.
 Pythium aphanidermatum survives in plant debris in soil producing oospores and
chlamydospores
 Rhizoctonia solani survives in plant debris in soil producing sclerotia
Epidemiology:
 A number of factors viz., inoculum density, soil moisture, temperature, pH, light
intensity, soil microbes determine the disease development and intensity.
 Papaya residue left out in the soil helps in increasing inoculum level and thus the
disease incidence.
 Other predisposing factors are higher nitrogen application, soil conditions, excess soil
moisture due to irrigation and heavy rain forming water logged condition.
 Younger plants are more susceptible than older plants.
Management:
 Use of disease free healthy seedlings
 Avoiding injuries to root and collar region of the stem at the time of planting
 Optimum irrigation
 Provision of adequate drainage facilities
 Avoiding direct contact of stem and irrigation water
 Removal and destruction of infected plants
 Seed treatment with captan @ 4 g / kg or P. fluorescens @ 10 g / kg
 Soil drenching with Bordeaux mixture 1% or COC 0.25% or Metalaxyl 0.1%
 Soil application of P. fluorescens @ 2.5kg /ha
2. Powdery Mildew – Oidium caricae
The disease is prevalent in whole of north India and Maharashtra and Karnataka
also.
Symptoms :
 The disease appears as of white powdery patches on both surfaces of the leaves
 More common on lower surface of the leaves.
 Affected areas become chlorotic and sometimes are surrounded by dark margin.
 Flower stalks and fruits are also affected with similar powdery growth.
 The affected portions of leaves later turn yellow and necrotic.
Casual Organism: Oidium caricae
Obligate parasite, hyaline septate ectophyte,
Conidia hyaline, granular
Mode of spread and survival
 The pathogen survives in infected plants parts.
  Wind –borne conidia
Epidemiology:
 Maximum disease incidence recorded during September – November with a peak in
October.
 The disease decreases with a fall in temperature and an increase in sun shine hours.
 The development of powdery mildew is promoted by high humidity (80-85%) and a
temperature range of 24-26°C.
Management:
 Removal and destruction of affected plant debris
 Spraying wettable sulphur 0.3% or Carbendazim 0.1% or Triademefan 0.1% or
Benomyl 0.1% or Topsin M 0.1%
3. Anthracnose: Colletotrichum gloeosporioides
Anthracnose is prevalent throughout India.
Anthracnose rot attains serious status during transit and storage causing economic
losses.
Symptoms:
 The disease attacks leaves, petiole flower and fruits.
 Initiates as minute dark brown specks on leaves
 They enlarge in size and are surrounded by chlorotic margins
 Spots coalesce covering the entire lamina.
 Shot holes are formed at the centre.
 Necrotic spots are produced on stem.
 Pustules like spots are produced on petioles.
 Flower infection causes flower drop.
 On fruits small circular water soaked dark spots appear.
 The spots enlarge as the fruits mature forming circular sucken lesions.
 The lesions coalesce forming sunken, brown rotting patches.
 The surface of spots has zones formation.
 Acervuli appear as concentric rings.
 The fungus invades fruit tissues producing rot and turning them soft and dark.
 The whole fruit become dirty dark brown and rots.
Causal Organism: Colletotrichum gloeosporioides
Perithecia aggregated, globose to obpyriform, dark brown to black, 85-300 µm in
diameter; the ostioles are periphysate and paraphyses are present.
The asci are 8- with short stalks, clavate to cylindrical, thickened at apex, 35-80 x 8-
14 µm.
The ascospores are hyaline, unicellular, narrowly oval to cylindrical to fusiform.
 Acervuli are produced on lesions, and usually setose.
Conidiophores are cylindrical phialidic.
The conidia are cylindrical with obtuse ends, 9-24 x 3-6 µm, unicellular, hyaline or
faintly brown. Appressoria are 6-20 x 4-12 µm, ovate to obovate, sometimes lobed
Mode of spread and survival:
 The pathogen survives in infected plants parts.
 Spread through conidia by wind and rain splash.
Management:
 Field sanitation
 Removal and destruction infected leaves.
 Spraying carbendazim 0.1% or Daconil 0.2% or Chlorothalonil 0.2% at 15 day
intervals.
4. Phytophthora Blight/ Fruit rot/ Stem rot: Phytophthora nicotianae var. parasitica
Symptoms:
 Small, water soaked discolured spots appear on the stem around fruit and leaf scar,
and on the fruits.
 The spots enlarge and girdle the stem causing wilting of the plants.
 The fruits are attacked at any stage primarily the matured fruits.
 The infected fruits shrivel, turn dark brown become mummified and finally fall down.
 A whitish mycelial mass develop on the rotting fruits and stem.
Mode of spread and survival:
 The pathogen survives in infected plants parts and soil as oospores.
 The pathogen spreads through wind or rain splash.
Epidemiology
 The optimum temp for disease development is 27.80C
Management:
 Removal and destruction of infected plants and fruits,
 Good drainage.
 Spraying COC 0.25% or Mancozeb 0.2%
 Ridomil MZ 0.2% Aliette 0.2% highly effective.
5. Asperisporium Black spot - Asperisporium caricae
Symptoms:
 The first symptoms are scattered small spots, visible on both leaf surfaces.
 On the upper surface, the lesions are round or angular, 1-4 mm in diameter, pale
yellow, with dark margins.
 Later the lesions become necrotic and whitish.
 Black pustules are produced on the abaxial surface of the leaf.
  The lesions are covered with masses of fungal spores which appear as dark dots.
 The disease is more intense on the lower leaves.
 Severe infection causes yellowing and premature shedding of leaves.
 The pustules also occur on fruits.
 The lesions are superficial and do not enter the flesh of the fruit.
 The damage to fruit is entirely cosmetic.
Causal Organism: Asperisporium caricae
Sporodochia hypophyllous, dark blackish brown to black. Stroma well-developed,
erumpent.
Conidiophores closely packed together and covering the surface of the stroma,
usually unbranched, hyaline to olivaceous brown, with several prominent conidial scars at
the apex, up to 45 x 6–9 μm.
Conidia solitary, ellipsoidal, pyriform or clavate, 1-septate, hyaline to mid pale brown,
verrucose,
14–26 x 7–10 μm
Mode of spread and survival:
 The pathogen survives in infected plants parts.
 Spread through conidia by wind and rain splash.
Management:
 Field sanitation
 Removal and destruction infected leaves.
 Spraying carbendazim 0.1% or Daconil 0.2% or Chlorothalonil 0.2% at 15 day
intervals.
6. Corynespora Brown spot - Corynespora cassiicola
 The symptoms occur on the stem, fruits, petioles and leaves.
 On the upper surface, the lesions are greyish to whitish, sunken, with dark margin
and yellow halo.
 Sometimes the centre of the lesion shows crack.
 On the lower surface, the lesions are brown, necrotic, and sunken, with brown-
reddish margins.
 On petioles the lesions are similar to those of the leaves.
 On fruits, black, rounded, sunken, dried dark velvet lesions occur.
 Lesions coalesce and cover extensive areas of the fruit surface.
 Causes post-harvest rot of fruits, entering the fruits through wounds.
Causal Organism: Corynespora cassiicola
 Conidiophores hypophyllous, erect, simple, sparingly septate, dark brown, up to 600
x 4–11 μm, with successive cylindrical proliferations variable in length, 10–100 μm, lighter in
colour towards the apex.
Conidia solitary, obclavate to cylindrical, straight or often slightly curved, tapering
towards the apex, pale olivaceous brown, smooth, 4–20 pseudoseptate, 32–220 x 8–22 μm,
up to 520 μm long in culture, hilum conspicuous
Mode of spread and survival:
 The pathogen survives in infected plants parts.
 Spread through conidia by wind and rain splash.
Management:
 Field sanitation
 Removal and destruction infected leaves.
 Spraying Dithane M-45 (0.2%)
Papaya Ring spot: Papaya Ring spot Virus (PRSV)
Serious disease in India
One of the limiting factors in papaya cultivation
Incidence varies from 20 – 100%
Loss 5-20%
Symptoms:
 Vein clearing, severe mosaic mottling, puckering and blistering
 Deformation of leaves into thread like structure called shoe – string symptoms.
 The margins and distal parts of young leaves roll downwards and inwards.
 The diseased plants are stunted
 The diseased plants are denuded with tuft of small deformed leaves at the apex.
 The petiole length shortened.
 The number of lobes in the leaves increased which become thin and distorted.
 On the fruits, numerous, circular, coalescent concentric ring spots are seen.
 Various degrees of apocarps are also common.
 If affected early no fruit formation
 If affected late a few fruits are produced.
 Fruit size and weight also reduced
Casual Organism:
Belongs to genus Potyvirus of the family Potyviridae. Filamentous flexuous rod
measuring roughly 760 – 800 nm long 12nm wide ss RNA. The virus particle or virion
consists of a nucleocapsid, Virus particles typically contain 94.5% protein and 5.5% nucleic
acid by weight, and have no outer membrane (non-enveloped).
Transmission:
 Mechanical inoculation, grafting and by aphids - Aphis gossypii and Myzus persicae
– must efficient vector.
Neither soil nor seed transmitted.
Alternate hosts – Cucurbita maxima C. moschata, C.pepo var pattypan, Luffa
aegyptiaca etc.
Papaya leaf curl – Tobacco Leaf Curl Virus (TLCV) and Nicotiana Virus 10
 The disease is characterized by severe curling,
 Crinkling, vein clearing and distortion of leaves.
 The leaf lamina is very much reduced.
 The margins are rolled downwards and inwards in the form of inverted cups.
 The veins get thickened and turn dark green.
 The leaves become leathery and brittle.
 Petioles get twisted into Zig – Zag manner.
 The affected trees fail to flower or bear fruits.
Casual Organism: Tobacco Leaf Curl Virus (TLCV) and Nicotiana Virus 10
Belongs to Gemini – virus group
Transmitted by only grafting and white fly Bemisia tabaci.
Alternate hosts: Tobacco, tomato, sunnhemp, chilli, Petunia, Zinnia hollyhock, Datura
stramonuim.
Papaya Mosaic: Papaya Mosaic Virus, Carica virus1
 The disease produces typical mosaic symptoms showing chlorosis with dark green
blisters on the leaves.
 Vector (Aphids): Myzus persicae, Aphis malvae, A. medicaginis, A. gossypii and
Macrosiphum sonchi.
Management of virus diseases:
 Raise papaya seedlings under insect-proof conditions.
 Use disease free seedlings.
 Raise sorghum / maize as barrier crop before planting papaya.
 Removal and destruction infected plants.
 Field sanitation i.e. removal of weeds which act as reservoir hosts or alternate hosts.
 Avoiding intercropping with alternate hosts
 Control insect vectors – Monocrotophos 0.05% or Dimethoate 0.03%
 Transplanting in September and November supplemented with 50g of Neemcake;
100g, of N; 100g of P205 and 200 g of K2O is recommended for the control of PRSV.
 Use of cross protection with mild strain of PRSV also found to be helpful.
Post harvest diseases
1. Anthracnose – Colletotrichum gloeosporioides
 2. Phytophthora blight – Phytophthora nicotianae var. parastica
3. Watery fruit rot – Rhizopus stolonifer
4. Macrophomina fruit rot – Macrophomina phaseolina
5. Stem end rot – Botryodiplodia theobromae
6. Ascochyta fruit rot – Ascochyta caracae
7. Phomopsis fruit rot – Phomopsis caracae papayae
Watery fruit rot – Rhizopus stolonifer
 Irregular water soaked lesions are produced.
 They enlarge and covered with white and dark brown fungal growth.
 The fruits collapsed and become watery and emit a foul odour.
Macrophomina Fruit rot – Macrophomina phaseolina
 Causes 5-20% loss during summer
 Small water soaked circular specks on the fruits.
 They rapidly enlarge and become sunken.
 The pathogen advances deep into the fruit and causes rotting and
disintegration of fruits.
 The fruit pulp turns brown to black.
 The tissues harden and dotted with sclerotic.
Stem end rot – Botryodiplodia thobromae
 The disease mostly attacks ripe and half ripe fruits.
 The rot begins as dark green, water soaked spots.
 The affected portion becomes shriveled and turns dark brown and roughened
due to erumptent pycnidia confluent.
 The spots are surrounded by a dark green water soaked area.
 Infection of fruit stalk results in fruit drop.
Ascochyta fruit rot – Ascochyta caricae
 Attacks half grown or mature fruits.
 Small circular water – soaked spots are produced.
 They become sunken and brownish black.
 The rot spreads outwards and irregularly.
Phomopsis fruit rot – Phomopsis caracae papayae
 The affected area becomes soft and pulpy.
 The rotten area turns brown to black,
 Later they get depressed and cracks.
Minor Diseases
Phyllosticta leaf spot – Phyllosticta sulata
  They spots are small and round or irregular (or) oval or elongated.
 The spots are white at centre and bounded by yellowish or brownish margin
which gradually merges into the green colour.
 Shot holes are seen.
 Spreads though wind.
 Spraying Bordeaux mixture.
Cercospora leaf spot – Cercospora papayae
 The spots are sub circular to irregular.
 Ash coloured on the upper surface.
 Immarginate and in district in lower surface.
Chocolate spot – Strain of Colletotrichum glolosprioides
Chocolate spot: Post-harvest, superficial lesions, seldom slightly sunken, irregular to
rounded, up to 1 cm in diameter, well defined, with characteristic reddish-brown colour. As
the fruit ripens the lesions can either remain superficial or grow and become sunken,
resembling anthracnose. Sometimes these symptoms together with latex exudation on the
centre of the lesion can be observed several days before harvest.

DISEASES OF TOMATO

Tomato has become one of the common vegetables all over the country and is grown
extensively in many parts almost the year and tomato plants are severely affected by various
diseases of microbial origin. There are > 20 diseases of tomato reported from different parts
of the country.
1. Damping off: Pythium aphanidermatum; P. indicum; P. debaryanum; P.ultimum
The disease is most common in many parts of India. Tomato seedlings are highly
susceptible to Damping off. The disease is responsible for poor germination and stand of
seedlings in the nursery. In nursery beds the disease may start in patches and in the course
of 2-4 days the entire lot of seedlings may be destroyed.
Symptoms:
Damping off of tomato and other vegetables occurs in two phases (i) Pre emergence
damping off (ii) Post emergence damping off.
Pre emergence Damping off
 It is a decay of germinating seeds
 The radical and plumule when they come out of the seed undergo complete rotting.
 Seedlings are infected and died before the emergence from the soil
  Causes poor and uneven stand of seedlings in nursery beds
Post emergence Damping off
 Occurs after the emergence of seedlings from the soil
 The affected seedlings become chlorotic and pale green and suddenly collapse
 Dark-brown water-soaked lesions develop at the collar region that rapidly spread
over the entire seedling.
 Affected portion shows shrinking and brown discolouration due to rotting
 Eventually, the lesions girdle the hypocotyl, causing seedlings to wilt and die.
 Brown, water-soaked lesions that start on the roots and later extend up the hypocotyl
characterize post-emergence Damping-Off.
 The root cortex becomes macerated and easily sloughs off.
 The affected seedling become collapsed and toppled down
 Post emergence mortality of seedlings very conspicuous
Causal organism: Pythurin aphanidermatum; P. indicum; P. debaryanum;

P.ultimum

Mycelium - hyaline, coenocytic freely branched – reproduction asexually and

sexually. Sporangia - irregular, lobed – terminal or intercallery – germinate by producing
tubes with vesicle
Zoospores - biflagellate – encysted in ½ hr - germinate to produce germ tube –
mycelium
Sexual – oogonuim and anthridium – oospore – zoosporangium – zoospores –
mycelium.
Mode of survival and spread
 Soil borne. All the causal organisms are soil inhabitants and they build up in soil with
the available hosts. Generally these pathogens have wide host range.
Epidemiology
 Damping-off is generally most severe under conditions of high soil moisture and/or
compaction, overcrowding, poor ventilation and cool, damp, cloudy weather.
 Water-splashing moves infested soil from diseased to healthy plants.
Management
 Partial sterilization of the soil by burning trash or by steam sterilization done
 Provision of better drainage
 Avoidance of same bed for repeated sowing
 Improving the soil texture by adding soil organic amendments
 Preparation of raised nursery beds.
 Thin sowing using optimum seed rate
  Optimum irrigation
 Application of more well decomposed FYM
 Seed treatment with captan or thiram @ 3g or Trichoderma viride @ 4g per kg of
seed
 Soil drenching with Bordeaux mixture 1% or copper oxychloride 0.2% @ 4l / sq.
metre.
 Spray 0.2% Metalaxyl when there is cloudy weather
2. Early Blight: Alternaria solani
Early blight is also called as Alternaria leaf blight or target spot. Early blight is a
common leaf-spotting fungal disease of tomato. This is a common disease of tomato
occurring all over world. In severe attacks the loss may be upto 80%. In India more severe in
June – July crop compared to winter crop.
Symptoms
 The fungus causes leaf blight and may also cause seedling disease, collar rot, stem
canker or fruit rot.
 When seedlings are affected dark brown cankers may develop and girdle stems of
seedlings at the soil line resulting in seedling disease and collar rot.
 The older leaves are first attacked and the disease progresses upwards.
 The first symptom to appear is small, brown to black, round to angular spots on the
leaves.
 As these spots enlarge become irregular, dark brown to black lesions with a series of
dark concentric raised rings of necrotic tissues.
 It gives the characteristic symptom of target effect or target appearance.
 The spots are surrounded by yellow halo due to the production of a toxin called
alternaric acid.
 When several lesions coalesce together, larger area affected giving blight
appearance.
 Severely affected leaves eventually turn brown, shrivel and fall down prematurely.
 Severe infestations of this disease can cause 100% defoliation of the plant.
 Extensive defoliation exposes fruits to sunscald and increases fruit rot.
 Stem lesions on older plants usually remain confined to one side of the stem.
 Stem and petiole show sunken and dark necrotic lesions.
 Fruits are also infected.
 Dark brown – black, sunken, dry, leathery lesions occur most frequently on the stem
end of the fruit and also have a zonate or “target-like” appearance.
 Spots are velvety appearance and may be covered by a blackish “dust,” consisting of
numerous microscopic spores of the fungus.
  Infected fruit often drops off soon after infection.
Causal organism: Alternaria solani
Mycelium: septate, branched, light brown which become dark at age, intercellular and
later intracellular
Conidiophores - dark coloured emerge through stomata.
Conidia - born in chain, club – shaped, muriform with 5-10 cross septa and 1-5
longitudinal septa with long beak.
Mode of survival and spread
 The fungus survives on infected debris in the soil, on seed, on volunteer tomato
plants and other solanaceous hosts, such as Irish potato, eggplant, and black
nightshade.
 Survives in infected plant debris in soil upto 3 years
 The early blight fungus is spread by wind and splashing rain,
 Seed borne also
Epidemiology
 Infection occurs rapidly under warm, humid conditions.
 Thousands of spores are produced in spots of infected leaves that are capable of
causing more infections.
 Plants under stress from nitrogen deficiency, heavy fruit load, or other factors are
most susceptible to the disease.
 Relatively warm temperatures, abundant rainfall, and high relative humidity favor
disease development.
 Water stress also predisposes infection
 Opt. temp 28 – 300C
 The disease becomes serious in frequent rains followed by warm and dry weather.
Management
 Use of disease free seeds
 Field sanitation
 Crop rotation
 Avoid diseased transplants
 Regular irrigation to avoid water stress
 Clipping of lower leaves upto 20 cm ht
 Avoid overhead irrigation
 To prevent rain splash, use mulch.
 Avoid composting diseased plant material.
 Seed treatment with Captan / Thiram (4g / kg).
 Spraying Mancozeb 0.2% or Ziram 0.2% Captan 0.3% Chlorothalonil 0.2%
  Maintain adequate but not excessive soil fertility.
 Proper irrigation and fertilizer management to maintain plant vigour
3. Late blight: Phytophthora infestans
It is prevalent in hilly regions of TN and Karnataka Where rainfall is abundant. It is
very destructive and fast-spreading.
Symptoms
 Affects leaves, stem and fruits
 Indefinite, pale green to brownish, irregular water soaked greasy lesions appear at
the tip and margin of the leaves.
 In moist weather enlarge rapidly with central necrotic tissue changing to dark brown
or black.
 A pale green halo is often observed around the leaf spots as they enlarge.
 The lesions cover whole leaf and spread to petioles.
 During wet weather, lesions on the abaxial surface of the leaf may be covered with a
gray to white moldy growth.
 As the disease progresses, the foliage turn yellow then brown, curls, shrivels, and
dies.
 When several lesions coalesce together, larger area affected giving blight
appearance.
 On petioles and stems, lesions begin as indefinite, water-soaked spots that enlarge
rapidly into brown to black linear elongated lesions that cover large areas of petioles
and stems.
 Affected stems and petioles may eventually collapse at the point of infection, leading
to death of all distal parts of the plant.
 Green fruits are sensitive to this disease
 Brown to green olivaceous greasy spots develop at stem end of the fruits.
 When the infection spreads the fruits rot and become covered with whitish mycelium.
 Infected fruits rapidly deteriorate into foul-smelling masses.
Causal organism: Phytophthora infestans
Mycelium: Hyaline endophytic coenocytic highly branched inter- and intracellular
Sporangiophores: hyaline, branched arise in cluster through stomata.
Sporangia pear- shaped hyaline papillate, multinucleate, zoospores biflagellate (low
temperature) germ tube (high temperature).
Amphigynous antheridium, oogonium spherical.
There are several races of the pathogen found. In India 77 races carrying 8 gene
complexes have been identified.
Mode of survival and Spread
 P. infestans survives in plant debris or on volunteer tomato plants and on perennial
weeds such as nightshade; where both mating types are present (A1 and A2),
P. infestans generates the thick-walled oospores that are long term survival
propagules.
Dispersal of the pathogen is by wind, rain, irrigation water or human assisted via
movement of infested or infected materials such as seed or tools, contacts among leaves
and leaf eating insects etc.
Epidemiology
 Excessive RH (>90%) with suitable temperature are important.
 Opt temp for germination of sporangia by zoospores (direct germination) 12 – 130 C
and by germ tubers (indirect germination) 21 – 240 C.
 Opt temp for growth of the mycelium 16 - 180 C.
 Daytime temperatures between 60 and 70°F, night temperatures between 50 and
60°F, and relative humidity near 100% are the ideal conditions for infection and
spread of late blight disease.
 Predisposing factors include cool, wet weather and high relative humidity, and large,
densely planted crops of tomato.
Late blight disease forecasting systems
1) BLITECAST system
Based on temperature, relative humidity, and rainfall, this is a regional disease
forecasting system used by potato and tomato farmers in the North-eastern United States.
2) NoBLIGHT system (Maine)
This is similar to BLITECAST, but differs in the calculation of severity values for
relative humidity; see Johnson 2005.
3) HYRE system
This is based on temperature and rainfall.
4) WALLIN system
This is based on temperature and relative humidity.
Management
 Seed material should be selected from disease free crop in disease free area.
 Use of disease free transplants
 Field sanitation
 Wider spacing
 Reduced nitrogenous fertilizers
 Avoid use of sprinkler irrigation
 Avoid working with plants when foliage is wet to avoid spreading of disease
  Spraying 1% Bordeaux Mixture in early stages at fortnightly interval when the crop is
at 15-20 cm ht. If weather is more favourable once in 7 days. Later mancozeb 0.25%
is effective.
 Other fungicides recommended are defoliation, zineb 0.2% and Duter 0.1 – 0.2%
Daconil 0.1%, COC (0.25) @ 1.5 – 2.5 kg / ha
4. Septoria leaf spot / Defoliation disease: Septoria lycopersici
It occurs in TN, HP, JK and Karnataka. The disease is as important as the early
blight for causing defoliation.
Symptoms
 Plants are attacked in all stages of growth.
 The disease first appears on the upper surface of the lower leaves after the fruit set.
 Several small round water soaked spots appear on the lower leaves.
 As the spots enlarge they develop dark brown margin and sunken grayish white
centres
 The light-coloured centre of the spots is the most distinctive symptom.
 Minute, black dot like fruiting bodies (pycnidia) of the fungus develop at the centre of
the spots under favourable conditions.
 Heavily infected leaves turn yellow, wither, and eventually fall off.
 Complete defoliation of the affected plants is noticed during rainy weather.
 Stem and flowers are also affected.
 If infected in early growing season, plants can become 100% defoliated before fruit
set.
 During favourable conditions, the disease can cause extensive defoliation, resulting
in sun scalding of fruit and reduction in yield.
Causal organism: Septoria lycopersici
Pycnidia are immersed amphigenous globose honey yellow to brown
Conidia hyaline filiform 2-6 septa.
Mode of survival and Spread
 The fungus survives in infected tomato debris remaining in the soil from a previous
tomato crop or weed hosts like horsenettle.
 It may also be introduced on seed. Both externally and internally seed borne
 Spread by rain splash and windblown water hands and clothing of tomato pickers.
Epidemiology
 Persistent dew or long periods of high humidity at 250C,
 muggy weather or drizzling for 2-3 days
 The disease is favored by moderate temperatures and extended periods of high
relative humidity.
 Management
 Use of disease free seeds
 Field sanitation
 Crop rotation
 Avoid diseased transplants
 Regular irrigation to avoid water stress
 Clipping of lower leaves upto 20 cm ht
 Avoid overhead irrigation
 To prevent rain splash, use mulch.
 Avoid composting diseased plant material.
 Seed treatment with Captan / Thiram (4g / kg).
 Spraying Mancozeb 0.2% or Ziram 0.2% Captan 0.3% Chlorothalonil 0.2%
 Maintain adequate but not excessive soil fertility.
 Proper irrigation and fertilizer management to maintain plant vigour
 Avoid composting diseased plant material.
5. Leaf Mould: Passalora fulva (Fulvia fulva)
It is the most severe foliar pathogen of glass house crop and also causes major
losses in field crop in tropical and subtropical areas during cooler periods when RH is high.
Symptoms
 The first visible symptoms are pale green or yellowish or chlorotic spots on the upper
surface of older leaves.
 Spots are not distinct as they lack a clearly defined border, in contrast with most
other foliar diseases.
 Thus affected leaves may look like they have a general yellowing due to a nutrient
deficiency.
 They spread quickly under favourable conditions of high humidity.
 The pale green or chlorotic spots turn to distinctive yellow spots.
 An olive-green to tan, velvety fungal growth appears on the lower surface of the
spots
 Spores are produced on the lower surface beneath the chlorotic areas producing a
characteristic velvety, olive green mould consisting of light grey fructification
becoming brown or olive green.
 As the disease progresses the leaves wilt and die.
 Under favorable conditions, complete defoliation can occur.
 Occasionally, the fungus attacks stems, blossoms and fruits.
 Green and mature fruit can have a black, leathery rot on the stem end.
Causal organism: Passalora fulva (Fulvia fulva)
 Mode of survival and spread
 Air – borne and sometimes seed borne also.
 The pathogen can survive in soil at least one year as spores or in infested plant
tissue from the previous planting.
 This pathogen can be seed-borne.
 The spores are easily moved by wind and splashing water or rain and tools.
Epidemiology
Opt. temp 22 – 240C and high humidity
The fungus is dependent on high relative humidity and high temperature for disease
development.
Management
 Use of disease free seeds
 Field sanitation
 Crop rotation
 Avoid diseased transplants
 Avoid overcrowding of plants
 Clipping of lower leaves upto 20 cm ht
 Avoid overhead irrigation
 To prevent rain splash, use mulch.
 Seed treatment with Captan / Thiram (4g / kg).
 Spraying Mancozeb 0.2% or Captafol 0.2% Chlorothalonil 0.2% or Carbendazim or
thiophanate- methyl 0.1%
6. Botrytis blight or Gray mould: Botrytis cineria
Symptoms
 Occurs both in the greenhouse and in the field.
 Affected leaves show light tan or gray spots
 The infected areas become covered by a brown to gray fuzzy fungal growth.
 Infected leaves and blossoms wither and die.
 The fungus proceeds into the stem producing tan, elliptical cankers with concentric
rings.
 Stem cankers cause wilting of vines
 Botrytis may develop on dying flowers and subsequently infect the fruit calyx.
 White circular (halo) spots appear on the green fruit and are termed "ghost spots."
 The lesions on ripe fruits appear as irregular light brown to gray spots.
 Later, a dark gray, velvety growth develops on the fruit surface, followed by a watery,
soft rot.
 Infected fruit become soft and watery, and the flesh turns light gray.
 Causal organism: Botrytis cineria
Mycelium is septate and branched, hyaline but become dark in color upon age.
Conidiophores are branched and bear conidia at the apex.
Conidia are continuous or one septate, oblong and dark.
Mode of survival and spread
 The fungus overwinters as sclerotia or as mycelium in plant debris and may be seed
borne.
 The fungus is easily dispersed long distances by wind.
 Also disseminated shorter distances by splashing and windblown rain
Epidemiology
 High relative humidity is necessary for prolific spore production.
 The fungus has a very wide host range that includes many vegetable crops.
 Fungus sporulation and infection, is favored by cool, wet and humid weather.
 The fungus requires a water film of several hours from rain, dew, fog, or irrigation for
spore germination, and a longer period of surface wetness for symptom
development.
 Optimum relative humidity for spore production is about 90%, and most spores are
produced during the night when the temperature is lower and the relative humidity is
higher than during the day.
 Temperatures of 17–23℃ are ideal for disease development.
 Plants approaching maturity are more susceptible. The fungus can also penetrate
dead flower tissue or dying foliage.
 Excessive application of nitrogen makes plants such as young transplants more
susceptible to gray mold.
 Dense plant canopies will limit air movement within the crop, thus creating conditions
for extended surface wetness at night and subsequent increased gray mold severity.
Management
 Use of disease free seeds
 Field sanitation
 Crop rotation
 Avoid diseased transplants
 Avoid overcrowding of plants
 Avoid overhead irrigation
 Avoid excessive application of nitrogen
 To prevent rain splash, use mulch.
 In the greenhouse, maintain a relative humidity of less than 80%, especially during
night.
  Good drainage
 Seed treatment with captan / thiram (4g / kg).
 Spraying Mancozeb 0.2% or Captafol 0.2% Chlorothalonil 0.2% or Bordeaux
Mixture1%
7. Powdery Mildew: Leveillula taurica
More serious in seedlings in Bangalore region of Karnataka. Occurs during July –
October
Symptoms
 Whitish floury patches appear on the lower surface of the leaves stems
 Corresponding upper surface shows bright yellow spots
 Infected leaves may be dwarfed, stiff, and narrow followed by drying of leaves.
 The fungus progressively attacks new leaves, spreading over leaves, stems, twigs,
and even the fruit.
 Terminal growth of the affected shoot is stunted or killed.
 The fruit yield is reduced and the affected fruits are smaller in size.
Causal organism: Leveillula taurica
Oidiopsis type, endophytic,
Mycelium: hyaline, septate, inter and intracellular,
Conidiophores, hyaline septate, arise through stomata
Conidia cleavate hyaline
Mode of survival and spread:
 Survives as ascospores in infected plant debris which serve as primary inoculum.
 The secondary spread is through air borne conidia.
Epidemiology
 Dry weather coupled with low humidity is favourable for initiation and spread.
 Infection in favoured by temperature range of 18 – 240 C and RH 70 – 100%.
Management
 Field sanitation
 Destruction of collateral weed hosts.
 Spraying wettable Sulphur 0.2% or karathane or Carbendazim or Benomyl or
thiophanate- methyl 0.1%
8. Buck Eye Rot: Phytophthora parasitica
Fruit rot or buckeye rot is a serious disease in all the tomato growing areas. The
disease is serious is hilly tract of TN, UP & KK. Spoils 30 – 40% fruits before harvest. All the
commercial varieties are susceptible. Loss is 35 – 40 %. Fruit rot upto 90%
Symptoms
 The pathogen does not affect the foliage and thus the disease is distinct from late
blight.
 Buckeye rot is a destructive fruit rot of green or ripe fruit.
 The fruits which contact the soil or where soil frequently splashes onto fruits are
frequently affected
 Small grayish-green or pale brown circular water-soaked spots are produced on
immature and mature green fruit at blossom end.
 The spot rapidly enlarges to cover up to half of the fruit diameter.
 The rot then appears brown with definite concentric or target-like appearance that
resembles buckeye chestnut.
 The affected fruits shrink and mummify
 White flocculent superficial mycelial growth develops profusely in warm and humid
conditions.
 The fruits remain firm and retain the shape till they are spoiled by other saprophytes.
 Over time, infected fruit will become soft and mushy.
Causal organism: Phytophthora parasitica
Similar to late blight pathogen Phytophthora infestans

Mode of survival and spread:

 The fungus survives as chlamydospores in the soil and infected plant debris.
 The secondary spread by surface water and rain splash
Epidemiology
 The fungi are common in many soils.
 The disease is most severe in poorly drained areas.
 The disease is most common during periods of prolonged warm, wet weather
 Peppers are also susceptible to this disease.
Management
 Use of disease free seeds
 Use deep tillage to reduce soil compaction and improve internal soil drainage.
 Field sanitation
 Rotate with corn or other grass crops
 Avoid diseased transplants
 Avoid overcrowding of plants
 Avoid overhead irrigation
 Mulch beneath plants to reduce soil contact with fruit.
 Staking plants and removing foliage and fruits upto a height 15-30 cm from ground
level
  Good drainage
 Seed treatment with captan / thiram (4g / kg).
 Spraying Mancozeb 0.2% or Captafol 0.3% or Chlorothalonil 0.2% or Bordeaux
Mixture1% or copper oxychloride 0.25% or Ridomil M2 (0.25%) will give fairly good
control of buckeye rot.
9. Anthracnose: Colletotrichum phomoides, C. coccodes, C. dematium, and C.
gloeosporioides
Symptoms
 Anthracnose is a common and widespread rot of ripe or overripe tomato fruit.
 Green fruits are infected but do not show symptoms until ripening.
 Fruit becomes more susceptible as they approach maturity.
 At first, infected fruit show small, circular, slightly sunken, water soaked spots.
 These spots enlarge, become darken, depressed and have concentric rings.
 Masses of the pink fruiting bodies of the fungus can be seen on the surface of the
lesions in moist weather.
 During humid weather, masses of buff-colored conidia are extruded from the fruiting
structure giving the lesion creamy-pink coloration.
 Under warm and humid conditions, the fungus penetrates the fruit, completely
destroying it. Secondary rotting organisms may invade anthracnose lesions to
completely rot.
Causal organism: Colletotrichum phomoides, C. coccodes, C. dematium, and
C. gloeosporioides
Mode of survival and spread
 The fungus survives the winter on diseased tomato vines, in the soil, and in seeds.
 These acervuli survive in soil for three years and cause infections either directly or by
producing secondary spores.
 The fungus then spreads from infected to healthy fruit as spores are splashed by rain
or overhead irrigation, or by pickers working wet plants.
Epidemiology
 Anthracnose is favored by warm rainy weather, overhead irrigation, and heavy
defoliation from foliar disease.
Management
 Use of disease free seeds
 Field sanitation
 Avoid overcrowding of plants
 Avoid overhead irrigation
 Use drip irrigation to reduce moisture levels on fruit and humidity in the plant canopy.
  Mulching prevents splashing of spores from the soil onto the fruits.
 Keep the garden weed free
 Staking plants
 Harvest fruit as soon as possible after ripening.
 Seed treatment with captan / thiram (4g / kg).
 Seed treatment by soaking in hot water (122 ºF) for 25 minutes to destroy the fungus.
 Spraying Mancozeb 0.2% or Captafol 0.3% or Chlorothalonil 0.2% will give fairly
good control of anthracnose.
10. Fusarium wilt: Fusarium oxysporum f.sp. lycopersici
This is one of the most common and important wilt diseases of tomatoes around the
world
Symptom
 Fusarium usually enters its host through feeder roots and subsequently multiplies
and colonizes the food and water conducting vessels of the plant.
 Infection may occur at any time during the life of the plant.
 The affected plants show clearing of veinlets and chlorosis followed by yellowing of
lower leaves
 Symptoms can be seen on one side of a leaf midrib, or on a single branch, or on
several branches on one side of the plant, or on all the lower branches.
 Drooping of the petioles downwards called epinasty symptom.
 The drooping starts from bottom and proceeds to top until all the foliage is killed and
the plant dies.
 The leaves gradually wilt and die.
 In due course entire plant wilts.
 The affected plants are stunted in growth.
 Affected plants die early and produce few, if any, fruit.
 Fruits ripe prematurely
 Dark brown or reddish brown or black discolouration of vascular tissues in the form of
streaks can be seen from the base of the stem upto the root tip.
 Microscopic examination of sections of the infected tissues would reveal the fungal
hyphae both as inter and intracellular.
 In the final stage rotting of roots may be observed but no bark shredding.
 The discoloration can extend from the roots upto the stem through the branches and
into the petioles of the plant.
Causal organism: Fusarium oxysporum f.sp. lycopersici
Mycelium: Hyaline at first creamy at later, septate, inter and intracellular
Microconidia produced in chain, hyaline spherical
 Macroconidia: sickle shaped, 3-5 celled, hyaline
Chlamydospores terminal or intercalary, spherical
It attacks only Lycopersicon spp.
Mode of survival and spread
 The fungus survives as chlamydospores and persists indefinitely in infested field soil.
 The fungus is also seed borne and is thought to spread long distances in this manner
 Persists on plant debris and weed hosts
 The fungus spread by anything that moves soil about, including irrigation.
Epidemiology
 The disease is most serious in sandy soils and at temperatures between 80-90o F.
 Soils become infested by planting infected transplants and from movement of
infested soil by wind and water erosion or on farm implements.
 It is favoured by sandy, acid soils, low soil moisture, hot weather, low RH, and short
day length
 The disease is most severe when air and soil temperatures are between 780 and
90o F
 More likely to occur in poorly drained soil.
 Soil temperature of 20-30º C, hot and dry periods followed by rains,
 Alternating high and low soil temperature and humidity levels
 Presence of root knot nematodes increase the disease development
Management
 Use of disease-free seeds, transplants and soil.
 Field sanitation
 Application of Lime in acid soils to raise the pH to 6.5-7
 Use nitrate forms of nitrogen fertilizer and avoid ammonium forms.
 Avoid flood irrigation because these water supplies can be contaminated with the
fungus and spread the disease.
 Long-term rotations with cereals (five to seven years out of tomato) may help.
 Crop rotation should be used in conjunction with varietal resistance to maintain
sustainable control and limit the development of new races.
 Control of nematodes with carbofuran or Nemagon
 Seed treatment with Thiram or Carbendazim or Trichoderma viride
 Soil mulch with polyethylene sheets in hottest months
 Apply FYM or organic amendments
 Apply 2.5 kg/ha of Trichoderma viride commercial formulation with 50kg farmyard
manure
 Soil fumigation with methyl bromide in controlled condition
  Spot drenching with Carbendazim 0.1%
11. Verticillium Wilt: Verticillium albo-atrum, V. dahliae
These pathogens cause economically important disease of tomato.
Symptoms
 The affected plants are stunted in growth.
 Yellow blotches develop on lower leaves;
 Yellowing of lower leaves progress slowly upward
 There is necrosis of veins surrounded with chlorotic or tan-colored areas at the
margins of leaf tips.
 This discoloration may become characteristic V-shaped or fan-shaped and more
yellow over time.
 The leaves rapidly turn completely yellow, wither, and drop off
 Unlike Fusarium wilt, symptoms of Verticillium wilt do not progress along one side of
a leaflet, branch, or plant.
 Vascular brown discolouration can be seen on cutting through stem or roots.
 Many adventitious roots develop at the base of the stem.
Fusarium wilt Verticillium wilt
No interveinal chlorosis. Develops more Develops interveinal chlorosis with less
intense yellowing of leaves intense yellowing of leaves
Slow development Rapid development
Dark brown or black vascular tissue Light brown vascular tissue
Prefers light sandy soil Prefers heavy soil
More localized distribution within an area Wide distribution
Requires higher optimum temperature Requires low optimum temperature

Causal organism: Verticillium albo-atrum, V. dahliae

Mycelium first prostrate and hyaline become floccose and white to grey.
Microsclerotia –dark resting spores.
Mode of survival and spread
 The fungus is soil-borne and can persist for many years in soil and plant debris.
 The fungus survives as microsclerotia in infected crop debris and can attack many
other plants.
Epidemiology
 This disease is favoured by long-term tomato cultivation, cool weather and high soil
pH. Verticillium wilt is increased by root wounding from cultivators or root-knot
nematode feeding.
 Management
 Field sanitation
 Long-term rotations with cereals and pulses
 Removal of weed host plants
 Seed treatment with Thiram or Carbendazim or Trichoderma viride
 Soil mulch with polyethylene sheets in hottest months
 Apply FYM or organic amendments
 Apply 2.5 kg of Trichoderma viride/ha commercial formulation with 50kg farmyard
manure
 Soil fumigation with methyl bromide in controlled condition
 Spot drenching with Carbendazim 0.1%
12. Bacterial Wilt: Ralstonia solanacearum
Bacterial wilt is a devastating disease of tomato, tobacco, and potato. It is also called
as southern bacterial wilt. Wide spread worldwide. Most severe in tropical and subtropical
climates with high rainfall. In India total loss has seen reported. In Philippines 15% loss has
been reported in India it is a threat to tomato in KK, MP Maharashtra and WB.
Symptoms
 Sudden drooping of leaves with rapid wilting and death of plants without yellowing or
spotting of the foliage
 The lower leaves may droop first before wilting occurs.
 Downward curling of leaves occurs.
 There may be excessive production of adventitious roots along the stem above the
soil.
 The pith appears as water soaked in early stages; later, the pith will turn brown and
sometimes become hollow.
 The discoloration of pith distinguishes this disease from Fusarium and Verticillium
wilt.
 The vascular system become yellowish brown
 Stems cut cross-wise may ooze a thick, off-white to yellowish liquid.
 Sticking the cut end of an infected stem partially into a glass of water reveals a milky-
white stream of bacteria in the water within three to five minutes.
 The root system may also develop a brownish rot as the plant dies.
Causal organism: Ralstonia solanacearum
Rod shaped Gram negative 1-4 flagellate
Three major races
Race l infects tomato, potato, chilli, egg plant etc.
Race 2 Infects bananas and Heliconia sp.
 Race 3 infects potato alone.
Mode of survival and spread
 The bacterium can survive in the soil for months, especially in well-drained soils.
 It is spread by soil and water movement or by diseased plants or infected debris or
equipment.
 Bacteria infect plants through the roots or stem, most often where tissue has been
injured by cultivating, or by some other physical means such as nematodes.
Management
 Use of disease-free seeds, transplants and soil.
 Field sanitation
 Avoid flood irrigation because these water supplies can spread the disease.
 Long-term rotations with cereals.
 Grow on raised beds to promote drainage
 Application of Bleaching powder @ 15 kg / ha before transplanting.
 Soil fumigation with methyl bromide in controlled condition
13. Bacterial spot: Xanthomonas euvesicatoria (Xanthomonas axonopodis pv. vesicatoria
Bacterial spot reduces tomato yield and quality by defoliation and spotting of fruit.
Symptoms
 Leaves, stems, and fruit may be infected at any growth stage
 Small, brown, water soaked, circular to irregular spots appear on stem and leaves.
 As lesions enlarge, they often become surrounded by a yellow halo.
 They become dried looking sunken and grayish brown in colour.
 Leaf spots appear greasy when leaves are wet
 If spots are numerous, they coalesce, and leaves wither and turn brown
 A general yellowing of heavily spotted areas on leaves occurs, followed by leaf
scorch.
 Bacterial ooze may form and dry to form a creamy film
 Spots on green fruit first appear as black, raised, pimple-like dots surrounded by
water-soaked areas.
 As the spots enlarge they become gray-brown and corky scabby with sunken, pitted
centres irregular margins and raised haloes
Causal organism: Xanthomonas euvesicatoria (Xanthomonas axonopodis pv.
vesicatoria
Rod shaped, Gram positive
Mode of survival and spread
  The bacterium overwinters on the surface of seeds (seed borne), in infected debris,
and in soil.
 The organism survives in alternate hosts, on volunteer tomato plants and on infected
plant debris.
Epidemiology
 Rainfall and humidity levels promote disease development.
 Warm, rainy weather favors rapid spread of bacterial spot.
 Moist weather and splattering rains are conducive to disease development.
 Prolonged heavy rainfall, high RH and temp around 240C
Management
 Use of disease-free seeds and transplants
 Field sanitation
 Crop rotation
 Avoid working in plantings when foliage is wet.
 Soaking seed in a solution of one part household bleach (5.25% sodium
hypochlorite) and two parts water for one minute followed by rinsing and drying. (or)
Disinfect suspect seed with 1% bleach for 10 minutes.
 Hot-water treatment involves soaking seed at exactly 122°F for 25-30 minutes
followed by cooling and drying.
 Using drip irrigation reduces bacterial spread and the leaf wetness periods that favor
infection compared to sprinkler irrigation
 Spraying with Agrimycin-100 (100 ppm) thrice at 10 days intervals effectively controls
the disease.
14. Bacterial canker: Clavibacter michiganensis sub sp. michiganensis
One of the major diseases of tomato in the world. Yield reduction up to 70% in USA.
Symptoms
 Bacterial canker can be difficult to diagnose because a variety of symptoms may
occur and the canker symptom (stem lesion) is not always produced.
 Plants affected in early stage wilt and die and the disease may be confused with
bacterial wilt.
 Plants that are infected early are killed while those that become infected later
develop leaf scorch and fruit symptoms.
 Infected older plants develop a leaf scorch (browning) at the margin and begin die
back.
 The petioles droop down.
 The leaves eventually become brittle and dry, and drop from the plant.
 Long brownish stripes appear on the stem, shoots and petioles
 They may split open to show creamy white or yellow or reddish brown discoloured
cavities in the pith and bacterial exudation.
 Eventually the pith becomes reddish brown in color and mealy in texture.
 Whitish cankers develop on stems and petioles under certain conditions.
 Infected fruits show small round raised white spots which later develop light brown
roughened centres surrounded by a white halo resembling the characteristic bird’s
eye.
Causal organism: Clavibacter michiganensis sub sp. michiganensis
Coccoid and curved or straight rods, Non motile, Gram positive
Mode of survival and spread
 Survive for short periods in soil, contaminated greenhouse structures, and wooden
tomato stakes
 The bacterium survives for longer periods in plant debris, Solanaceous weeds and
volunteer tomato plants.
 The bacterium can survive in soil on infested plant material for at least 1 year.
 The bacterium is carried on seed (Internal and external seed borne) and on
transplants.
 In the field, the bacterium is spread by splashing water and wind-driven rain;
contaminated equipment; and by pruning, staking, and harvesting activities.
Epidemiology
 Disease development is favored by moderately high temperatures (75 to 850 F) and
wet, humid conditions.
 Presence of root knot nematode increases the severity of the disease.
Management
 Use of disease-free seeds and transplants
 Field sanitation
 Crop rotation with non-host crop helps in reducing the disease incidence.
 Avoid working in plantings when foliage is wet.
 Using drip irrigation reduces bacterial spread and the leaf wetness periods that favor
infection compared to sprinkler irrigation
 Avoid overhead irrigation
 Sanitize tools such as pruning shears and stakes.
 Use mulch to prevent rain splash.
 Hot water treatment of seeds at 50°C for 25 minutes is effective.
 Seed treatment with 5% HCL for 5 hr (or) hot water at 560C for 30 min (or) 1.05% Na
hypchlorate for 40 min
 Spraying streptomycin followed by CuSO4
 Virus diseases
15. Mosaic: TMV (ToMV), CMV, PVX, PVY
Symptoms
 Tobacco mosaic virus (TMV), also known as tomato mosaic virus (ToMV)
 Symptoms of the disease are variable and depend on the virus strain present, the
tomato variety grown, and temperature.
 Generally the virus causes mottled areas of light and dark green color called mosaic
mottling
 Infected leaves may also be small, curled, and malformed.
 Sometimes younger leaves become distorted crinkled.
 In severe cases entire leaf area become pale yellow to white with scattered small
dark green islands.
 Sometimes the leaflets become indented resulting in "fern leaf" symptoms.
 Affected plants are stunted.
 Affected stems are brittle, easily broken, and contain brown areas in the pith and
cortex.
 Ordinarily the fruit does not show any marked disfiguration.
 Some strains (referred to as the acuba strains) may cause a striking yellow mosaic,
whereas other strains may cause leaf malformation and "fern leafing," suggestive of
cucumber mosaic virus infection.
 The most pronounced symptom produced by CMV is the extremely distorted,
extreme filiformity or shoe string-like leaves
 Both the number and size of the fruit are reduced.
 Occasionally fruit mottling and bronzing, develop.
 At times, fruit may develop a "brown wall" or "internal browning" defects.
 Crop losses upto 20% of the world production
 Many host range N. glutinosa, N. tabacum, D.stramonum, G. Globosa, etc.,
 TMV is spread primarily by humans handling infected plants and mechanically
transmitting the virus to healthy plants via the sap.
 TMV can be seed borne in tomato upto 94%
 CMY is transmitted by aphids in a non persistent manner.
 Management: Use of disease free seeds
 Seed treatment with 10% Trisodium phosphate Na3PO4 for 20 min plus hot water
treatment at 70 0 C for 2 – 4 days.
16. Tomato spotted wilt: Tomato Spotted Wilt Virus (TSWV)
 Tomato spotted wilt, caused by the virus Tomato spotted wilt virus (TSWV), is one of
the most economically devastating diseases of tomato around the world. TSWV was first
discovered in Australia in 1919. Tomato production losses of 75–100% from tomato spotted
wilt have been reported in Hawaii. This is the most serious virus disease of tomatoes in
recent years, causing widespread damage to both commercial and home garden plantings.
Infected fruit cannot be sold.
Symptoms
 The tomato plants are affected at all stages of growth but seedlings are more
vulnerable.
 Produce symptoms on leaves stem and fruits.
 The first observable symptoms are small, chlorotic lesions on the leaflets that often
have a darker green “halo.”
 These chlorotic lesions may coalesce and become necrotic, giving the foliage a
“bronzed” appearance.
 These necrotic regions spread to terminal shoots, causing them to “wilt.”
 Tops of plants may suddenly die back (snuff-top) and some plants may wilt on one
side, suggesting a wilt disease.
 Leaves curl inwards and downwards
 Stunting of plants
 Cessation of growth
 Under favourable condition bronzing leads to necrosis which continues and leads to
death of the plant.
 Early-infected plants produce few or no fruit while later-infected plants produce
discoloured fruit.
 Green fruit may have slightly raised bumps with faint, light green to whitish circles.
 The circles and rings are more obvious as the fruit ripens, staying yellowish while the
fruit turns red
 The most conspicuous symptoms are discolored blotches or concentric rings on the
fruit
 Disease infection leads to reduction in size of the fruits.
 The virus infection causes asymmetrical growth of plant. i.e. one side dry and other
side will not dry.

Early blight or Alternaria leaf spot TSWV

Necrotic lesions with concentric rings Necrotic lesions without concentric rings
Yellow halo present surrounding the lesions No Yellow halo
 No bronzing Bronzing present
No death of plant or asymmetrical growth Death of plant or asymmetrical growth is
present
Brown necrotic lesion in the form of Brown necrotic lesion in the form of concentric
concentric rings are present on fruits rings are absent on fruits
Raised bumps with faint, light green to Green fruit may have slightly raised bumps
whitish circles are absent on Green fruit with faint, light green to whitish circles.
Yellowish circles and rings are absent on Yellowish circles and rings are more obvious
the red fruits on the red fruits
Discolored blotches or rings are absent on The most conspicuous symptoms are
the fruits discolored blotches or rings on the fruit

Causal organism: Tomato Spotted Wilt Virus (TSWV)

Isometric particles 70 – 90nm in dia
Transmission
TSWV is transmitted by several species of thrips, including common blossom thrips
(Frankliniella schultzei), western flower thrips (F. occidentalis), chilli thrips (Scirtothrips
dorsalis), and onion thrips (T. tabaci).
Nympus acqure the virus from inf. palnt but adults transmit the virus. Long latent
period in vector. 4-18 days. Min Ac. feeding period 15 min % of transmission increased by
length of feeding period. Seed transn. also recorded but only 1% also sap transmissible.
Management
 New crop should not be planted near older crops or other susceptible crop (egg
plant, chilli potato)
 Field sanitation – removal of infected plants, alternate hosts etc.
 Raising barriers crop with Crotalaria junacel
 Using antiviral principles.
 Leaf extracts of sorghum, prosopis, Mirabilis jalapa contain AVP which effectively
control the disease.
 Leaf extracts of 10% is prepared.
 1 Kg of dried leaf powder – 5 l water – 600C – 30 min - filter – add 5 lit of water.
 Sprayed 15, 25, 35 and 45 DAP.
 Checking the population of thrips can reduce the disease incidence. 2-3 foliar sprays
with Dimethoate (0.05%) or Monocrotophos (0.05%) at 10 days intervals controls the
thrips population.
17. Tomato yellow leaf curl: Tomato yellow leaf curl virus (TYLCV)
 Tomato yellow leaf curl is a most destructive viral disease of tomato caused by
Tomato yellow leaf curl virus (TYLCV). In tropical and subtropical regions, total losses of
tomato crops have been reported. TYLCV is widespread and can be found in most
places where tomato is grown. Incidence is more in summer months since the vector
population will be more. Losses are high when crops are affected during the half of their
growing period. (20 DAP – 92% yield less; 35 DAP – 74% yield less and 50 DAP – 29%
yield less.
Symptoms
 Characteristic symptoms are dwarfing of plants.
 Interveinall chlorosis, mosaic mottling, vein clearing and crinkling of leaves
 Smaller leaves than normal, upward rolling giving them a cup-like appearance,
puckering of the leaves.
 On the under surface of the leaves there will be small leaf like out growth called
enations
 The veins become thickened.
 The leaves become leathery and brittle.
 Reduction in of nodes and internodes length
 The infected plants remain stunted
 The infected plants look pale and produce more lateral branches giving a bushy
appearance.
 Abscission of flowers and fruit is common.
 If tomato plants are infected early in their growth, there may be no fruit formed.
Causal organism: Tomato yellow leaf curl virus (TYLCV)
Gemini virus group
Transmission
No sap transmission Transmission by white flies Bemissia tabaci. A single
viruliferous insect is enough for successful transmission. Females are more efficient than
males because females are more voracious feeder. Minimum acquisition feeding period is
30 min. Incubation periods in the body of the vector are 6 hr. Inoculation feeding period is 30
min.
It has wide host range including tobacco, chilli papaya Acanthospermum hispidum.
Physalis Crotalaria etc.
Management
 The affected plants should be removed and destroyed.
 Alternate or collateral hosts harbouring the virus should be removed
 Checking the white fly population can reduce the disease incidence.
  Soil application of granular insecticide like Furadan (1 kg a.i./ha) at the time of
sowing seeds in the nursery bed checks whitefly population. Another dose of
Furadan (1.5 kg a.i./ha) is given one week after transplanting.
 2-3 foliar sprays with Dimethoate (0.05%) or Monocrotophos (0.05%) at 10 days
intervals controls the white fly population.
 Barrier crops like maize, jowar, bajra are good to protect the crop from TLCV
infection. Five or six rows of these crops all around the main tomato plot should be
sown at least 50-60 days before transplanting of tomato. These crops check
incoming viruliferous whiteflies from entering into tomato crop.
 Use of polythene mulching or reflective mulches (aluminum or silver-colored) in the
soil just before transplanting of tomato. Polythene sheets of white, blue, grey and
black colours are effective.
 Combined application of polythene mulching and Furadan application in the soil is
recommended.
18. Tomato Big bud: Candidatus Phytoplasma
 Infected plants are scattered in field
 The first indication of infection appears at the tips of the actively growing shoots.
 The youngest fruit truss, assumes an upright position.
 The buds on the truss also point in a vertical direction,
 Vein clearing and chlorosis of leaves
 Stunted growth with shortened internodes and thickened stem.
 Proliferation of auxiliary shoots with numerous small more rounded, thin leaves giving
rosette appearance.
 The calyx segments remain united almost to the tips, and the whole calyx enlarges to
form like a bladder with a toothed opening at the top.
 The affected leaves become yellow-green and roll along their margins.
 The size of the leaves reduces as the disease advances.
 Fruit that is well developed but still green at the time of infection becomes hard and
tough and colours extremely slowly or not at all.
 Occasionally leaves and auxillary shoots show purple pigmentation.
 Transmitted by leafhopper Orosius argenatatus, grafting, dodder etc
 Controlled by rouging and insecticide spraying.
------------------------------------------------------------------------------------------------------
 DISEASES OF BRINJAL
Damping off: Pythurin aphanidermatum; P. indicum; P. debaryanum; P.ultimum
The disease is most common in many parts of India.
Brinjal seedlings are also susceptible to Damping off.
The disease is responsible for poor germination and stand of seedlings in the

nursery.

In nursery beds the disease may start in patches and in the course of 2-4 days the
entire lot of seedlings may be destroyed.
Symptoms:
Damping off of tomato and other vegetables occurs in two phases (i) Pre emergence
damping off (ii) Post emergence damping off.
Pre emergence Damping off
 It is a decay of germinating seeds
 The radical and plumule when they come out of the seed undergo complete rotting.
 Seedlings are infected and died before the emergence from the soil
 Causes poor and uneven stand of seedlings in nursery beds
Post emergence Damping off
 Occurs after the emergence of seedlings from the soil
 The affected seedlings become chlorotic and pale green and suddenly collapse
 Dark-brown water-soaked lesions develop at the collar region that rapidly spread
over the entire seedling.
 Affected portion shows shrinking and brown discolouration due to rotting
 Eventually, the lesions girdle the hypocotyl, causing seedlings to wilt and die.
 Brown, water-soaked lesions that start on the roots and later extend up the hypocotyl
characterize post-emergence Damping-Off.
 The root cortex becomes macerated and easily sloughs off.
 The affected seedling become collapsed and toppled down
 Post emergence mortality of seedlings very conspicuous
Causal organism: Pythurin aphanidermatum; P. indicum; P. debaryanum;

P.ultimum

Mycelium - hyaline, coenocytic freely branched – reproduction asexually and

sexually. Sporangia - irregular, lobed – terminal or intercalary – germinate by producing
tubes with vesicle
Zoospores - biflagellate – encysted in ½ hr - germinate to produce germ tube –
mycelium
 Sexual – oogonuim and anthridium – oospore – zoosporangium – zoospores –
mycelium.
Mode of survival and spread
 Soil borne. All the causal organisms are soil inhabitants and they build up in soil with
the available hosts. Generally these pathogens have wide host range.
Epidemiology
 Damping-off is generally most severe under conditions of high soil moisture and/or
compaction, overcrowding, poor ventilation and cool, damp, cloudy weather.
 Water-splashing moves infested soil from diseased to healthy plants.
Management
 Partial sterilization of the soil by burning trash or by steam sterilization done
 Provision of better drainage
 Avoidance of same bed for repeated sowing
 Improving the soil texture by adding soil organic amendments
 Preparation of raised nursery beds.
 Thin sowing using optimum seed rate
 Optimum irrigation
 Application of more well decomposed FYM
 Seed treatment with captan or thiram @ 3g or Trichoderma viride @ 4g per kg
 Soil drenching with Bordeaux mixture 1% or copper oxychloride 0.2% @ 4l / sq. m
 Spray 0.2% Metalaxyl when there is cloudy weather
Fusarium Wilt: Fusarium solani
The common disease is common in Tamil Nadu. The disease affects brinjal in all
stages of its growth.
Symptoms
 It attacks seedlings as well as matured plants.
 Leaves turn chlorotic.
 The leaves become flaccid and hang down.
 In the course of a week time, the plant wilts and dries up.
 The roots exhibit varying degrees of rotting.
 If the bark of the stem is peeled, Vascular browning is seen as brown streaks
at the base of the stem and roots.
 Whitish fungal growth is seen on base of stem and roots.
Causal organism: Fusarium solani
Mycelium is septate and hyaline.
Microconidia are hyaline, wedge shaped, 2-celled and are formed in chain.
 Macroconidia are falcate and septate.
Chlamydospores are globose, intercalary or terminal.
Mode of survival and spread
 The fungus survives as chlamydospores and persists indefinitely in infested field soil.
 Persists on plant debris and weed hosts
 The fungus spread by anything that moves soil about, including irrigation.
Epidemiology
 The disease is most serious in sandy soils and at temperatures between 80-90o F.
 Soils become infested by planting infected transplants and from movement of
infested soil by wind and water erosion or on farm implements.
 It is favoured by sandy, acid soils, low soil moisture, hot weather, low RH, and short
day length
 More likely to occur in poorly drained soil.
 Alternating high and low soil temperature and humidity levels
 Presence of root knot nematodes increase the disease development
Management
 Use of disease-free seeds, transplants and soil.
 Field sanitation
 Avoid flood irrigation because these water supplies can be contaminated with the
fungus and spread the disease.
 Long-term rotations with cereals (five to seven years out of tomato) may help.
 Control of nematodes with carbofuran or Nemagon
 Seed treatment with Thiram or Carbendazim or Trichoderma viride
 Apply FYM or organic amendments
 Apply 2.5 kg of Trichoderma viride/ha commercial formulation with 50kg farmyard
manure
 Spot drenching with Carbendazim 0.1%
Verticillium Wilt (Verticillium albo-atrum, V. dahliae)
It is now recognized as one of the most destructive disease in TN. Losses caused by
the disease extend from about 5-10% in midly affected crops to 90% in severely affected
crops.
Symptoms
 Although seedlings can be infected, symptoms usually are not observed until plants
are older.
 A yellowing of lower leaves followed by wilting is the first sign of disease.
 A characteristic symptom of infection is a V-shaped lesion that develops on older leaf
tips that later expands to cover the leaf.
  Brown, necrotic tissue within lesions is surrounded by a large, irregular area of
yellowing due to a systemic leaf toxin produced by the fungi.
 As the disease progresses, stunting and chlorosis become severe with diurnal
wilting.
 Wilting can be asymmetric, with sections of the plant remaining turgid.
 Permanent wilt and plant death follow.
 Dissecting through the crown of affected plants reveals dark-brown vascular
discoloration, which can extend into the pith and up into the stem and branches.
 Fruit that form are small and deformed with internal discoloration.
Causal organism: Verticillium albo-atrum, V. dahliae
Mycelium first prostrate and hyaline become floccose and white to grey.
Microsclerotia –dark resting spores.
Mode of survival and spread
 The fungus is soil-borne and can persist for many years in soil and plant debris.
 The fungus survives as microsclerotia in infected crop debris and can attack many
other plants.
Epidemiology
 This disease is favoured by long-term tomato cultivation, cool weather and high soil
pH.
 Verticillium is favored in its development if the soil is alkaline.
 Verticillium wilt is increased by root wounding from cultivators or root-knot nematode
feeding.
Management
 Field sanitation
 Long-term rotations with cereals and pulses
 Removal of weed host plants
 Seed treatment with Thiram or Carbendazim or Trichoderma viride
 Soil mulch with polyethylene sheets in hottest months
 Apply FYM or organic amendments
 Apply 2.5 kg of Trichoderma viride/ha commercial formulation with 50kg farmyard
manure
 Soil fumigation with methyl bromide in controlled condition
 Spot drenching with Carbendazim 0.1%
Leaf spot: Alternaria melongenae and Alternaria solani
Symptoms
 Irregular, brown and necrotic spots with concentric rings are seen on leaves.
 Spots coalesce to cover large necrotic areas.
  Leaf dries and then fall down.
 Fruit infection shows dark brown and sunken spots.
 Fruit turn yellow and drop.
Causal organism: Alternaria melongenae and Alternaria solani
Mycelium: septate, branched, light brown which become dark at age, intercellular and
later intracellular
Conidiophores - dark coloured emerge through stomata.
Conidia - born in chain, club – shaped, muriform with 5-10 cross septa and 1-5
longitudinal septa with long beak.
Mode of survival and spread
 The fungus survives on infected debris in the soil, on seed, on volunteer tomato
plants and other solanaceous hosts, such as Irish potato, tomato, and black
nightshade.
 Survives in infected plant debris in soil upto 3 years
 The fungus is spread by wind and splashing rain,
 Seed borne also
Management
 Field sanitation
 Regular irrigation to avoid water stress
 Avoid overhead irrigation
 To prevent rain splash, use mulch.
 Avoid composting diseased plant material.
 Seed treatment with Captan / Thiram (4g / kg).
 Spraying Mancozeb 0.2% or Ziram 0.2% Captan 0.3% Chlorothalonil 0.2%
 Proper irrigation and fertilizer management to maintain plant vigour
Cercospora Leaf Spot: Cercospora melongenae
This is common but minor disease in tropics.
Symptoms
 Symptoms appear on the leaves, petioles, and stems of eggplant.
 Initially, small, circular to oval chlorotic spots with light to dark tan centres appear
 They may develop angular or irregular shapes.
 Elliptical to oval lesions may occur on the leaf blades, veins, and petioles.
 Appear more abundantly on the lower surface.
 They are brown to steel-gray on the upper surface and light brown on the lower
surface (Anonymous 2011).
 Conidiophores appear in fascicles (clusters) of 3 to 12. pale to medium brown, paler
towards the apex, occasionally septate, and unbranched,
  Conidia, hyaline mildly curved (Mycobank Database 2012).
 Soil as well as seed borne
 Survives in plant debris and affected fruits.
 Spread through air, water and insects etc.
Management
 Maintain proper field sanitation
 Use disease-free transplants
 Irrigate in the morning to reduce humid and damp conditions overnight.
 Avoid over-irrigation to reduce relative humidity.
 Avoid overhead sprinkler irrigation in order to minimize leaf wetness and spread
of the pathogen in splashing water droplets.
 Increase the spacing between plants to improve aeration and drying of wet
foliage.
 Keep plants adequately fertilized.
 Spraying Mancozeb 0.2% or Ziram 0.2% Captan 0.3% Chlorothalonil 0.2%
Phompsis blight and fruit rot: Phomopsis vexans
Common throughout the world. Although it appears as damping off, Leaf blight, the
most destructive phase of the disease is the fruit rot. The pathogen attacks only brinjal. In
India fruit rot phase causes heavy damage in the field and also during transit.
Symptoms
 The disease affects brinjal from seedling to maturity in one or other form of the
disease.
 In nursery it causes damping off of seedlings also.
 After transplanting the leaves which come into contact with soil first affected.
 Defined, circular or irregular, grey to brown spots with light coloured centre develop
on leaves.
 At later stage numerous fruiting bodies, called pycnidia, can be observed as small,
black pimples, embedded in the host tissue.
 The affected leaves turn yellow and die.
 The petiole and stems also affected.
 Stem symptoms include brown or dark sunken lesions slightly above the soil surface,
and can result in cankers.
 Stem lesions are dark brown becoming grey at the centre as black pycnidia develop.
 Mostly the stem base is attacked and is characterized by constriction of the base or a
grey dry rot.
 The stem is girdled
  The skin peels off and the inner tissues are exposed in strong wind.
 The infected plants toppled down due to breaking of the main stem.
 The fruits are attacked while on the plant.
 Pale sunken oval spots develop on the surface of the fruits.
 These subsequently enlarge and become depressed
 With one lesion or several spots coalescing, large portions of the fruit are affected
 The spots contain many black pycnidia arranged in concentric rings.
 The internal portion of the fruits rots.
 The whole fruits will be mummified due to dry rot.
Causal organism: Phomopsis vexans
Mycelium is septate
Pycnidia with or without beak erumpent, brown to black globose or irregular with
ostiole,
Pycnidia produce two types of conidia. viz. Alfa conidia and beta conidia.
Alfa conidia are hyaline, sub cylindrical, single celled, fusoid, curved aseplate.
Beta conidia (stylospores) are filiform, hyaline and one-celled.
Perithecia are in clusters containing clavate, sessile, 8-spored asci.
Ascospores are bluntly fusoid and 2-celled.
Mode of survival and spread
 This fungus can survive in plant debris or in mummified fruit in the soil.
 Seed produced on plants grown in affected fields can be infested with fungal spores
and may initiate disease on seedlings.
 The major means of spread is by rain splashing or overhead irrigation splash tools
and insects.
Epidemiology
 Disease develops fast in wet weather with temperature around 260 C storage rot is
maximum at 250 C.
 Disease is favored by hot and wet weather.
 The optimum temperature for fungal growth is 29°C and it grows well up to 32°C.
Management
 Remove and destroy all infected plant material to reduce initial inoculum.
 Use disease-free seed and transplants
 A 3-4 year crop rotation is beneficial, since the fungus does not infect other crops.
 Weed control is advisable since pathogen can survive on solanaceous weeds such
as nightshades.
 Deep summer ploughing
  Mulch and furrow irrigate to help reduce splashing of water and soil.
 Hot water seed treatment at 500 C for 30 min
 Spraying difolaton 0.2% or Captan 7-10 days interval – five sprays.
Sclerotinia blight: Sclerotinia sclerotiorum
In Tarai region of N. India, it is a more serious disease.
Symptoms
 Dark -green, water-soaked lesions develop on foliage, stems and fruit.
 Stem infections girdle the stem at the soil line, causing plants to wilt and die.
 Fruits are infected directly from the soil surface or through the peduncle rot quickly
 Affected fruits rot and turn into a watery mass..
 In advanced stages, white, cottony mycelium blankets affected tissue, and sclerotia
form on the surface.
Causal organism: Sclerotinia sclerotiorum
Mycelium hyaline much branched septate, inter and intracellular,
apothecia – funnel shaped cup
produces asci – ascospores.
Mode of survival and spread
 Soil borne. Survives in soil & plant debris as sclerotia.
 Secondary spread through air borne ascospores
Epidemiology
 Dec – Jan more prevalent.
 Dew, fog and frequent rain generally favor disease development.
 Optimum temperature 15.5 to 210 C
Management
 Field sanitation
 Deep summer ploughing
 Use wide row spacing
 Good drainage
 Flooding & Drain if possible
 Crop rotation with rice or beat onion spinach or maize, small grains and grasses
 Spraying ziram or carbendazim have been reported to give some relief.
Bacterial Wilt: Ralstonia solanacearum
In many areas of India considered as one of the very serious disease.
Symptoms
 Symptoms are sudden drooping of leaves with rapid wilting and death of plants
without yellowing or spotting of the foliage
 The lower leaves may droop first before wilting occurs.
  Downward curling of leaves occurs.
 Sometimes there is an excessive production of adventitious roots along the stem
above the soil line.
 The pith appears as water soaked in early stages; later, the pith will turn brown and
sometimes become hollow.
 The vascular system become yellowish brown
 Stems cut cross-wise may ooze a thick, off-white to yellowish liquid.
 Sticking the cut end of an infected stem partially into a glass of water reveals a milky-
white stream of bacteria in the water within three to five minutes.
 The root system may also develop a brownish rot as the plant dies.
Causal organism: Ralstonia solanacearum
Rod shaped Gram negative 1-4 flagellate
Three major races
Race l infects tomato, potato, chilli, egg plant etc.
Race 2 Infects bananas and Heliconia sp.
Race 3 infects potato alone.
Mode of survival and spread
 The bacterium can survive in the soil for months, especially in well-drained soils.
 It is spread by soil and water movement or by diseased plants or infected debris or
equipment.
 Bacteria infect plants through the roots or stem, most often where tissue has been
injured by cultivating, or by some other physical means such as nematodes.
Management
 Use of disease-free seeds, transplants and soil.
 Field sanitation
 Avoid flood irrigation because these water supplies can spread the disease.
 Long-term rotations with cereals.
 Grow on raised beds to promote drainage
 Application of Bleaching powder @ 15 kg / ha before transplanting.
 Soil fumigation with methyl bromide in controlled condition
Little leaf – Candidatus Phytoplasma
First reported from India in 1938. It occurs only in India & Sri Lanka. In almost all the
states of the country it has become a serious problem facing brinjal cultivation. Loss upto
100% in diseased plants.
Symptoms
 The most characteristic symptom is the reduction in size of leaves and petiole.
 The petioles are so short that the leaves appear to be sticking to the stem.
  The leaves become thin, narrow, soft glabrous and pale green in colour.
 The internodes also shortened.
 The auxiliary buds stimulated to produce >100 branches.
 The number of leaves produced will be more giving a bushy appearance.
 In early infection no flowers are formed
 Even if formed the floral parts are modified into green leaf like structures.
 After infection no fruits are formed.
 In late infection the fruit size is very much reduced.
Causal organism: Candidatus Phytoplasma
The phytoplasma is transmitted by the jassid Hishimonas phycitis
Acquisition feeding period 1 hr
Latent period in the vector 16 days
Inoculation feeding period <1 hr
No transsovarious transmission.
Alternate hosts – Potato, Tomato (Big bud) chillies, Datura, Cathranthus roseus,
Argemon mexicana
Management
 Roughing of infected plants
 Eradication of weed hosts.
 Spraying systemic insectides like malathion, Metasystex to control vectors,
 Pusa purple cluster, Arka sheel Aushy, Manjari Gota and Banarus Giant are
moderately resistant to resistant in field.
Mosaic: Potato virus Y (PVY) Tobacco mosaic virus (TMV)
Potato Virus Y
Mosaic mottling of leaves and stunting of plants are the characteristic symptoms
Mosaic symptoms are mild in early stages but later become severe.
Infected leaves are deformed, small and leathery.
Very few fruits are produced on infected plants.
Tobacco Mosaic Virus
Conspicuous mottling of leaves
Leaves also develop blisters in advanced cases.
Severely infected leaves become small and misshapen.
Plants infected early remain stunted.
PVY is easily sap transmitted. It is transmitted in the field through aphids, Aphis
gossypii and Myzus persicae and perpetuates on weed hosts like Solanum nigrum and
S. xanthocarpum.
 TMV is transmitted by sap, contaminated implements and clothes, soil debris and
hands of labour. It can perpetuate on many cultivated plants like cucurbits, legumes,
pepper, tobacco, tomato and weed hosts. The virus survives in plant debris

DISEASES OF BHENDI
1. Powdery mildew: Erysiphe cichoracearum
It is very severe in this crop. Normally occurs during September – December.
Symptoms
 The infection is first seen on older leaves.
 The disease symptoms appear as subtle, small, round, whitish spots on leaves and
sometimes stems.
 The spots enlarge and coalesce rapidly
 White or grayish powdery growth or patches resembling talcum powder on the upper
surface of older leaves or other plant parts.
 The fungal growth is diffused without any marked boundary
 The talc-like powder is composed of fungal mycelium, conidiophores and conidia.
 Heavily infected leaves become yellow, and then become dry up and brown.
 The affected leaves may roll upward,appear scorched and fall off prematurely
 Severe infection causes very much reduction in fruit yield.
Causal organism: Erysiphe cichoracearum
Mycelium: ectophytic external, hyaline, septate haustoria are button-shaped
Conidiophores short hyaline
Conidia are single celled, hyaline, barrel shaped and in long chains basipetally.
Cleistothecia are globose and dark brown myceloid appendages.
The asci are pedicellate, ovate or ellipsoid.
The number of ascospore is usually 2 rarely 3 per ascus.
The ascospores are single celled, hyaline and oval to sub cylindrical
Mode of spread and survival
 Fungus overwinters on plant debris or alternate host
 Spread through airborne conidia
Epidemiology
 Disease is favoured by warm, dry weather with cool nights that result in dew
formation
Management
 Removal of weed host plants
 Field sanitation
  Plants should be well manured and applied fertilizers to maintain the vigour of plants
 Spraying Sulphur dust 8-10kg / ac or Wettable Sulphur 0.3% (or) Benlate 0.1% or
tridemorph 0.1% or dinocap 0.1% or propiconazole 0.05 % or Rubigon 0.025% or
Bavistin (0.1%)

2. Cercospora leaf spot: Cercospora abelmoschi , Cercospora malayensis

Symptoms
 Cercospora abelmoschi causes no definite spots but grows as a sooty black to dark
olivaceous mould on the lower surface of the leaves.
 Severely affected leaves dry up.
 Cercospora malayensis produces dark brown circular or irregular spots with grey
centre.
 Both the leaf spots cause severe defoliation
Causal organism: Cercospora abelmoschi , Cercospora malayensis
Conidiophores are pale to medium olivaceous brown, multiseptate, some times
branched, geniculate and irregular.
Conidia are obclavate to cylindric, olivaceous brown and straight to curved.
Mode of spread and survival
 The fungus survives in the diseased crop material.
 Spread thro air borne conidia.
Epidemiology
 Both the leaf spots are common during humid seasons
Management
 Removal of weed host plants
 Field sanitation
 Plants should be well manured and applied fertilizers to maintain the vigour of plants
 The leaf spot disease can be controlled by spraying with any one of the fungicides
viz, carbendazim 0.1% or Mancozeb 0.2% or Difolatan 0.2%.
3. Wilt: Fusarium oxysporum f.sp. vasinfectum
Symptoms
 The infected plants appear as stunted
 Leaves become yellow before the appearance of typical wilt symptoms
 The leaves show epinasty and vein clearing.
 They lose turgor.
 Finally the plant dies.
 If a diseased stem or root is cut longitudinally the vascular tissues appear as dark
streaks.
4. Vein Clearing or Yellow vein mosaic:
Bhendi yellow vein mosaic was first reported in okra plants in 1924 in India and Sri
Lanka. This is the most important, serious and destructive viral disease in bhendi. The
disease infects at all the stages of crop growth and severely reduces growth and yield. If the
plants are affected early there will be a total loss. The extent of damage declines with delay
in infection of the plants in a field. Plants affected 50 and 60 DAS suffer a loss of 84 and
49% respectively.
Symptoms
 The disease is initially characterized by yellowing of the entire network of the veins in
the leaf lamina.
 Then the leaves turn completely yellow
 In severe infections the younger leaves also turn completely yellow
 The leaf size becomes reduced.
 In extreme cases, the infected leaf becomes totally light yellow or cream coloured
and there is no trace of green colour.
 The veins and veinlets are thickened.
 The affected plants become stunted in growth.
 Due to infection flowering may be restricted.
 The fruits if formed they are small in size, malformed, yellowish green in colour,
fibrous and harder than the healthy fruits.
Causal organism: Yellow vein mosaic virus.
The causal agent is the single-stranded DNA Bhendi yellow vein mosaic
virus (BYVMV), which is associated with a beta satellite, both of which are required for
infection. BYVMV belongs to the genus Begomovirus, family Geminiviridae.
Transmitted by Bemisia tabaci
Weed Hosts: Croton sparsiflora, Malvastum tricupsidatun, Ageratum sp, Hibisus
tetraphyllus
Commelina nudiflora
Management
 Rouging and destruction of infected plants
 Raising of new crops near older crops should be avoided.
 Removal of weed hosts.
 Growing resistant varieties like Pusa Savani, Arka Anamika, Parbhani Kranti, Arka
Abhay and Varsha Uphar.
 Use of yellow sticky traps
 Spraying systemic insecticides starting soon after emergence of the plants
 Raising border crops – maize, jowar or Bajra with spraying in insecticides
 DISEASES OF CRUCIFERS
Diseases of Cabbage and Cauliflower
Damping off: Pythium aphanidermatum; P. debaryanum
Symptoms
Damping off of tomato and other vegetables occurs in two phases (i) Pre emergence
damping off (ii) Post emergence damping off.
Pre emergence Damping off
 It is a decay of germinating seeds
 The radical and plumule when they come out of the seed undergo complete rotting.
 Seedlings are infected and died before the emergence from the soil
 Causes poor and uneven stand of seedlings in nursery beds
Post emergence Damping off
 Occurs after the emergence of seedlings from the soil
 The affected seedlings become chlorotic and pale green and suddenly collapse
 Dark-brown water-soaked lesions develop at the collar region that rapidly spread
over the entire seedling.
 Affected portion shows shrinking and brown discolouration due to rotting
 Eventually, the lesions girdle the hypocotyl, causing seedlings to wilt and die.
 Brown, water-soaked lesions that start on the roots and later extend up the hypocotyl
characterize post-emergence Damping-Off.
 The root cortex becomes macerated and easily sloughs off.
 The affected seedling become collapsed and toppled down
 Post emergence mortality of seedlings very conspicuous
Causal organism: Pythurin aphanidermatum; P. debaryanum

Mycelium - hyaline, coenocytic freely branched – reproduction asexually and

sexually. Sporangia - irregular, lobed – terminal or intercallery – germinate by producing
tubes with vesicle
Zoospores - biflagellate – encysted in ½ hr - germinate to produce germ tube –
mycelium
Sexual – oogonuim and anthridium – oospore – zoosporangium – zoospores –
mycelium.
Mode of survival and spread
 Soil borne. All the causal organisms are soil inhabitants and they build up in soil with
the available hosts. Generally these pathogens have wide host range.
Epidemiology
  Damping-off is generally most severe under conditions of high soil moisture and/or
compaction, overcrowding, poor ventilation and cool, damp, cloudy weather.
 Water-splashing moves infested soil from diseased to healthy plants.
Management
 Partial sterilization of the soil by burning trash or by steam sterilization done
 Provision of better drainage
 Avoidance of same bed for repeated sowing
 Improving the soil texture by adding soil organic amendments
 Preparation of raised nursery beds.
 Thin sowing using optimum seed rate
 Optimum irrigation
 Application of more well decomposed FYM
 Seed treatment with captan or thiram @ 3g or Trichoderma viride @ 4g per kg of
seed
 Soil drenching with Bordeaux mixture 1% or copper oxychloride 0.2% @ 4l / sq.
metre.
 Spray 0.2% Metalaxyl when there is cloudy weather
Club root: Plasmodiophora brassicae
Club root, caused by the slime mold Plasmodiophora brassicae, was first recognized in
Europe during the 13th century. It has since become the most serious disease of crucifer
crops worldwide. Club root is a most persistent and devastating disease of cruciferous crops
which affects nearly all cultivated, as well as many wild and weed members of the cabbage
family. Potentially most dangerous disease of Cruciferaceae. Very common in temperate
region. Once the disease has appeared in the area if becomes difficult to raise a profitable
crop of crucifers in that area. Affected plants are usually a total loss. Most cruciferous weeds
are susceptible and can serve as reservoirs of the pathogen from one year to another.
Symptoms
 Symptoms become apparent only after the pathogen has advanced considerably in
the root system.
 Clubroot may develop extensively on plant roots before the first sign (an abnormal
wilting and yellowing of leaves, especially on warm days) is noticed aboveground.
 If the soil is moist, these symptoms may not become apparent until water stress
occurs.
 Infection in the nursery stage results in the death of seedlings
 Infected plants at first show pale green to yellow leaves.
 Later, infected plants show wilting in hot, sunny midday, which recover during night.
  The aerial parts of the plants shows stunting, chlorosis, reduction in size of head,
flagging of leaves and non specific unhealthy symptoms
 Infected older plants remain alive but stunted and fail to produce marketable heads.
 Most characteristic symptoms are seen on the roots.
 When the roots are examined the characteristic symptoms consist of small or large,
spindle or spherical or knobby or club shaped swellings due to hypertrophy and
hyperplasia which cause enlarged thick fleshy growths of the roots.
 The clubs are generally widest in the middle and taper toward the ends.
 Hypertrophy causes malfunctioning of xylem, which results in flagging of the leaves.
 The malformation may be seen either at the base of the tap root or at the lateral roots
or the entire root system.
 The infected plants ultimately die.
 Older and larger clubbed roots disintegrate before the end of the season because of
invasion by saprophytes.
Causal Organism: Plasmodiophora brassicae
The fungus is slime mold.
It produces resting spores inside the host cells. They are hyaline spherical, gives rise
to zoospores
Zoospores are irregular amoeboid with uninucleate protoplasm with two flagella.
Devoid of cell wall. These zoospores penetrate the cell wall enter and multiply causing
hyperplasia and hypertrophy.
Pathogen: Obligate endoparasite
Thallus is Plasmodium (Naked slimy mass of protoplasm containing numerous
nuclei) gives zoosporangia / resting spores released into soil when decayed and produce
zoospores.
i. Primary phase occurs in root hairs
ii. Sec. phase occurs in cortical cells of roots
Primary phase – Resting spores germinate and produce zoospores (primary) with
two flagella. Encysted zoospores attach with root hair, myxamoeba enters the root hair cell,
divides to several uninucleate amoebae and nuclei divides and form multinucleate plasmodia
which again divide and form thin walled zoosporangia which contain 4-8 uninucleate
zoospores, escapes in the soil, fuse as gametes and form quadriflagellate binucleate zoo
Sec. phase – Quadriflagellate binucleate zoospores (secondary) reinfect the root and
form binucleate plasmodium, penetrate the root cortex – plasmodium repeatedly divides and
host cells hypertrophied and the plasmodium transformed into masses of resting spores
released into soil as the root decay.
 Disease cycle
Within the infected plant roots, the organism develops rapidly, causing an increase in
the number and size of cells, which results in "clubbing." During the development of the
organism in the plant, new zoospores are produced; these are capable of infecting the same
plant or adjacent plants and, thus, repeating the cycle. Eventually, resting spores are formed
within the diseased plant tissue, and these are released into the soil when the plant roots
disintegrate.

Mode of survival and spread

 P. brassicae spores can remain viable in the soil and infected plant debris in soil for
at least 20 years, even in the absence of a susceptible host. After the roots decay,
spores are released into the soil where they remain dormant until conditions are
suitable for germination, e.g. when another cruciferous crop is grown.
 The fungus can be spread through contaminated soil from place to place.
 Farm machinery, boots, animals, the dung of animals that have eaten diseased roots,
and compost containing remains of a diseased crop are some of the means of
spreading club root.
 The resting spores of the fungus can be spread from field to field by infested soil,
contaminated water supplies, infected transplants, infested soil on farm machinery,
and even by roving animals such as cattle.
 The most important means of spread is on the roots of infected transplants,
contaminated irrigation water and surface flood water. Reports indicate that dam
 water, especially water from dams receiving run off from infected fields, can become
contaminated with the fungus.
 Spore dispersal by wind is also possible, especially under dry conditions.
Epidemiology
 The disease is favoured by wet acid soil
 Optimum soil temperature is 20 -250 C for disease development; although infection
can also occur at temperatures as low as 12°C.
 High soil moisture is more important for disease development.
 Sensitive to alkaline condition
 The germination of resting spores requires moist, acid soil and can occur over a wide
temperature range of 12°- 27° C.
 Disease development is favored by high soil moisture and soil temperature between
18°-25° C.
 Although clubroot has been found in soils exhibiting a wide pH range from 4.5-8.1,
the disease is primarily associated with acid soils.
 No spore germination at pH 7.2 or above.
 Development of the disease is favored by a low soil pH (below 7.0), cool soil, and
excess soil moisture.
 Cool, wet and acidic soils favour the development and spread of the disease.
 Clubroot is more prevalent on poorly-drained soils, particularly low-lying areas.
 Clubroot is more pronounced in acidic soils (pH<7.0), although at high spore
concentration levels the disease can develop in alkaline soils (pH>7.0).
Management
 Eradication of crucifer weeds.
 Field sanitation
 Long rotations (7 years or longer) with non-cruciferous crops
 Avoid over-watering the soil and using practices that flood the soil, such as furrow
irrigation.
 Improve drainage in poorly drained soils and low lying areas
 Use of only disease-free transplants
 Use of seedlings from disease free area
 Raise the soil pH to 7.2 by application of hydrated lime 6 week before planting and
keeping the soil uniformly wet. Lime inhibits disease development, but will not
prevent a disease outbreak if the spore load in the soil is sufficiently high. In some
soils, large amounts of lime may be required. Be careful, because such applications
may result in nutritional problems or encourage diseases such as common scab in
potatoes and white rot in onions.
  The quantity of lime is determined by initially measuring the pH of the soil. Suppose a
soil is with pH 5 it requires 2.5 t / ha.
 Soil application of PCNB 0.1%
 Solarisation is only economic to use on heavily-infested fields during periods of high
temperature
 Seed treatment with cabendazim 2g/kg
 Nursery drenching with carbendazim or chlorothalonil 0.1%.
 Spot drenching with carbendazim/chlorothalonil 0.1%.
 Soil fumigation with chloropicrin, methyl bromide
 Application of formalin 2 % @ 10 lit/sq. m. of seed bed drenching the soil with PCNB
1.0% is found effective
 Seedling dipping in 0.1% HgCl2 (or) 0.8% Benlate or Carbendazim for 15-20 minutes
Downey Mildew: Hyaloperonospora parasitica (synonym: Peronospora
parasitica)
It attacks cabbage, cauliflower, turnip and radish. Very serious on cauliflower. The
disease is very serious in nursery and it can also appear in field planting.
Symptoms
 Plants can be infected at any stage of development.
 In seed beds, cotyledons and primary leaves are invaded resulting in fungal growth
visible on the underside of the leaf.
 Later a slight yellowing develops opposite to the fungal growth on the upper side of
the leaf.
 The young leaf or cotyledon, when yellow, may drop off.
 In older plants, purplish brown spots appear on the under surface of the leaves, stem
and pods.
 These may remain as small or enlarge in size.
 The upper surface of leaves shows irregular chlorotic or yellowish translucent spots
delimited by veins.
 Under cool, moist conditions, grayish white fluffy downy growth appear on the under
surface of the lesion.
 As the lesions enlarge and dry out they become necrotic and the leaves become tan
and papery
 In severe infection the leaves shed
 The affected cauliflower curds look brownish to blackish at the top.
 The stem also get affected showing dark brown lesion which later develop downy
growth.
 Numerous sunken black spots appear on cabbage head.
 Causal Organism: Hyaloperonospora parasitica (synonym: Peronospora
parasitica)
It is an obligate parasite. The mycelium is coenocytic, intercellular and is with ovate
haustoria. Sporangiophores arise in groups through stomata, dichotomously branched and
bear sporangia. The sporangia are greyish, ovoid and thin walled provided with papilla at
the distal ends. Oospores are not common.
Mode of survival and Spread
 The fungus overwinters mainly in roots or in decaying portions of diseased plants on
cruciferous weeds, and occasionally on crop seed.
 Survives as thick-walled spores which remain in the soil after the crop decays.
 On growing plants, spores are blown about by wind and splashed by rain.
Epidemiology
 The fungus thrives well in cool moist environment. Chiefly in humid region.
 Moisture and temperature are important in the spread and reproduction of this
fungus.
 High relative humidity during cool or warm, but not hot, periods promotes its growth
and sporulation.
 Presence of a water film on the foliage from fog, drizzling rain, or dew allows spores
to germinate, infect, and produce more spores on a susceptible host in as few as 4
days.
 Rapid development and spread of the disease occur at 10 – 15 0C
 Heavy humidity, fog, drizzling rains or dews that remaining on plants until mid
morning for 4 days is ideal for development and spread.
 Abundant sporulation and rapid disease development occur at greater than 98%
relative humidity, when leaves are wet, and at 8-16°C.
Management
 Field Sanitation
 Crop rotation
 Clean seed beds.
 Use of disease free transplants
 All the weeds serving as alternate host to the fungus should be destroyed.
 The crop should be irrigated judiciously to avoid periods of high humidity.
 Seed treatment with hot water or organomercurials .
 Spraying Maneb 0.2% Ridomil MZ 72 0.25%
 Spraying the seedlings in the nursery beds with Copper Oxychloride (0.3%) is
effective
 In the field, the crop is sprayed with Copper Oxychloride (0.5%).
  Seed treatment with Metalaxyl (Apron 6g/kg of seed)
 Foliar spraying with Metalaxyl (Ridomil) 0.4%.
White rust: Albugo candida (Cystopus candida)
Symptoms
 All aerial parts are affected
 Symptoms manifest as chlorotic or necrotic spots on upper leaf surfaces.
 White or creamy yellowish raised blisters or pustules are seen on lower surface of
the leaves (Armstrong 2007).
 Other symptoms include chlorosis, necrosis, defoliation, swelling and distortion of
stems and flowers, stunted growth, and leaf curling (Babadoost 1990).
 The leaves may become thick fleshy and inrolled
 Severe infection reduces the leaf size.
 Spots coalesce together causing drying.
 The systemic infection affects stem and inflorescence
 If the disease becomes systemic, an infected plant may form swollen, twisted floral
parts called “stagheads” (Armstrong 2007).
 The inflorescence shows various deformations.
 They become thick fleshy and greenish leading to sterility.
 Floral parts show swelling and distortion due to hyperplasia and hypertrophy. This is
known as staghead.
 The petals become sepals like; stamens become leaf like; Ovules and pollen grain
are atrophied. Ovary is sterile
Causal Organism: Albugo candida (Cystopus candida)
It is an obligate parasite. Mycelium is intercellular. Knob like haustoria, hyphe collect
beneath the epidermis Sporangiophores are club-shaped hyaline and produce short chain of
sporangia basipetally. Sporangia are single celled, spherical, hyaline and are arranged in
chain.
Mode of survival and Spread
 Oospores serve as primary inoculum for this disease and can survive for many years
in soil and plant debris or as a contaminant of seeds.
 Sporangia produced in pustules are spread by wind, rain or insects to neighbouring
plants.
Epidemiology
 Cool moist weather favours development of the disease.
 Under optimum conditions, between 16 and 25° C and high relative humidity
(Damicone and Roberts n.d.), the sporangia germinate to produce biflagellate, motile,
 infective zoospores (Reddy 1996). If there is no free moisture available on the host
surface, the sporangia may simply re-infect the host plant without producing
zoospores. If free water exists on leaf surfaces, the zoospores drop their flagella,
encyst, and form germ tubes, which enter leaves through the stomata to cause
systemic infections.
 Infection is generally favoured by cool (13-18°C), wet weather in the form of
prolonged dews or fog.
Management
 Field sanitation
 Destroy the oospores on surface of seed by hot water treatment at 52°C for 20
minutes.
 Removal of Cruciferous weeds
 Spray 0.8% Bordeaux mixture or copper oxychloride 0.25% or Chlorothaloni0.1% or
metalaxyl 0.1 % or Mancozeb 0.2 %.
Alternaria leaf spot and Blight: Alternaria brassicae and A. brassiciola
It is a destructive disease on seed crop. The leaf spot phase reduces plant vigour
and renders the crop unsalable or unusable where leaves are the edible portion of the plant.
Besides the leaf spot phase, edible flower parts of cauliflower curds, seedlings, and flower
parts related to seed production can be diseased.
Symptoms
 On seedlings, the symptoms are small dark spots on the stem or black streaks on
cotyledons and hypocotyls that cause damping-off or stunting of the plant.
 On older plants, the bottom older leaves are infected first.
 Symptoms appear as small circular dark coloured spots on the leaves.
 Spots spread rapidly to form circular lesions upto 1-3 inches in diameter.
 The enlargement of the spots has characteristic concentric rings (target spots) and
possibly surrounded by yellow halos.
 Lesion centres may break apart, giving a shot hole appearance to the leaf
 Under favourable conditions, the lesions become covered with sooty black mass of
spores.
 Infected leaves soon turn yellow and drop.
 Several spots cause premature death of leaves.
 Petiole and stem also affected showing linear spots.
 The disease infects the base of heads and cause browning of cabbage and
cauliflower heads
 Flower clusters may also become infected during seed production, affecting seed
quality.
 Causal Organism: Alternaria brassicae and A. brassiciola
Conidiophores are thick and brown. Conidiophores are thick and geniculate. Conidia are
both transversely (11-15 septa) and vertically septate (0-3 septate), coloured and beaked.
Conidia are mostly solitary or chains up to 4.
Mode of survival and Spread
 Survives in plant debris in soil
 Cruciferous weeds may also harbour these fungi
 Primarily seed borne via mycelium within the seed or transitory spores on the seed
(both internally and externally seed borne)
 Conidia are disseminated by wind and water.
Epidemiology
 Occurs during warm, moist conditions
 Bright sunshine, frequent dews or showers, and temperatures between 60 and 90 °F
favor disease development.
 Disease development is favored by free moisture on plant surfaces and temperatures
between 20-27°C.
Management
 Use of disease free seeds
 Proper crop rotation
 Seed treatment with Thiram 2-3g/ kg
 Seed treatment with hot water (50OC for 30 minutes)
 Spraying at full bloom, pod set and pre- harvest stage with Captan (0.2%) or
Mancozeb or zimeb 0.2% or Copper Oxychloride (0.5%) for the control of disease.
Black leg of cabbage: Phoma lingam (sexual stage: Leptosphaeria macutans)
Black-leg is of major concern in crucifer production. It is a serious disease in
temperate region.
Most destructive one.
Symptoms
 Symptoms manifest as oval, sunken, light-brown cankers with purple-to-black
margins near the base of stems.
 These lesions extend below the soil surface, causing a black rot of lower stem and
roots.
 Cankers enlarge and girdle stems, causing plant collapse.
 Lesions may also develop on cotyledons and hypocotyls of young seedlings causing
Damping-off several weeks before transplanting
 Lesions appear on leaves as pale, irregular spots.
 Leaf spots gradually enlarge, becoming circular to oval with ashy gray centers.
  Under favorable conditions, small black fruiting structures (pycnidia) develop in stem
cankers and leaf spots.
 Vascular tissues may turn black in color prior to external rot symptoms.
 The fungus interferes with water conduction in tissues causing wilting and debilitating
plants.
 Severely infected plants are stunted and often wilt.
 The leaves remain attached and the plant turns a dull blue-red color.
 The root system may be destroyed, although new roots may form above the stem
cankers, allowing the plant to remain alive.
 Infection can spread to the base of leaves of cabbage heads in storage where brown
to black spots develop.
 Flower stalk and siliques and seed also affected
Causal Organism: Phoma lingam (sexual stage: Leptosphaeria macutans)
Mycelium septate, branched, hyaline at young and dark with age.
Two types of pycnidia can be found; one on infected, live plants (thinner-walled pycnidium
with a neck) and the other on crop residues (thicker-walled pycnidium with a narrow ostiole).
through infected plantings during wet conditions when pycnidia are present.
Pycnospores hyaline one celled.
Mode of survival and Spread
 Fungus survives on plant debris or living plants as pseudothecia, which release
ascospores that may be windborne for long distance.
 The fungus survives in association with infected plant residues until the plant debris
decomposes (1 to 4 years)
 It can survive for years as mycelia in infected seed.
 Sources of the fungus also include cruciferous weeds
 Survives in plant debris in soil for 3 years
 Seed borne
 Secondary spread by air borne ascospores
 Pycnidiospores are dispersed by splashing rain or irrigation water
 Disease also spreads by workers or equipment moving
Management
 Use disease-free or treat seeds with hot water.
 Hot water treatment of seeds at 500 C for 30 minutes is recommended.
 Practice a four year rotation in seedbeds and fields.
 Avoid cultivation in fields where crucifers have been continuously grown for 2
years.
 Seedlings before transplanting should not be dipped in water
  Rogue diseased plants from seedbeds.
 Improve soil drainage and air circulation.
 Control brassica weeds.
 Incorporate crop debris promptly after harvest to hasten decay.
 Avoid working in the fields when wet.
 Seed infection can be prevented by spraying the seed plants with copper
oxychloride or with an organo mercuric compound.
 Seed treatment with Captan or Thiram 4g/kg of seed, followed by seed treatment
with Trichoderma viride 4g/kg.
 Pusa Drumhead, a cabbage cultivar has been reported to be tolerant under field
condition.
Cabbage yellows or Fusarium wilt of cabbage: Fusarium oxysporum f.sp.
conglutinans
It was found first in the Hudson Valley in 1899. It now occurs in all states where
cabbage is grown in warm seasons. Yellows can attack all members of the cabbage family,
including cabbage and cauliflower. It is a vascular disease. It is common in warm condition.
Symptoms
 Plants will develop characteristic symptoms 2 to 4 weeks after transplanting
 The entire plant appears to have a dull cast, and lower leaves turn yellow-green in
color.
 A lateral warping or curling of the stem and leaves occurs.
 The lower part of the leaf blade adjoining the petiole or midrib wilts and dies first,
resulting in a curve in the midrib.
 The lower leaves turn yellow first, and then symptoms move to the upper leaves.
 The wilting of lower leaves may be more apparent on one side of the plant than the
other.
 The yellowed leaves turns brown dies and becomes brittle drop of prematurely
 Growth is stunted.
 When stems of infected plants are cut in a cross section, internal necrosis (browning)
usually is visible.
Causal Organism: Fusarium oxysporum f.sp. conglutinans
Mode of survival and Spread
The Fusarium yellows fungus is capable of surviving many years in the soil, even in the
absence of host plant debris.
Epidemiology
Infection is favored by warm soil temperatures (80-850 F) and does not develop well in
temperatures below 61 F.
 Fusarium yellows is a "hot weather" disease.
Soil moisture and pH have little reaction on the fungus.
Management
Field sanitation
Crop rotation
Seed treatment
Rhizoctonia disease of cabbage: Rhizoctonia solani (Thanetophorus
cucumeris; synonym: Pellicularia filamentosa)
The fungus causes damping-off and wirestem of cabbage, cauliflower, and other
crucifer seedlings in the seedbed; bottom rot and head rot of older plants in the field and
storage. Losses occur as reduced stands and lowered yield and quality.
Symptoms
1. Damping-off.
 Seeds may decay, especially in cold, wet soils.
 Stems of young seedlings become light brown and water-soaked near the soil
line.
 Affected seedlings quickly wilt, topple over, and die.
 Damped-off plants commonly occur in circular patches in plant beds or along
sections of rows.
2. Wirestem
 Wirestem is the most common and destructive phase of Rhizoctonia disease.
 This disease is more serious in nursery beds.
 The affected young seedlings show reddish brown discolouration of the stem
near the ground level.
 This area gets constricted and the plants bent or twist without breaking.
 In some cases, the seedling continues to grow even though the lesion girdles
the stem.
 The lesion is quite sunken, and the stem resembles a wire, hence the name
'wirestem'.
 The girdled seedling eventually dies.
 In transplanted plants, the stem above and below the soil line shrivels and
darkens, becoming tough and woody or wiry.
 In wet soil, the decayed outer tissues of the stem may slough off when the plant
is pulled.
 Growth of diseased seedlings after transplanting to the field is usually slow.
 Severely diseased plants soon die.
  Even if the plants are able to produce new roots above the affected stem after
transplanting, they are generally stunted, unthrifty, and they produce small
heads.
3. Bottom rot
 The lower leaves droop, decay, and turn black, but remain attached.
 Some plants may recover and produce heads.
 In cabbage, bottom rot usually develops into head rot.
4. Head rot
 A firm to slimy dark decay of the bases of the outer leaves and heads of
cabbage develops between early head formation and maturity.
 The outer leaves of the head wilt, become pale, and turn brown to black near
the main stem.
 As leaves are killed, they dry at the base and remain held in place by the
margin of the blade that folds over the top of the head.
 Foliage leaves die and drop off, exposing the stem beneath the head.
 A cobwebby brown mold may be conspicuous on decayed tissues and
between the head leaves in damp weather.
 Small brown sclerotia may develop and be visible on parts or the whole
surface of the head.
 Dark brown sunken spots are produced inside the head.
 A firm, persistent, dark decay continues to develop in transit and storage.
Causal Organism: Rhizoctonia solani (Thanetophorus cucumeris; synonym:
Pellicularia filamentosa)
Mode of survival and Spread
 The fungus survives indefinitely in the soil, primarily as small, hard, chocolate-brown,
kernel-like bodies called sclerotia.
 Crucifer seed infected with Rhizoctonia is also a primary source of inoculum;
Epidemiology
 The strain of Rhizoctonia solani causing bottom rot and head rot of cabbage grows at
temperatures ranging between 8° to 32°C.
 Cabbage may become infected at temperatures ranging between 11° to 32°C with an
optimum between 25° to 26°C.
 Cool, cloudy weather, high humidity, wet and compact soil, and overcrowding
especially favours development of the Wirestem disease.
 Damping-off develops most rapidly at temperatures of 75°F (23°C) and above in wet
soils following heavy rains or over-irrigation.
Management
  Disinfest the soil before seeding with steam or a soil fumigant.
 Grow plants in well-drained, fertile soil. Fertilize based on a soil test
 Treat the seed with hot water.
 When transplanting, discard all seedlings with discolored stems and roots.
 Do not plant crucifers for at least three years in fields where bottom rot, head rot, and
root rot have occurred.
 Cultivate the soil as soon as possible after heavy rains to aerate it and thus make
conditions less favorable for infection.
 Avoid covering parts of leaves with soil when cultivating.
 Banking soil around plants creates conditions favorable for development of bottom
rot and head rot.
 Harvest crucifer root crops when the soil is comparatively dry so that a minimum of
soil will adhere to the branch roots.
 Discard that show severe Rhizoctonia infection.
 A reduction in the inoculum level of Rhizoctonia has been reported following cropping
with cereals and incorporating the crop residue into the soil.
 seed treatment with antagonist fungal culture of Trichoderma viride (3-4 g/kg of seed)
or Thiram (2-3 g/kg of seed) are effective.
 Soil around the affected seedling should be drenched with Dithane M 45 (0.2%) or
Bavistin (0.1%) to control the spread of the disease.
Black Rot of crucifer: Xanthomonas campestris pv. campestris
Black rot is a potentially lethal bacterial disease that affects cruciferous vegetables
including cabbage and cauliflower. Black rot occurs worldwide wherever cruciferous plants
are grown and makes cruciferous vegetables unfit for the marketplace or the table. Black rot
of crucifers is considered the most destructive disease of crucifers worldwide. The disease
seldom occurs and causes little damage in cooler temperate climates but can cause severe
losses in transplant and field production in warmer subtropical climates. The disease causes
high yield and quality losses, especially in tropical and subtropical regions during the rainy
season. In warm and wet conditions black rot losses may exceed 50% due to the rapid
spread of the disease. The disease is usually most prevalent in low areas and where plants
remain wet for long periods. Conditions favouring plant-to-plant spread of the bacterium has
led to a total loss of crucifer crops. In India it was first reported in 1929 and then its
widespread occurrence all over the country is well recognized. It was introduced from west
to our country.
Symptoms
 The disease affects primarily above ground parts of plants at any stage of growth
 On young seedlings, cotyledons are infected showing blackening at the margin.
 Later, the cotyledon shrivels and drops off, but only after the bacteria have passed
into the young leaves and stem.
 Affected seedlings turn yellow to brown, wilt, and collapse.
 On older plants Initial symptoms are irregular, dull, yellow blotches that appear on the
edges of leaves.
 As the disease progresses, these blotches expand and progresses to form the
characteristic wedge or V-shaped lesion associated with this disease with the open
part along the edge of the leaf.
 The V-shaped areas are initially yellow, but eventually become brown and necrotic in
the center with a yellow border or halo.
 Within the affected area, leaf veins and veinlets turn black forming to a net-like
pattern, giving the disease its name – black rot.
 At advanced stages, affected tissue becomes brown and necrotic.
 Black leaf veins may extend from the affected leaf into the main stalk where the
darkened vascular system may be visible.
 As the disease progresses into the vascular system, lesions resulting from systemic
invasion may appear along leaf midribs and between leaf veins.
 The V-shaped areas enlarge and the entire leaf eventually turns yellow or wilts and
falls from the plant.
 A typical cross-section of an infected stem or petiole shows a black ring due to
invasion of the water-conducting vessels
 Systemically infected plants may be stunted
 More severe symptoms develop on one side of the plant.
 The lower leaves on infected plants are usually stunted, yellow to brown, and wilted
and often drop prematurely.
 Infected plants may consist of only a long, bare stalk topped with a tuft of leaves.
 In affected cabbage, heads are smaller and outer leaves may senescence.
 The disease can progress on cabbage during storage, making the heads
unmarketable.
 Plants may quickly rot immediately before or after harvest, due to secondary soft-
rotting bacteria.
Causal Organism: Xanthomonas campestris pv. campestris
It is a Gram negative and rod-shaped bacterium with single polar flagellum.
Mode of survival and Spread
 The bacteria can overwinter in plant debris, in and on seeds, and in and on weeds.
 The pathogen may survive in diseased crop residue buried in soil for up to 2 years,
but not more than 60 days free in soil.
 The major source of these bacteria is infected seeds, which enable long-distance
spread of the disease. As few as three infected seeds in 10,000 (0 03%) can cause
black rot epidemics in a field.
 The pathogen is spread within and between fields by splashing water, wind, insects,
machinery, irrigation or drainage waters, blowing of detached leaves or dust particles
and shipping and handling of infected plants.
Epidemiology
 Free moisture is required for infection by the pathogen.
 After infection, symptoms may appear on plants within 7 to 14 days under optimum
conditions (25 to 30 degrees C).
 The disease develops best under warm, wet conditions.
 Temperatures of 80 to 86 degrees F favour growth of the bacterium.
 Free moisture, in the form of rain, dew, or fog, is required for infection to occur.
 The disease may be more severe in low and shaded areas.
 This bacterial disease is common in areas having a warm and wet climate.
Management
 Disease-free seed and transplants
 Use clean, disinfested containers and planting materials.
 Good air and soil drainage
 Field sanitation
 Cultural practices such as deep tillage hasten the decomposition of infested crop
residue
 Crop rotation for 3 years
 Provide a balanced fertility program.
 Control of all cruciferous weeds in and around the production area.
 Do not work in fields when plants are wet.
 Destroy or bury all crop debris immediately after harvest.
 Planting should be done on raised beds to facilitate drainage.
 Avoid sprinkler irrigation
 Also, do not overcrowd or plant in poorly drained soil.
 Do not work in the seedbed or fields when plants are wet.
 Use clean or new harvest containers that are smooth and flexible.
 Spraying fields with fixed copper bactericides
 Seed treatment with 0.1% Hgcl2 (or) Aureomycin 0.1% or Agrimycin-100 (100ppm) or
Streptocycline (100 ppm) for 30 min (or) hot water 500 C for 20 – 25 min
  Soil application stable bleaching powder @ 10 – 12.5 kg / ha.
 Spraying agrimycin 100 or Streptocycline gives effective control.
 Spraying copper oxychloride 0.25% + Agrimycin 100 at 200 ppm.

Stalk rot/Cottony rot/ White blight/ white mould / white rot: Sclerotinia
sclerotiarum
It is considered to be a limiting factor in cauliflower and cabbage seed production in
N. India.
Causes 30% loss in cauliflower. This fungus can cause serious losses in the field, in
storage, and under transit and market conditions.
Symptoms
 Generally, damp weather favours the occurrence of the disease.
 Infections may occur on the stem at the ground level, on the leaves at their bases, or
where the foliage comes in contact with the soil.
 The infections begin as water-soaked, circular areas, which soon become covered by
white, cottony fungal growth.
 The affected tissue becomes soft and watery as the disease progresses.
 The fungus eventually colonizes the entire cabbage head and produces large, black,
mustard seed like structures called sclerotia on the diseased tissue.
Cauliflower mosaic virus
Mosaic mottling, vein clearing, vein banding, stunted growth, central leaves are
smaller, small sized head and poor quality
Spread by aphids Brevicoryne brassicae, Myzus persicae
--------------------------------------------------------------------------------------------

DISEASES OF SWEET POTATO

White rust

The disease is of world wide occurrence and attacks other members of Ipomola.

Irregular yellow specks appear on the lower surface of the leaves. Latter they become white

blisters and rupture to expose the white powdery mass of spores. Corresponding to this

yellowing or browing can be seen on the upper surface of the leaves. Severe infection

causes defoliation.

Black rot
 Occurs wherever sweet potatoes are grown primarily a storage rot disease. Also

occur in the field as well as in seed beds.

All underground parts of the plant are affected. Black spots appear on the young

sprouts which eventually girdle the plant . This result in yellow and sickly appearance of the

leaves the blackening extends to roots and stem. Dark circular depressed spots are grayish

black when dry and dark greenish. Black when moist at the centre small black fruiting bodies

develop.

C. Organism: Mycelium septate branched brown with age. Microconidia are hyaline

one celled cylindrical. Macroconidia or chlamydospores olive brown obovate oval terminal or

in chain perithecia flask shaped with long beak ascospores elliptical.

Spread: Chlamydosporesa nd perithecia in crop residue & tuber.

F. Condition: Infection occurs in field at 10 -30 C with opt at 25 C Amount of disease

increases with increase in soil moisture at storage opt temp 23 – 27 0C.

 Control: Use of disease free planting materials

 Field sanitation.

 Soil should be well drained.

 Heat treatment at 43 C for 24hr.

 Dipping the seed materials in Hg CL2 at 1:1000 (or) TBZ 3.32 g ai / l

 Cutting should be planted in soil free from pathogen for disease free crop.

Storage rots

Soft rot : The disease begins as soft rot which progresses rapidly decaying the whole

tuber within 4-5 days. When the skin inbroken a straw coloured liquid drips out of it. If the

skin is not broken the affected tubers lose moisture and become shriveled and mammidfied

when the skin is ruptured during the progress of the diseases fugal growth can be seen

covering the affected.

 Surface consisting of sporangiophores and sporangia of the fungus the tissues turn

brown with mild odour.

F. Condition: Most rapid decay of tuber occurs at 15 – 23 C and RH 75 – 84%

 Control: Aovid wound or bruises on the tubers during digging and storing.

 DRY IN SUN FOR 1-2 hr before storage.

 Storages should be clean and washed with 2.5% CUSO4 solution.

 The temp of the stores should be held at 26.5 – 30 C with 90% RH for 10 – 14 days

then declimed to 13C & 85 -90% RH.Clearing of tubers before storage.

Dry rot

It is of minor importance in the field but it may cause serious damage in the storage.

In the field the rot begins at the stem end of the root. The diseased roots are shrunken and

wrinkled. The surface is covered with minute mounds. The internal decayed tissue is coal

black in colour.

Charcoal rot

This rot is relatively slow in storage. The tissues becomes chocolate to cinnamon

brown and later dark reddish brown in colour. Minute balck sclerotia develop on the affected

tissues giving black appearance. The decay in spongy at first turning to hard mummified

consistency.

DISEASES OF BEANS

Anthracnose

 This is an imported disease.

 It causes greater loss in cool temperature regions than in the tropics.
Symptoms:

 All aerial parts are affected.

 Most striking symptoms appear on immature pods.
  On leaves initially blackened dead portions of veins appear on the under
surface of the leaves.
 Later similar spots appear on the upper surface of the leaves.
 Lesions are also formed on petioles stems and cotyledons.
 On pods black sunken cankers with lighter or grey central areas are seen.
 The central area shows pinkish mass of spores during central areas are seen.
 The infection may go deep into the seed.
 The seeds of infected pods show brown to light chocolate coloured sinken
cankers on the seed coad.
C. Organisms: Colletotrum lindemuthiamum

Similar to that of C. gloeosporioides.

Mode of spread and survival:

The fungus survive on infected seeds and plant debris.

The fungus is seed borne.

Epidemiology:

Optimum temp 17 – 27 C ; RH 90 – 100%

In hills of North India maximum intensity reaches in August – September.

The disease is severe in cool wet season or when over head irrigation is used.

Management:

 Use of disease free seeds.

 Crop rotation for three years.
 Field sanitation.
 Avoiding over head irrigation.
 Sowing between mid April to Mid May.
 Seed treatment with Carbendazim 2g/kg.
 Foliar spraying with Carbendazim 0.1% or Mancozeb 0.2%or Zineb 0.2%.
 Use of resistant varieties wells Red kidney sea way, maniton. In HP 2
accessions AB 136 and G 2333.

Rust
 The disease attacks mostly leaves rarely the stem petioles and pods.
 Initial symptoms are minute whitish slightly raised pustules are produced on
under surface of the leaves.
 Later they become distinct reddish brown circular sori or pustules.
 On formation or teleuospors they turn dark brown or black.
 Severe infection gives a rusty appearances to the leaves.
 Severely infected leaves may turn yellow and dry and fall off.
 C. Organism: Uromyces phaseoli typical
 Autoecious long cycle rust.
 Uredospores – globose or ellipsoid single celled echimulated,
  Teleospores – globose or broadly ellipsoid single – celled
 pedicellate chestunut brown smooth with few varicose marks.
Mode of spread – Avi borne conidia

Epidemiology:

 Cloudy and humid days with leaf wetness in the morning favour germination
of spores and infection.
 A medium to fairly high temperature is required for heavy infection.
 Long day hours favour the disease.
Management:

 Field sanitation.
 Crop rotation.
 Wider spacing.
 Foliar spraying with Mancozeb 0.2% or Triadimefan 0.05%.
Augular Leaf spot

In India the severity of the disease has been reported upto 70% resulting in > 56%
pod loss.
Symptoms:

 Angular spots appear in between veins and vein lets on the leaves.
 The spots are initially dark grayish on upper surface and light grayish on
lower surface of the leaves.
 Later the spots turn to dark brown covered with grey mould on the lower
surface.
 Severely infected leaves fall off prematurely.
 On pods the spots are circular having reddish brown centre with well defined
ashy black border.
 Severely infected pods either bean no seeds or produce shriveled seeds.

Mode of Spread and Survival:

 The pathogen perpetuates through seed and plant debris.

 Both seed and soil borne.
 The disease is severe in wet weather.
Management:

 Crop rotation 3-4yr.

 Disease free seeds.
 Deep ploughing.
 Wider spacing.
 Well drained weed free soil.
 Application of carbendazim 0.1% or Tridemorph 0.1%
 Use of res var EC 77007, EC 10037, EC 10039.
Powdery mildew.
  Similar to PM of Pea
Ashy stem blight / Ashy grey stem

 Also called as dry root rot or charcoal rot.

Symptoms:

 Black sunken canker appears near the base of the cotyledons.

 It spreads downward into the stem and first pain of the infolded leaves.
 This results in damping off and death of young seedlings.
 On older stem reddish brown shallow cankers are produced.
 They become grey at centre with numerous minute black pycnidia.
 Infected plants are killed.
 Root infection causes blackening of roots and hence called as charcoal root.
 Leaf infection shows irregular dead areas at the tip marked by pycnidia.
 The infection spreads down the veins reaches the petiole causing defoliation.
C. Organism: Macrophomina phaseolina

Seed and soil borne.

Warm weather conditions of 32 – 34 C favourable for disease incidence.

Management:

 Disease free seeds.

 Field sanitation.
 Removal and destruction of infected plants.
 Avoidence of excessive soil moisture.
 Seed treatment thiram or carbendazim.
 Soil drenching with COC or Carbendazim.
Common Blight

It is a major constrain in bean production in tropics.

Yield loss upto 84% reported.

Symptoms:

 The disease affects leaves stem pod and seeds.

 Starts as water soaked spots on the under surface of the leaves.
 Enlarge to form irregular sunken reddish to brownish spots with yellow halo.
 Reddish discolouration of veins and mid ribs.
 Reddish streaks are formed on the stem .
 Severe infection results indefoliation.
 On pods water soaked spots surrounded by district zones of reddish brown
or brick red band of tissues are formed.
 The seeds are discoursed and shriveled .
 Seedling arises from infected seeds exhibits wilting.
C. Organism: Xanthomonas axonopodis pv. phaseoli.
 Mode of spread and survival:

The bacterium overwinters in seed plant debris and weed hosts.

Primarily seed borne sec spread through wind splashed rain.

Epidemiology:

Warm and humid condition favour disease development.

Management:

 Disease free seeds.

 Field sanitation.
 Deep ploughing to bury the plant debris.
 2-3 yr crop rotation.
 Spraying COC + Mancozeb.
 Seed treatment with streptomycin sulphate 0.5% or Hot water treatment at 50
C for 10min.
 Res var Goliath waxy, Ruse 6, Tara valley.
Common Mosaic- Bean Common Mosaic Virus (BCMV or BV 1)

One of the most commonly prevalent viral disease.

Causes considerable loss amounting to 26 – 84%.

First reported in 1963 in India.

Symptoms:

 The leaves have irregular shaped light yellow and green areas frequently in a
mosaic pattern.
 During early stage of infection the leaves appear crinckled chlorotic, stiff with
downward curling.
 In advanced stage the leaf size is reduced with filform leaflets, the plants are
stunted and appear bushy.
 The pods are under sized and have few seeds.
 Vascular necrosis of the root stem leaves and pods is also common.
C. Organism:

Bean common mosaic virus

Seed transmission.

Also transmitted by aphids. Aphis craccivora, A. fabae, Myzuz persical.

Management:

 Use of disease free seeds.

 Adjusting planting date coinciding with reduced vector actively.
 Barrier cropping with maize.
 Closer spacing.
 Removal and destruction of infected Plants.
  Spraying Monocrotophos 0.05% or Dimethoate 0.05%
 Res . var Pusa Parvati Top crop Masterpiece Premier PDR 14.
Yellow Mosaic Virus – Bean Yellow Mosaic Virus

 Bean yellow mosaic virus small chlorotic spots surrounded by yellow halo
appear on leaves.
 These spots enlarge and the leaves appear yellowish.
 Young leaves become glossy stiff and curled upwardly.
 The mottling of contrasting yellow and green areas become more intense.
This distinguish from common mosaic.
 The disease causes stunting bunches and delayed maturity.
C. Organism: Bean Yellow mosaic Virus

Transmn by aphids Aphids fabae M. persical. Macrosiphum euphorbial.

Management: Refer common Mosaic except for res var.

Res. var Black Turtle soup.

DISEASES OF COCONUT

1. Bud Rot – Phytophthora palmivora and Phytophthora katsurae

2. Basal stem rot / Thanjavur Wilt – Ganoderma lucidum
3. Stem bleeding – Thielaviopsis paradoxa
4. Grey leaf spot – Pestalotia palmarum
5. Root (Wilt) Disease – Phytoplasma
Bud rot: Phytophthora palmivora and Phytophthora katsurae
This is one of the worst diseases of coconut. It is found in many parts of India. First
reported in India in 1906 by E.J. Butler. Common killer / fatal disease. The seedlings and
young trees are more susceptible.
Symptoms:
 Affects palms of all ages, but young palms of less than 20 years of age are more
susceptible especially during rainy / monsoon season
 The first external symptom is pale green or yellowish green discolouration of the
heart leaf or central shoot.
 At the base of the heart leaf irregular, sunken, water soaked brown spot appears.
 The disease is characterized by rotting of the terminal bud and surrounding tissues
quickly
 The infected portion will be degenerated to slimy mass emitting foul smell.
 The affected heart leaf comes off easily when it is pulled.
  Within a few days the infection spreads to adjacent older leaves which become
yellow and then brown.
 In adult palm, the first externally visible symptom is withering of the spear leaf, which
subsequently turns pale in colour, bends over at the base and hangs down
 Withering and yellowing of one or two younger leaves surrounding the spindle
 Rotting of the tender leaf base and soft tissues of the crown into a shiny mass of
decayed material that emit a foul smell which attracts flies
 Rotting progresses downwards, affects the meristem and kills the palms
 The internal tissues show discolouration assuming a pale pink with a brown border
 Drooping of successive leaves and falling of leaves one by one, leaving only mature
leaves in the lower whorls at the crown
 Young nuts cease to develop and fall off prematurely.
 Severely affected palms are killed due to death of growing buds.
 Retained nuts on the palm grow to maturity
 The palm ultimately succumbs to the disease, if not checked
Causal Organism: Phytophthora palmivora and Phytophthora katsurae
Oomycetous – Peronosporales – Pythiaceal
Mycelium hyaline coenocytic – intercellular
sporangiophores are simple or branched.
Sporangia – Pear –shaped hyaline thin walled formed singly on germination – motile
zoospores reniform with two flagella.
Also produces chlamydospores – intercallery or terminal sexual reproduction –
Anthernidia – Oogonia – oospores.
Mode of spread and survival
 The fungus survives as oospores, chlamydospores and mycelium in the soil and in
the frond base or basal part of the crown which act as primary source inoculums.
 Secondary spread by zoospores through irrigation water, wind and windblown rain
Epidemiology
 Heavy rainfall, high relative humidity of 94-100% and temperature below 24oC for 6
days are highly favourable for the disease spread
Management
 Unless the infection is noticed in the early stages no curative measures could save
the palm.
 In early stages of the disease, cleaning and removal of all affected tissues of the
crown along with some healthy tissues and application of Bordeaux paste and protect
it from rain by providing a mud pot or a polythene covering till normal shoots emerges
 Spray 1% Bordeaux mixture to the spindle leaves and 2-3 innermost whorls of leaves
  Burn all diseased tissues removed from the palm
 As a prophylactic measure, spray 1% Bordeaux mixture on the spindle leaves and on
the base of 3-4 innermost whorls of leaves of neighbouring palms
 In palms that are sensitive to copper containing fungicides, spray and spray drench
with Mancozeb 0.4% (4g/L)
 Small perforated sachets containing 2g Mancozeb may be tied to the top of the leaf
axil. When it rains, a small quantity of the fungicide is released from the sachets to
the leaf base, thus protecting the palm
 Adopt control measures for rhinoceros beetle and red palm weevil
 Provide adequate drainage in gardens
 Adopt proper spacing and avoid overcrowding in bud rot prone gardens
 In bud rot prone gardens, prophylactic measures should be done to all palms 2-3
times at 45 days intervals
 Clean the crown before monsoon and follow strict phytosanitation
 Regular application of organic matters favours the establishment of biocontrol agents
and suppression of pathogens
 Apply salt and ash mixture or paddy husk after removing the affected portion in the
crown and subsequently cover with a mud pot. They absorb moisture and keep the
protected portion dry
 Apply bleaching powder on the affected portion
Basal Stem Rot / Thanjavur Wilt / Foot Rot / Ganoderma Wilt / Anabe Roga:
Ganoderma lucidum, Ganoderma applanatum and G. boninense
Thanjavur wilt disease of coconut is a major constraint in the production of coconut
not only in TN but also in the neighboring states. The disease was first noticed in Thanjavur
district of TN after the cyclone of 1952 and 1955 and hence the name Thanjavur wilt.
Symptoms
Palms bear profusely just prior to and at the initiation of symptoms
The diseased palms show the following typical symptoms in different parts of the palm viz.,
stem, leaves, inflorescence and roots.
a. Leaves
 Initially the leaves in the outer one or two whorls wither and droop with yellowing and
browning.
 Yellowing and drooping of leaves progress to younger leaves in quick succession
leaving the spindle leaf alone.
 Spindle leaf stand erect with flacidity
 The spindle leaf becomes short and do not unfold properly.
  The dried outer whorl of leaves remaining hang down around the stem for a long time
to form a skirt of dead leaves around the trunk (Plate31)
 Leaves break or buckle very close to their bases
 The crown is reduced to a mere handful of short erect yellow leaves (Plate 32).
 Drooped leaves fall off one by one leaving only a few smaller leaves at the apex.
 Delayed production of new leaves
 The newly formed leaves are pale and smaller in size
 Finally smaller leaves wither and bud decays
 Crown is easily blown off by wind
b. Stem:
 Bleeding of reddish brown viscous fluid (honey like) from the base of the stem with the
decayed tissues beneath.
 It is restricted to basal portion of the stem (0.1-1.5 m) from the base
 Discolouration, necrosis and rotting of internal tissues up to the height of bleeding
(exudation) and emitting a bad smell.
 In advanced stage the basal portion of the stem decays up to the central core.
 Sometimes wilt without external bleeding.
 The bark peels off.
 Apex of the trunk tapers
 In the advanced phase or in dead palms, the fungus fructifications may be observed at
the base of the palm just above the ground level as a shiny, waxy, brown, corky and
woody bracket
c. Inflorescence and nuts:
 Production of new inflorescence is arrested
 Button shedding is common.
 The subtended bunches hang down.
 Shedding of immature buttons and formation of barren nuts
 When the disease progress slowly, only few normal nuts are produced.
 Often bear profusely just prior to and at the time of initiation of symptoms.
 Nut and kernel weight, water content, copra weight and oil content decrease.
d. Roots:
 Extensive damage of the root system following rotting and disintegration of cortical
tissues
 Decay and death of finer roots (70 %).
 Production of new roots is very poor.
Causal organism: Ganoderma lucidum, Ganoderma applanatum and G.
boninense
 The fungus is hetrothalic. Hyphae are hyaline, chlamydospores are intercallery or
terminal golden yellow colour granules.
Conidia are round and thin walled.
Mode of spread and survival
 Fungus is soil borne inhabiting in roots of dead as well as living woody plants in the
soil.
 The disease spread is mainly through root contact.
 Secondary spread through air borne basidiospores.
Epidemiology
 Trees in the age group of 10 – 30 years are more susceptible.
 Prolonged drought, high soil temperature, low rainfall, extensive flooding, sandy or
sandy loam soils, presence of hard pan in the sub-soil and neglected gardens are
conditions favourable for the disease incidence
Management:
 The stumps of already infected and dead palms should be removed and burnt.
 The palms with advanced stage of infection and economical palms should be cut
along with root system and removed.
 Isolate the affected palm from the healthy ones by digging a trench of 1m deep and
50cm wide at 2.0m away from the bole of the infected palm
 Avoiding repeated ploughing and deep tillage to prevent root injury
 Provision of adequate soil moisture through irrigation or conserve moisture by
coconut husk burial during summer
 Flood irrigation should be avoided. (follow basin or drip irrigation)
 Provision of good drainage system
 Intercropping with crops like banana, turmeric etc.,
 Apply FYM or green leaf manure 50kg/palm/year to increase soil organic content.
 Balanced application of fertilizers.
 Soil application of neem cake @ 5 kg / palm /year.
 Apply 200g phosphobacteria+200 g Azotobacter / palm / year
 Soil application of Trichoderma viride 200g + P. florescence 200g fortified in neem
cake /compost / vermicompost / other organic wastes / palm/year
 Drench the basin with 40 litres of 1% Bordeaux mixture or 0.1% calixin after soaking
soil, at quarterly interval for one year
 Root feeding of 2 g Aureofungin-sol + 1g of Copper sulphate or Calixin 2ml or
hexaconazole 2 ml in 100 ml water at quarterly interval
 Avoid growing leguminous crops in and around the garden
Stem bleeding: Thielaviopsis paradoxa - Conidial stage (imperfect) Ceratocystis
paradoxa - Ascigerous stage (perfect)
The disease is mostly found in Thanjavur and Kanyakumari districts of TN and
Northern Kerala.
Symptoms
 Dark brown to black fluid exudes through the stem cracks on the basal part of the
trunk
 On drying the fluid forms black encrustation with brownish orange margin
(Plate38)
 Bleeding patches progress both upwards and downwards and cover major
portion / part of the trunk
 Lesions / patches coalesce to form larger patches
 Tissues beneath the bleeding points decay and become yellowish
 Except vascular bundles the other tissues are disintegrated
 Leaf size reduces leading to reduced crown size
 The rate of leaf production slows down
 Bunch production is reduced
 Nuts and buttons shed heavily
 In advanced stages uniform yellowing and dropping of leaves leads to complete
death of the palm
Causal Organism: Thielaviopsis paradoxa - Conidial stage (imperfect)
Ceratocystis paradoxa - Ascigerous stage (perfect)
Wound parasite
The fungus is airborne.
Epidemiology
Growth cracks on the trunk, sudden heavy manuring or heavy rains followed by
extensive dry period, poor drainage, soil moisture stress, hard pan formation in the soil,
imbalance in nutrition, excessive soil salinity, stem injury, lightning attack, insect attack etc.
act as predisposing / aggravating factors of this disease
Management:
 Chisel out the affected tissues completely and paint the wound with Calixin 5%
(5ml/100ml water)
 Apply coal tar or rubber kote after 1-2 days (Plate42)
 Burn the chiseled out material
 Avoid any mechanical injury to trunk
 Apply neem cake 5 kg per palm in the basin along with other manures and fertilizers
  Root feeding with Calixin 5% (5ml/100 ml water) during September-October,January-
February and April-May (Plate43)
 Drench the wet basin with 25 ml of Calixin in 25 litres of water once in 3-4 months
 Trail pepper on coconut to prevent direct exposure of cracks to pathogen
 Irrigate basins regularly during summer months and conserve moisture by coconut
husk burial
 Adequate manuring to increase the vigour of the palms
 Apply normal dose of organic manures (50 kg/palm/year) and balanced fertilizers
Grey blight: Pestalotiopsis palmarum
It is one of the widely distributed diseases. It reduces considerably the vitality of the
palm. The disease is particularly severe in Kerala and Tamil Nadu. Palms of 20-40 year old
are highly susceptible
Symptoms:
 Appears on the leaflets of mature leaves of the outer whorls of palm
 Yellowish brown oval spots with brown margins appear on leaflets
 The centre of the spots become greyish white, with dark brown margin
 Many spots coalesce to form large irregular necrotic patches causing extensive blight
 The acervuli of the fungus appears as black minute dots / specks on the lesions
 In advanced stages, the tips and margins of the leaflets dry and shrivel giving a burnt
appearance
 Premature shedding of leaves and reduction in the number of leaves prolong the pre
bearing age of young palms
Causal Organism: Pestalotiopsis palmarum
Mode of spread
Spread is through air borne conidia.
Epidemiology
Disease intensity is severe during rainy season with low temperature and high
humidity.
Poor soil nutritional status, especially potash deficiency and poor drainage increases
the disease incidence. Neglected gardens are severely affected.
Management:
 Recommended agronomic practices should be followed
 Good drainage facilities.
 Remove severely affected older leaves and burn
 Spray the crown with 1% Bordeaux mixture or 0.3% tilt (3ml/L) or COC or Dithane M
45
 Apply higher dose of potash (25% extra) along with recommended dose of NPK
  Apply increased dose of farmyard manure and composted coir pith (@100
kg/palm/year)
 CGD, COD and their hybrids are tolerant
Root Wilt: Phytoplasma
The disease was first reported following the heavy floods of 1882 in Kerala. Now the
disease has spreads to almost all coconut growing areas of Kerala and parts of adjoining of
TN especially in Coimbatore, Tirunelveli and Kanyakumari districts. Also called as Kerala wilt
disease. It is non lethal but debilitating.
Symptoms
 The disease is not a fatal one but a slow decline disease causing drastic yield
reduction
 The characteristic and earliest diagnostic symptom is the abnormal inward
bending of leaflets termed as ribbing or flaccidity resembling the ribs of mammals
(Plate1)
 Flaccidity of leaves of the central and outer whorls
 Whole frond develops a cup like appearance (Plate2)
 Foliar yellowing and marginal necrosis of leaflets of the outer whorls of leaves
(Plate3)
 Leaves produced subsequently become smaller and thinner
 Paling of the younger leaves and stunting of the crown due to the reduction in
number and size of the leaves
 Deterioration and decay of roots and rootlets from tip backwards and reduction in
regeneration of fresh roots
 Root cortex turn brown and dries up in flakes
 Superimposing of leaf rot disease root (wilt) diseased palms
 Drying up of the spathes and necrosis of spikelets from tip downward in
unopened inflorescence
 Inflorescence necrosis, production of little or no female flowers, pollen sterility
and shedding of immature nuts and buttons
 Reduction in size and number of nuts
 Production of poor quality nut / copra, thinner husk, less firm shell, weaker fibres,
uneven thickness of kernel
 Thinner kernel never dries up into copra but remains soft and flexible with very
less oil content
 Insipid tender coconut water
Causal organism: Phytoplasma
Vectors – Lace wing bug – Stephanitis typicus
 Plant hopper - Proutista moesta
Epidemiology
 Occurs in all major soil types but the spread is faster in sandy, sandy loam, alluvial
and heavy textured soils. Laterite soils have lower incidence and intensity of the
disease.
 Higher incidence in water logged low lying areas adjacent to rivers and canals and
also in neglected gardens
Management
Efficient management of root (wilt) affected palms demand control of all pests and
diseases, imparting natural resistance and health to the palms through proper manuring and
agronomic practices. A package of management practices for the effective management of
root (wilt) disease is given below
 Total eradication of all the disease affected palms in mildly affected areas of Northern
Kerala
 In heavily disease affected tracts, rougue out all severely affected uneconomic adult
palms yielding less than 10 nuts per year and all diseased palms in the pre-bearing
age
 Replant with disease tolerant like CGD varieties or high yielding hybrids like
Chandrasankara and CGD X WCT
 Apply balanced dose of NPK fertilizers in the form of urea, rock phosphate and
potash
Average management : 0.34 kg N, 0.17 kg P2O5 and 0.68 kg K2O per palm per year
Good management : 0.50 kg N, 0.32 kg P2O5 and 1.20 kg K2O per palm per year
 Add organic manures (cattle or green manure) @ 50 kg per palm per year
 Lime : 1 kg per palm per year and MgO (Magnesite Magnesium source) : 100g (In
Onattukara region: 500g)
 Grow green manure crops like sunhemp, sesbania, cowpea, calapagonium etc in the
coconut basin and incorporate in situ
 Adopt mixed farming by raising fodder crops in the interspaces and maintaining milch
cows
 Mixed cropping with cocoa and intercropping with tapioca, yams and elephant foot
yam
 Under rainfed conditions apply fertilizers in 2 splits, 1/3 at the time of south-west
monsoon and 2/3rd before the north-east monsoon. Under irrigated conditions apply
fertilizers in three equal splits during April-May, August-September and December-
January
  Apply fertilizers and manures in 10 cm deep circular basins at a radius of 2m from
the bole of the palm
 Desilt the channel and strengthen the bunds during summer months when the crop is
grown under the bund and channel system
 Adopt strictly all the prescribed prophylactic measures against leaf rot disease, red
palm weevil, rhinoceros beetle etc.
 Initial stage of the disease, spray the crown and drench the basin with 500 ppm
tetracycline
Leaf Rot: Fungal complex predominantly by Colletotrichum gloeosporioides,
Exserohilum rostratum and Fusarium spp.
Symptoms
 Affects palms of all ages, especially palms below 25 years
 Water soaked lesions with different shape and colours on the emerging spindle and
young tender leaves (Plate7)
 Dark brown spots develop on the tender leaves which later enlarge and dry up as the
leaf emerges (Plate8) and leaflets will not open fully (Plate9)
 Successive central shoots are affected, resulting in rotting of all the leaves on the
crown
 These lesions enlarge, coalesce leading to extensive rotting of spindle leaves
(Plate10)
 Extension of rotting into the interior of spindle resulting in decay and sometime rotting
of buds
 Tips of leaflets and midribs often become blackish, shriveled and fall off in wind,
giving a ‘fan’ like or ‘arrow leaf’ appearance to the leaves (Plate11)
 Successive infection of the emerging spindles results in appearance of symptoms in
most of the leaves of the crown
 Extensive lesions and their coalescing results in severe blighting of lamina (Plate12)
 Breaking of ends of leaves which subsequently become yellow and eventually hang,
dry and fall of
Causal Organism: Fungal complex predominantly by Colletotrichum gloeosporioides,
Exserohilum rostratum and Fusarium spp.
Mode ofSpread
Primary spread through air-borne conidia.
Epidemiology
Free water, raindrops, high relative humidity and low temperature especially during
monsoon season are highly favaourable. The prevalence of leaf rot due
to C. gloeosporioides is maximum during monsoon months where as the incidence due to E.
rostratum is maximum during winter season
Management
 Remove and destroy severely affected / senile and uneconomic palms
 Replant with healthy seedlings from elite palms and hybrid varieties tolerant to the
leaf rot - root (wilt) disease complex. CGD and hybrids of CGD X WCT are tolerant
under field conditions
 Adopt all recommended practices viz agronomic, cultural, plant protection etc as
applicable to root (wilt) disease endemic region
 Clean the crown in general during pre-monsoon period.
 Remove and destroy the rotten portions from the spear leaf and the 2-3 adjacent
leaves
 Pour 300 -1000 ml of fungicidal solution of Hexaconazol (Contaf 5E) - 2ml or 3g
mancozeb in 300ml water at the base of spear
 Spray crowns and leaves with 1% Bordeaux mixture or 0.5% Copper oxychloride
formulation (5g/L) or 0.4% Mancozeb (4g/L) in January, April-May and September.
While spraying, care should be taken to spray the spindle leaf and 2-3 adjacent
leaves
Mahali / Fruit Rot / Nut Fall: Phytophthora palmivora and Phytophthora
katsurae
Symptoms
 Female flowers and immature nuts rot and shed especially during rainy season
 Nuts of 2-5 months old are highly susceptible
 Water soaked dark green lesions appear, usually near the fruit stalk of immature
nuts, which later turn brown and become irregular in shape (Plate19)
 Lesions spread on the husk and endosperm resulting in their discolouration and
rotting
 Nuts fall prematurely (Plate20)
 Fluffy white mycelial growth forms on the fallen nuts or buttons (Plate21, 22)
 Water soaked lesions on the inflorescence and rachis result in rotting and drying of
inflorescence and rachis
Causal Organism: Phytophthora palmivora and Phytophthora katsurae
Spread of Disease
The fungus survives as oospores, chlamydospores and mycelium in the soil, frond
base or basal part of the crown.
Epidemiology
 Heavy rainfall, high relative humidity of 94-100% and temperature below 24oC are
highly favourable for the disease spread. Dissemination of the disease is primarily by wind
and wind blown rain and also by contact between bunches, dripping of rain water from the
diseased to healthy bunches and also through insects
Management
 Spray 1% Bordeaux mixture or copper oxychloride (5g/L) on the bunches and crown
during monsoon and subsequently twice at 40 days interval along with stickers as
prophylatic measure in disease prone area
 Collect and destroy the fallen nuts
 In disease prone areas, adopt proper spacing of palms
 Provide proper drainage
 Regular manuring and proper cultural practices reduce the disease incidence
Anthracnose and Leaf Blight: Colletotrichum gloeosporioides
Symptoms
 Affect palms of all ages especially on outer whorls of mature leaves
 Burnt or dried appearance of outer whorls of leaves
 Reddish brown oval to irregular sunken lesions with dark brown margin on leaves
 Salmon or reddish brown fruitification of the fungus as dots on the affected leaves
 Lesions coalesce resulting in leaf blight
 Disease progress to mid whorl of leaves causing premature drying and falling of
leaves
Causal Organism: Colletotrichum gloeosporioides
The disease is air borne
Management
 Remove and destroy severely affected leaves
 Spray 1% Bordeaux mixture or Mancozeb 0.4% (4g/L) on outer and mid whorls of
leaves at 45 days intervals
 In severe case, spray 0.3% (3ml/L) tilt / contaf at monthly interval
Mid Whorl Yellowing / Quick Yellow Declining: Phytoplasma
Symptoms
 A fatal disease caused by Phytoplasma
 Affects palms of all ages and spread rapidly
 Affected palms die within months (4-10 months)
 Lower and mid whorl leaves exhibit yellowing which subsequently spreads to inner
whorls leaving the spindle leaf (Plate44)
 The whole foliage become yellow and necrotic within months (Plate45)
 Developing and opened inflorescence, rachis and flowers become black
  Female flowers are severely reduced
 All nuts fall prematurely
 Basal regions of leaves rot resulting in drooping and falling of leaves in quick
succession
 Sometimes leaves show bronzing and fall off in quick succession without hanging
around
 Spear leaves and growing point rots resulting in the death of the palms
Causal Organism: Phytoplasma
Vector: Plant hoppers – Myndus crudus
Management
 Remove and destroy diseased palms
 Grow resistant variety – Malayan Yellow Dwarf.
 Adopt management followed for Root (wilt) disease
Inflorescence Blight and Nut Fall: Colletotrichum gloeosporioides, Gloeosporium spp.
Symptoms
 Serious disease after monsoon and during summer
 Sunken black or dark brown lesions on rachis
 Lesions coalesce resulting in drying of rachis from tip downward
 Inflorescence dries extensively resulting in severe button shedding and immature nut
fall
 Sunken dark grey, brown or black lesions with black to dark brown margins develop
anywhere on the soft portion of immature nuts
 Lesions enlarge to irregular form and coalesce to cover larger parts of the nuts
 Dark brown or salmon coloured fruiting bodies of the fungus appear on affected parts
 Longitudinal ruptures develop on the affected fruits, allowing the fungus and other
organisms to enter and causing rotting of mesocarp, shell and endosperm
Causal Organism: Colletotrichum gloeosporioides, Gloeosporium spp.
Fungus is air borne
 Remove and destroy dried inflorescence and fallen buttons and nuts
 Spray 1% Bordeaux mixture or Mancozeb 0.4% (4g/L) on inflorescence and also on
developing buttons and nuts as prophylactic measure at 45 days interval
Botryodiplodia Nut Fall: Botryodiplodia theobromae (Lasiodiplodia theobromae)
Symptoms
 Occurs during summer months and affects nuts of all stages
 Disease appears as black extensive patches at the stalk end of the fruit
 Later these black patches progresses to cover the major portion or entire nuts
without definite margins.
  Black fruiting bodies of the fungus seen as dots on affected nuts and rotting of
nuts
 Nuts rot and shed prematurely
Causal Organism: Botryodiplodia theobromae (Lasiodiplodia theobromae)
Airborne
 Remove and destroy dried inflorescence, fallen button and nuts
 Spray 1% Bordeaux mixture or Mancozeb 0.4% (4g/L) on inflorescence and also on
developing buttons and nuts as prophylactic measure at 45 days interval
 In diseased gardens, spray the inflorescence and nuts with 0.1% Calixin / Contaf /
Tilt after harvesting the mature nuts
Tatipaka Disease
Symptoms
 First appeared in Tatipaka village of East Godavari district of Andhra Pradesh,
following a cyclone in 1949.
 Palms in the age group of 25 to 60 years are more susceptible.
 Development of an abnormally large crown with dark green inner leaves and
higher yield is the precursor of disease incidence. Subsequently the crown
becomes smaller in size producing progressively shorter leaves.
 The stem begins to taper. The leaves give a fascinated appearance due to
improper unfolding of leaflets. The affected tree produces smaller bunches with
atrophied barren nuts.
 The causal agent is suspected to be Phytoplasma.
Differences between Basal stem rot, Stem bleeding and Root wilt diseases.
Description Basal Stem Rot / Stem bleeding Root Wilt
Thanjavur Wilt /
Foot Rot /
Ganoderma Wilt /
Anabe Roga
Bleeding symptoms Seen at the base or Seen at the base or Not seen.
collar region. any part of the trunk.
Sometime may not
be seen externally.
(Reddish brown Brownishto black, --
viscus fluid) non viscus fluid)
Internal decay Present upto the Confined to bark --
central core tissues.
Maximum height of Upto 4-5m Upto trunk apex --
bleeding symptoms
Root decay Extensive root decay Not present Present
present
Brackets of Produced in the Not produced Not produced
Ganoderma advanced stage of
the disease or after
the death of the
palms
Crown symptoms Yellowing, drooping Only reduction of Yellowing, Flacidity
and drying of leaves crown size and and inward bending
one after another tapering of crown at of leaflets. No. & size
from outer whorl advanced stages. of leaflets reduced.
Rib like leaf lets Absent Absent Present
Death Within 6 to 24 Longer period Longer period
months

DISEASES OF ARECANUT

Mahali/Fruit Rot/Koleroga: Phytophthora meadii (major species), P. arecae, P.heveae

 This dreaded disease occurs in all the arecanut growing regions receiving heavy
rainfall
 The crop loss varies from 10-90%
 Characteristic symptom is rotting and extensive shedding of the immature nuts during
south west monsoon
 The first symptom appears as dark green/yellowish water soaked lesions on the nut
surface usually near the soft inner perianth region and infected nuts lose its natural
green luster
 The lesions gradually spread covering the entire nuts (before or after shedding)
which consequently rot and shed
 A felt off white mycelial mass envelopes on entire surface of the fallen nuts
 As the disease advances the fruit stalks and the axis of the inflorescence rot and dry,
sometimes being covered with white mycelial mats
 Infected nuts are lighter in weight and possess large vacuoles
 Dark brown radial strands on kernel make them unfit for chewing
  Infection occurring later in the season results in rotting and drying up of nuts without
shedding called ‘Dry Mahali’
Causal Organism: Phytophthora meadii (major species), P. arecae, P.heveae
Mode of Spread and survival
 The fungus survives as oospores, chlamydospores and mycelium in soil, on fallen
nuts, on dried nuts and inflorescence remaining in the crown. The spread of the
disease is by wind and windblown rain
Epidemiology
 Mahali is weather dependent and seen during monsoon season from June-October
 Continuous heavy rainfall with intermittent bright sunshine hours, low temperature of
20-230 C, constant high relative humidity of more than 90%, wind, cloudy weather,
plantations situated in valley surrounded by rubber plantations etc. favours the
outbreak of the disease
Management
 Prophylactic spray of 1% Bordeaux mixture with stickers once before the onset of
south west monsoon followed by second and third applications at 40-45 days interval
 Cover bunches with polythene sheets before monsoon rains
 Collect and destroy all fallen and infected nuts
 Remove and destroy all completely affected inflorescence and immature bunches
Bud Rot or Crown Rot: Phytophthora meadii, P.heveae, P. arecae
 Occurs independently (bud rot) or following severe fruit rot infection (crown rot)
 Spindle leaf shows discolouration from the natural light green colour to yellow
and then to brown followed by withering
 Infection spreads inside the bud causing rotting of growing bud and the
surrounding young leaves
 The spindle slumps/droops and can be drawn out with a gentle pull
 Infection spreads to the adjacent leaves, which becomes yellow, droops and drop
off one by one leaving a bare stem
 Secondary organisms colonize the infected tissues and converts it into a slimy
mass emitting a foul smell
 Severe fruit rot infection, especially on bunch and inflorescence stalks, which
spreads to the stem and outer leaf sheaths
 Inner portion of the leaf sheath exhibits water soaked lesions and base of leaf
sheath rots resulting in yellowing of outer leaves
 Disease spreads to subsequent upper leaf sheath base resulting in their rotting
and yellowing of middle whorls of leaves
  Tender portion of the stem and growing bud becomes infected resulting in rotting
of the internal tissues of the crown and finally death of the palm
Causal Organism: Phytophthora meadii, P.heveae, P. arecae
Spread of Disease
 The fungus survives as oospores, chlamydospores and mycelium in soil, on fallen
nuts and on dried nuts and inflorescence remaining on the crown. The spread of the
disease is by wind and windblown rain
Epidemiology
 Continuous heavy rainfall with intermittent bright sunshine hours, low temperature of
20-230 C, constant high relative humidity more than 90%, wind, cloudy weather,
plantations situated in valley surrounded by rubber plantations etc. favours for the
outbreak of the disease
Management
 Remove and destroy dead palms, fruit rot affected dried bunches, fallen nuts and
crowns of palms affected by bud/crown rot
 When the spindle leaf starts withering, remove and destroy all affected tissues of the
spindle along with healthy tissues
 Apply Bordeaux paste and protect it by covering with a polythene cover or a mud pot
 Spray drench the spindle leaf base and the base of the other leaves with 1%
Bordeaux mixture
Basal Stem Rot/Foot Rot/Anabe Roga/Ganoderma Wilt: Ganoderma
lucidum (frequent), G. applanatum (associated)
 A fatal disease affecting the palm in the age group of 5-10 years
 Destroy 5-8 % of the palms in neglected and water logged gardens
 The diseased palm cannot be identified in the initial stages of the disease
 The palm in the advanced stage of infection shows symptoms on the crown, stem
and root system
 Leaflets of the outer whorls of the leaves develop yellowish-orange discolouration
which gradually spreads to the inner whorls of leaves
 The pale discolouration spreads to the whole leaf and the entire crown becomes
progressively yellow with the dried outer whorl of leaves drooping down and covering
the stem
 Later the inner whorl of leaves also becomes yellow leaving only the spear leaf green
 Development of inflorescence and nuts is arrested
 In the advanced stages, spindle gets dried up and the crown topples down leaving
the bare stem
  Stem tapers, internodal length is reduced and its internal tissues are completely
damaged
 The infected brittle stem breaks off easily during heavy wind
 The base of the stem up to 1m height shows brown disolouration and oozing of a
dark fluid
 Bracket shaped fruitification of the fungus develops at the base of the trunk, usually
after the death of the palm, or on the stump or on the live palm
 Roots exhibit varying degrees of discolouration and rotting, which become brittle and
dry with a musty smell. Uptake of water and nutrients is affected
Causal Organism: Ganoderma lucidum (frequent), G. applanatum (associated)
Spread of Disease
 The disease is severe in neglected, ill-drained and overcrowded gardens especially
with hard, black loamy acid soils of higher iron and calcium contents
 Soil borne, but secondary spread is through air borne spores
Management
 Remove and destroy all severely affected palms and stumps of dead palms,
including roots
 Drench the soils with 1% Bordeaux mixture before planting healthy seedlings
 Isolate affected palms by digging deep trenches all around, one metre from the base
and drench with 0.1% Calixin / Contaf (1ml/L). Minimum of 10 litres of fungicide
solution is required for a bearing palm
 Improve drainage
 Avoid dense planting
 Avoid flood irrigation and water flowing from infected palms to healthy palms
 Avoid repeated ploughing and digging in the diseased gardens
 Balanced manuring and fertilizer application
 Apply 2 kg neem cake/palm/year
 Discourage growing of collateral hosts of the fungus, such as Delonix regia
andPongamia glabra in the vicinity of gardens
 As a prophylactic measure, apply biocontrol agents Trichoderma harzianum fortified
in organic manures into the soil
 Root feeding of palms with 100 ml of 2.0 % Calixin (20ml/L) through 2-3 roots in the
early stage of infection at quarterly intervals
Stem Bleeding: Thielaviopsis paradoxa (Ceratocystis paradoxa)
 Young palms of 10-15 years are more susceptible but older palms are rarely infected
 Small discoloured depressions or spots on the basal portions of the stem
 Spots coalesce to form larger patches followed by cracking
  Fibrous layers of the stem disintegrate which eventually hollows up to varying depths
along the infected portions
 Dark brown gummy exudates ooze out from cracks
 Stem tapers near the crown
 Crown size and yield is reduced
 Severely affected palms die off
Causal Organism: Thielaviopsis paradoxa (Ceratocystis paradoxa)
Spread of Disease
 The disease is severe in neglected gardens with poor drainage. Higher water table
predisposes the palms to this disease
Management
 Improve drainage
 Balanced manuring/fertilizer application
 Scrap off the affected portion of tissue and smear with hot coal tar or rubber kote
mixed with Calixin @ 5ml/kg or Bordeaux paste
 Swab 5% Calixin (5 ml/100 ml) after the removal of the infected portion along with
healthy tissues and drench soil with 0.1% Calixin or root feeding of 100 ml of Calixin
2.0% (20ml/L) through 2-3 roots
 Trailing pepper
Yellow Leaf Disease; Phytoplasma
 Also known as Kattuveezhcha / Chandiroga / Arasiroga
 Most serious disease of arecanut and is present in all districts of Kerala in
moderate to severe form
 The yield loss is as high as 50% over a period of three years immediately
following the disease incidence
 Affects palms of all age groups (Plate1,2)
Symptoms
 Symptoms appear as translucent spots of 1-3 mm diameter and characteristic
yellowing of the tips of leaflets in two or three leaves of outermost whorls.
(Plate3)
 Yellowing gradually extends to the middle of the lamina showing a clear cut
demarcation of yellow and green parallel bands on both sides of the midrib of
leaflets (Plate4)
 Progressive drying up of tips of the chlorotic leaves
 As the disease progresses the yellowing extends to the whole lamina, leaving
only the leaf stalk green
  Sometime one or two leaflets in any part of the crown or the entire foliage may be
affected in the initial stage
 In the advanced stage, leaves are reduced in size, stiff, pointed, closely bunched
rosetted and abnormally puckered
 Internodal length is reduced, stems tapers and inflorescence not produced
(Plate5)
 Mature and immature nuts shed in large numbers, endosperm becomes soft and
black
 The crown falls off leaving a bare trunk
 Varying degrees of rotting on roots
 Lateral root production reduced
 Tips of absorbing young roots blacken and rot, especially in water logged
conditions.
 Roots exhibit vascular discolouration
Causal Organism: Phytoplasma
Vector: Planthopper (Proutista moesta)
Managent
 Apply recommended dose of fertilizers
 Add extra 160 g of rock phosphate to increase new root formation
 Apply lime at the rate of 500 g per palm once in 2-3 years during June-July
 Apply organic manure @ 12 kg each of compost and green leaves per palm
 Provide irrigation during summer months
 Avoid water stagnation in the garden by providing drainage facilities
 Grow cover crops in the garden and apply in situ
 Remove infected palms
 Replant the affected gardens with high yielding local varieties like Kasargod local,
Dakshin Kannada local, Sirsi local and also with dwarf varieties like Hirahalli
dwarf and Mohit nagar
 Apply 100 g Magnesite and 100g of micronutrient per palm per year
 Spray Rogor/Dimethoate 30 EC (1.5 ml/L) to control insect vectors
Inflorescence Die-Back and Button Shedding: Colletotrichum gloeosporioides
 Wide spread in areca nut plantations often resulting in heavy yield loss
 The disease is seen throughout the year, but becomes severe during summer
months from February to May
 Yellowing of rachillae of inflorescence
 Yellowing progresses from the tip of the rachillae towards the main rachis
  As the disease progress, the entire rachillae turn dark brown causing wilting and
drying of inflorescence (inflorescence die back)
 Shedding of female flowers (buttons) in large numbers
 Discolouration of the inner soft calyx region of the female flowers and buttons results
in their shriveling, drying and shedding
 Concentric rings of light pink coloured mass of spores appear on the discoloured
infected inflorescence
 On severe infection the female flowers and buttons shed completely or dries up and
remains on the crown
Causal Organism: Colletotrichum gloeosporioides
Spread of Disease
 Spread is through air borne conidia
Management
 Remove and destroy completely dried inflorescence, buttons and all fallen nuts
 Spray 0.4% Zineb or Mancozeb (4g/L) twice, first one just after the setting of female
flowers and then again at 3-4 weeks interval as prophylactic measure. Bordeaux
mixture 1% and 0.3% Captan (3g/L) are also very effective
 In diseased gardens, spray 0.1% contaf/tilt/topas/bavistin or 50 ppm(50mg/L) of
aureofungin sol
Leaf Rot: Colletotrichum gloeosporioides
 Seedling and young bearing palms are more susceptible
 Water soaked lesions on margins and tips of young leaves and emerging spindle leaf
 Lesions develop into dark brown sunken spots which enlarges and dries up due to
extensive rotting
 Dried/shrivelled tips and margins of leaflets shred off leaving only the mid-veins
 On severe infection, lesions develop on mid-veins, midrib and even to the growing
spindle leaf resulting in rotting of spindle leaves and growing bud
Causal Organism: Colletotrichum gloeosporioides
Spread of Disease
 Air borne disease, spreading through conidia
Management
 Remove and destroy affected portion of the leaves
 Spray 0.4% Mancozeb(4g/L)/1% Bordeaux mixture on spindle leaf and inner whorls
of leaves and also spray drench the axil of inner whorls of leaves with either of the
fungicides
 In severe case, spray the crown with 0.1% Contaf / Tilt(1ml/L) / bavistin (1g/L) at
fortnightly intervals
Leaf Blight/Grey Blight: Pestalotiopsis palmaraum and Phomopsis palmicola
 Seedlings and young palms are affected, especially during summer months
 Characteristic reddish brown or dark brown discoloured spots on mature outer whorls
of the leaves
 Spots enlarge to form irregular patches with brown margin and grey centre which
have minute black dot like structures
 In advanced stages of infection, extensive blighting of leaves results in stunted
growth
Causal Organism: Pestalotiopsis palmaraum and Phomopsis palmicola
Spread of Disease
 Spread of the disease is through air borne conidia
Management
 Remove and destroy severely affected older leaves
 Apply recommended dose of manures and fertilizers
 Provide shade to the nursery plants
 Spray 1% Bordeaux mixture or 0.4% Mancozeb (4g/L)
Leaf Spot/Anthracnose: Colletotrichum gloeosporioides
 Seedlings and palms of all ages are affected
 Outer whorls of the leaves are more susceptible
 Small yellow specks appear on the leaf lamina
 Specks enlarge to form irregular sunken lesions with dark brown margins and light
brown centre having minute dot like structures
 Characteristic prominent yellow halo develops around the sunken lesions
 Lesions advance and coalesce to form larges patches resulting in premature
yellowing, blighting, drying, drooping and shredding of leaves
 Severe infection causes stunted growth and death of the seedlings
Causal Organism: Colletotrichum gloeosporioides
Spread of Disease
 The fungus spread through air borne conidia
Management
 Remove and destroy severely affected leaves
 Provide shade to nursery plants
 Spray 1% Bordeaux mixture/0.4% Mancozeb (4g/L) at fortnightly intervals
 In severe cases, spray 0.1% contaf/tilt (1ml/L)/bavistin(1g/L) at fortnightly intervals
Bacterial Leaf streak: Xanthomonas campestris pv arecae
 Dark green, water – soaked, translucent limear lesions or stripes produced paralled
to mid of the leaflets.
  Later the lesions are covered with abundant creamy white and slimy bacterial
exudates on the lower surface.
 On drying the exudates forms a waxy film or Creamy white to yellowish falkes.

DISEASES OF TEA
1. Blister blight: Exobasidium vexans Massee
This disease was first reported from Assam in 1868. Since then it spreads to most
other tea growing states of North and South India. It also occurs in Burma, Indonesia, Japan,
Malaysia, Singapore, Sri Lanka and Taiwan. Since 1946 it has become severe year after
year in South India causing heavy damage to the industry.
Blister blight produces losses up to 50%.
Losses due to blister blight extend up to 43% on annual crop basis.
Heavy attack can result in death of the whole plant. Even with fungicide control
11.3% yield loss occur in Sri Lanka, in the peak attack at the altitudinal range of 1500m -
<1800 m (FUCHS, 1989).
Symptoms:
 It is a disease of both nursery and planted crop.
 In nursery, seedlings are stunted and produce many thin stems instead of a single
stalk.
 Repeated attacks cause death of seedlings.
 Succulent leaves and green shoots of newly pruned tea are highly susceptible
 The fungus attacks the first flush of 2-3 young leaves and kills the young shoots and
buds. Thus the new growth is largely ruined.
 Mature leaf is not affected.
 The first symptom is the appearance of small, circular, oily, pale or pinkish,
translucent spots on the tender leaves
 These spots enlarge in size in due course upto an inch in diameter.
 Later the spots turn into deep red shiny blisters.
 The spots become depressed into a shallow cavity on the upper surface of the
leaves.
 Correspondingly the under surface of the leaf bulges as a concave trough-like
depression forming a classic blister – like swelling.
 The lower bulged surface is covered with white fungal growth.
 Leaves become curled and distorted.
 Later, the blisters turn to dark brown and shrink to flattened patch.
 The infection spreads to petiole and young succulent stem resulting in serious
damage.
  On stem, spots are produced without blister.
 The fungus penetrates the stem.
 Stem infection leads to goose neck shape, dieback and snapping at the point of
infection.
 The leaves and buds above the point of infection wilt and wither
Causal organism: Exobasidium vexans Massee
Mycelium – Septate inter & intracellular - collect in bundles below lower epidermis to
produce erumpent hymenial layer from which vertical hyphae are projected by rupturing the
epidermis on the surface of the spots.
Two kinds of spores – the conidia and the basidiospores are produced
Conidia – borne singly at the tips of long stalks. Hyaline elliptical, single celled or two
celled (when mature), straight or slightly curved
Basidia are intermingled with conidial stalks and sterile hyphae. Paraphyses single,
septate, apically rounded Basidia are long club shaped, clavate, 30 - 35 x 5 - 6 µm. generally
bearing two sterigmata
Basidiospores are ovate to oblong, ellipsoid, hyaline initially unicellular, becomes 1-
septate at maturity, 13-27 x 4.3-6.5 µm
Sporulation occurs after 10-19 days and spore discharge period extends upto 8 days.
Number of spores ejected in 24 hours is 1.3 million/sq.cm and the pathogen completes its
life cycle 11- 28 days.
Mode of spread and survival:
 Air borne
 Survives in the pre existing infected bushes
Epidemiology:
 Favourable conditions for infection are cloudy weather (monsoon months);
continuous leaf wetness for 11-13 hours coupled with relative humidity >60% and
temperature between 17 to 22oC.
 RH plays an important role in the epidemics.
 The disease is favoured by cool day and night with wet or humid conditions.
 More severe outbreaks occur under shade or adjacent to jungle or wind breaks or in
damp low lying areas where mist persists.
 Cool moist, relatively still air favours infection.
 Moist and shade are therefore more conductive for the development of severe
attacks.
 Temperatures > 24oC are fatal to the disease. Because of that periodical appearance
and disappearance of the disease occurs.
Management:
  Removal of affected leaves and shoots by pruning and destruction
 Spraying Bordeaux mixture or Copper fungicides found to be effective.
 Copper fungicides are often used with nickel salts which have eradication effect.
 (A mixture of 210 g of copper oxychloride + 210 g of nickel chloride per ha at 5 days
interval from June – September and 11 days interval in October – November gives
economic control)
 Spraying with 420 g of COC + 27 g of Agrimycin 100 per also gives better control
 Chlorothalonil gives both protective and therapeutic effects.
 Systemic fungicides like Tridemorph, Bayleton, Baycor offer good disease control.
 Chemical fungicides such as copper oxychloride as protectant (inhibits germination of
spores), tridemorph (Calixin), hexaconazole (Contaf 5E) and propiconazole (Tilt
25EC) are recommended for blister blight control in both pruning and plucking fields.
Grey blight: Pestalotiopsis theae
It occurs both in North and South India.
In South India, it occurs in Karnataka, Kerala and Tamil Nadu.
Symptoms:
 The disease generally attack older leaves.
 The disease initiates as minute round brown spots.
 Soon the spots enlarge and turn grey with dark brown margin.
 The lesions become necrotic
 Fructification (acervuli) appears as minute black dots in the form of concentric rings.
 The fungus also attacks plucking points causing die back.
 If young leaves affected the leaves become blackened and unfolded.
Brown blight: Glomerella cingulata
Symptoms:
 Small, oval, pale yellow-green spots first appear on young leaves.
 Often the spots are surrounded by a narrow, yellow zone.
 As the spots grow and turn brown or gray, concentric rings with scattered, tiny black
dots become visible
 Eventually the dried tissue falls, leading to defoliation.
 Leaves of any age can be affected.
Mode of spread and survival:
 Survives in the pre existing infected bushes
 Air borne conidia
 Pathogen gains entry through wounds
Epidemiology:
 The infection is predisposed by sun scorch insect plucking wounds.
  The incidence is more frequent on weak bushes especially if potassium is deficient
 More prevalence in shear harvesting fields during monsoon, stripping and wounds.
Management:
 Spraying of mancozeb at 0.3% or carbendazim or thiophanate methyl 0.05 % at 10-
15 days interval
Black rot: Corticium invisum, C. theae
 Small, dark brown irregular spots appear on leaves.
 Spots coalesce to form dark brown patches covering the entire leaf lamia.
 Leaves and twigs turn brown.
 Dead leaves are hanging on thin threads from the branches
 The affected leaves drop off.
 Before the leaf turns black, the lower surface shows white powdery appearance.
Causal organism: Corticium invisum, C. theae
Mode of Spread:
 Air borne
Epidemiology:
 The disease develops rapidly when the temperature and humidity are high.
 Basidiospores germinate only in wet weather or when the leaf is covered with dew.
Management:
 Pruning in December
 Removal and destruction of affected debris
 Spraying copper oxychloride
Red Rust: Cephaleuros mycoidea and Cephaleuros parasiticus
The disease is widespread and imported in India, Africa, Sri Lanka and America.
Symptoms:
 On leaves the alga occurs sometime as parasite or some time as epiphytic.
 The alga occurs as orange yellow, roughly circular patches on the upper surface of
the leaves.
 The patches may be few or numerous, crowded or scattered and may occupy most
of the leaf.
 Under favourable conditions the alga penetrates the leaf tissues.
 The penetration filaments are intercellular.
 They never penetrate host cells but get nourishment by osmosis.
 The host cells in contact get killed and become brown and dried up.
 On stem the alga is normally parasitic producing cankers and killing the tissues.
 It occurs as red hairy patches.
Causal organism: Cephaleuros mycoidea and Cephaleuros parasiticus
 The cell contents of the alga orange red, hence the misapplication of the name rust.
Epidemiology:
 Poor soil drainage, imbalanced nutrition, and exposure to relatively high temperature
and humidity predispose tea plants to infection
 Rainy season is more favourable for multiplication of alga
Management:
 Removal and destruction of affected plant parts
 Increasing the vigour of bushes by proper fertilizer applicaton
 Spraying with Bordeaux mixture 1%
Root diseases
Primary Root diseases
a. Brown root disease: Fomes noxius
 Common in low elevation area
 Slow spreading and quick killing pathogen
 The roots are encrusted with a mass of earth and small stones cemented to the root
by the mycelium
 Mycelium tawny brown resembling sambar skin
 Between the bark and wood there is a thin layer of white or brown mycelium
 Wood turns soft and spongy and honey- comb like reticulations on the wood
 Fructification seen on stumps- bracket shaped, irregular and hard
 Infection spreads mainly through root contact
 More common in sandy soils than claying soils/
 The disease originates from decaying stumps leaf out in soil.
b. Black root disease: Rosellinia arcuata
 First identified root disease of tea
 It is a common disease on tea
 Occurs in India and Sri Lanka
 The fungus originates from the heaps of dead leaves.
 The fungal attack usually begins at collar regions.
 Black woolly strands of mycelium closely adhere to the roots and collar as loose cob
webby mass.
 These enter the bark and spread out into star – like sheets of white mycelium.
 Girdling and canker seen at collar region
 The mycelium then ramifies between the bark and wood.
 The mycelium divides into number stands at the entry point which radiate over the
surface of the wood forming a white star upto 1 cm diameter.
 A swollen ring of tissue is formed round the stem above and below the dead patch.
  Mycelium grows freely through surface soil and organic matter and spreads rapidly in
damp weather.
 Removal of surface mulch around 10 meters
 Drenching the soil with Dithane M 45/Captan 30 g/10 litres of water.
 Avoid soil rehabilitation.
c. Red root disease: Poria hypolateritia
 Fast spreading and slow killing pathogen
 It occurs in Assam and TN.
 The fungus is confined to underground parts.
 Mycelium white, later turns red, in advanced stages may appear black
 Interwoven with adhering soil; on washing soil goes off – blood red mycelium seen.
 When the bark is peeled off, characteristic, flat, black rhizomorphs are seen.
 These strands form branched markings on the surface of the wood.
 ‘The roots show mottled appearance of red and white.
 The bark is softened.
 The wood may be discoloured as bluish black.
d. Xylaria root disease: Xylaria sp.
 Roots covered by black, ribbon like mycelial strands;
 Extensive necrosis of feeder roots;
 High casualty soon after drought.
SECONDARY ROOT DISEASES
a. Armelliella root rot: Armelliella mellea
 Usually the disease becomes apparent after it has severely damaged the root system
 The foliages become chlorotic, wilted and droped off.
 Death of whole plants then follows.
 Sheets of creamy mycelium are seen beneath the bark along with flattened brown
rhyzomorphs.
 In advanced stages sporophores are produced at the collar region.
 The sporophores occur in clumps and are pale brown and mushroom – shaped.
 Infected large root pieces provide main source infection.
 Rhyzomorphs can grow through soil and reach healthy hosts.
b. Inter root disease: Botryodiplodia theobromae
 Commonly seen in low and mid-elevations area
 The disease appears 3 months after pruning.
 Weak appearance of frame
 Presence of unhealthy leaves,
 Failure of bushes to recover after pruning,
  Die back of new shoots
 Presence of white powdery spots with black centres on root surface
 The bark is rough and abnormally thickened,
 The fructifications are minute, black, and spherical embedded in the bark.
c. Charcoal stump rot: Ustulina zonata
 The leaves wither turn brown and drop off.
 Sudden death of bushes
 White fan shaped mycelium on the surface of wood beneath the bark
 Charcoal like encrustation on bark seen in advanced stages
d. Violet root rot: Sphaerostilbe repens
 Leaves turn yellow and droop, gradual death of bushes,
 Presence of enlarged lenticels on root bark;
 Roots become inky black/violet;
 Develop rancid odour- vinegar smell
 White colour mycelium, later turns to purple, seen on wood.
 Avoid planting in water logging areas
 Improved drainage controls
e. Collar canker: Phomopsis theae
 Observed mostly in young tea
 Pathogen invades the stem through open wound.
 Chlorosis, cessation of growth, profuse flowering and canker on stem
 Predisposing factors are deep planting, planting in gravelly soils, mulching closer to
collar, wound caused by weeding implements, fertilizer application close to the collar,
pegging, low moisture status in bark and surface watering during dry weather.
 Preventive measures include avoid planting of susceptible clones in gravelly soils
and drought prone areas, improving organic matter of marginal soils and using plants
with good root system. Removal of affected portion by pruning to healthy wood and
application of copper fungicide or spore suspension of biocontrol agents
like Trichoderma and Gliocladium to cut ends are the curative measures.
Minor diseases
Pink disease: Pellicularia salmonicolor
 A number of silky thread unit to a thin film on stem and leaves.
 Young branches lose the leaves and die back.
 Bark killed in patches.
 The branches become irregularly swollen.
 The fungus forms pink fructification over affected f stem.
 Basidiospores are wind borne.
 Application of potash promotes recovery.
Cercospora leaf spot / Birds eye spot: Cercospora theae
 Small spots with brown centre and reddish brown margin are formed on leaves.
 Several spots coalesce to form irregular patches with shot holes.
 Severe infection causes pre mature leaf fall.
 The disease is severe after heavy rains.
Thread blight: Pellicularia koleroga
 The disease is common in Assam and other parts of India.
 Sterile white threads or strands pass along the branches.
 Spread into a fine web like film on the under surface of the leaves.
 This causes browning and death of leaf cells.
Sooty mould: Capnodium spp.
 The leaves and shoots are covered with black sooty.
Twig die back/ Stem canker/Branch Canker: Macrophoma theicola
 Cancerous growth around the longitudinal wounds on the branches of tea bush.
 Control measures are to cut off the affected branches
 Spraying any of the systemic fungicides (Tridemorph, hexaconazole and/or calixin) at
0.5 % (50g in 10L) over the infected portions.
Leptothyrium die-back: Leptothyrium theae
 Common in higher altitudes
 Pathogen enters through the pruning cuts
 Dieback of shoots below the cut ends
 Infected branches snap off easily.
 Application of copper oxychloride & linseed oil paste on cut ends prevents the
disease.

DISEASES OF COFFEE
Collar rot: Rhizoctonia solani
The disease occurs on 1-3 months old seedlings in nursery.
Prevalent in all coffee growing areas of India
Seedling loss uto 10-20%
Symptoms
Causes both pre – and post - emergence damping off
Pre emergence Damping off
 The fungus invades embryo and endosperm before germination
 It causes decay of germinating seeds
 Young radical and plumule undergo complete rotting
  Seedlings are infected and died before the emergence from the soil
 Causes poor and uneven stand of seedlings in nursery beds
Post emergence Damping off
 Occurs after the emergence of seedlings from the soil
 Watery, soft rot develops at the collar region of the stem
 Affected portion shows shrinking and brown discolouration due to rotting
 The affected seedling become collapsed and toppled down
 Mortality of seedling is very conspicuous
Mode of spread and survival
 soil-borne sclerotia
Epidemiology
 Excessive soil moisture in the nursery bed
 Thick overhead pandal shade
 Hot and humid condition
 Overcrowding of seedlings
Management
 Expose the nursery soil to the sun for 2-3 months
 Preparation of raised – bed nursery
 Application of decomposed FYM
 Good drainage.
 Excess watering should be avoided.
 Overcrowding of seedlings should be avoided.
 Use of filtered overhead shade using green leaves coir mats / nylon mats
 Removal and destruction of affected seedlings
 Seed treatment with carbendazim (1g/kg) carboxin (0.7g/kg)
 Soil drenching with carbendazim 0.05% or Mancozeb 0.05% or Captan 0.05%
Coffee Leaf rust / Oriental leaf disease / Coffee rust: Hemileia vastatrix
Coffee originates from high altitude regions of Ethiopia, Sudan and Kenya and the
rust pathogen is believed to have originated from the same mountains. The earliest reports
of the disease hail from the 1860s. It was reported first by a British explorer from regions of
Kenya around Lake Victoria in 1861 from where it is believed to have spread to Asia and
the Americas. Rust was first reported in the major coffee growing regions of Sri Lanka in
1867 and the causal fungus was first fully described by the English mycologist Michael
Joseph Berkeley and his collaborator Christopher Edmund Broome after an analysis of
specimens of a “coffee leaf disease” collected by George H.K. Thwaites in Ceylon. Berkeley
and Broome named the fungus Hemileia vastatrix, Hemileia referring to the half smooth
characteristic of the spores and vastatrix for the devastating nature of the disease.
 It is unknown exactly how the rust reached Ceylon from Ethiopia but over the years
that followed, the disease was recorded in India in 1870, Sumatra in 1876, Java in 1878,
and the Philippines in 1889. During 1913 it crossed the African continent from Kenya to the
Congo, where it was found in 1918, before spreading to West Africa, the Ivory Coast (1954),
Liberia (1955), Nigeria (1962-63) and Angola (1966).
It is the most devastating disease of coffee. Found in every coffee growing region in
the world. It has reached epidemic proportion on many occasions resulting heavy economic
loss. The severe epidemic of the disease was first reported in Ceylon in 1867. In India it was
first reported from Karnataka in 1870. In Sri Lanka, severe epidemic of the disease changed
the growers to convert coffee plantations to tea or rubber cultivation. Coffee Leaf rust can
cause yield losses in excess of 75% where outbreaks are severe. It causes 50 – 60% loss in
India.
Symptoms
 The disease is mainly restricted to leaves but sometimes seen on berries and on
tender shoots.
 Young leaves are highly susceptible than matured ones.
 The rust infects mainly leaves, but also young fruit and buds.
 The disease initiates as small yellow or blotchy, orange powdery pustules, or lesions
on the under surface of the leaves.
 Corresponding to the pustules chlorotic patches appear on the upper side
 Soon the spots enlarge on the under surface of the leaves.
 The colour turns orange brown with powdery masses of spores called uredosori.
 As the spots become older their centre becomes necrotic and the spores are
confined to the outer areas.
 Several spots coalesce to form large necrotic patches
 Severely affected leaves shed prematurely.
 Vegetative growth is reduced.
 Die -back of the branches also occur.
 Premature ripening of berries and production of poor-quality, 'light coffee beans
Causal organism: Hemileia vastatrix
Spermogonia and aecia unknown.
Uredinia hypophyllous, densely scattered and giving a powdery appearance on yellowish-
orange rounded blotches about 3-25 mm in diam., consisting of numerous narrow
interwoven ‘feeder” hyphae and ± rounded cells below the stomata, bearing clavate
filaments emerging through the stomata, whose tips bear numerous pedicels on which the
spores are borne. The urediniospores are packed together like segments of an orange,
giving each spore a kidney-like shape, curved with short 28-36 x 18-28 µm, wall hyaline,
strongly warted on the convex face, smooth on the straight or concave face, 1 µm thick
(Laundon & Waterston 1964b). Teliospores are rarely found. Telia as the uredinia,
hypophyllous; teliospores often produced in uredinia, sometimes in teliosori borne in
cluster on short pedicels, 1-celled, more or less spherical to limoniform or spherical or
napiform and smooth with aterminal papilla, wall hyaline to yellowish, smooth 16-25 ×
19-22 µm, borne.
Although assumed to be heteroecious, the life cycle of H. vastatrix is not completely
known. It is generally agreed that the rust does not complete its life cycle on the coffee tree,
but no alternate host is known (Coutinho et al 1995).
Mode of spread and survival:
 The fungus survives in off season by uredinospores
 Dispersed primarily by wind and rain splash
 When the spores erupt, they enter the air current where they can travel a few
centimeters to the next leaf, or hundreds of kilometers to another site (spores have
been recorded travelling 1,000 m up in the high altitude air streams).
 There are also documented cases of spores being transported to new sites by small
insects such as Thrips and parasitoid wasps.
 Spores may also be dispersed or carried from one farm to another by people, insects
and animals.
 Not usually seed-borne but coffee berries and seeds may become contaminated by
urediniospores that are then carried elsewhere.
 Telespores not infect coffee.
Epidemiology:
 Rainy weather, mist or dew conditions and moderate temperature favour the
development of the disease.
 The showers and sunny weather with occasional mist prevailing during NE monsoon
period is ideal for severe infection.
 Severe epidemic occurs during July – December.
 Disease incidence is reduced during January – March.
 The disease is also severe in shaded coffee due to high humidity and low light
intensity.
Management
 Use of resistant varieties like Sln. 5B, Sln. 8 Sln. 9
 Wider spacing
 Shade managenet
 Pruning of dead and dying twigs after harvest
  Apply balanced nutrients to maintain plant vigour
 Diseased fallen leaves should be collected
 Spraying Bordeaux mixture 0.5% during pre blossom (May- June) and post blossom
(September – October)
 Spraying triadimephon 0.05% a.i. or bayleton 160 g or contaf 400 ml or tilt 160 g or
opus 42 ml in 200l water during August – September
 Biological control with Verticillium hemileiae during winter
Anthracnose: Colletotrichum coffeanum
The disease also known as die back or brown blight or black berry or Nilgiri twig
disease
In India it occurs in Karnataka and Tamil Nadu.
Symptoms:
 The fungus causes spots on leaves and berries.
 On leaves circular to irregular grayish spots are produced.
 On berries small dark sunken spots are formed.
 The infection spreads to internal tissues and affects the bean turning black.
 Infection on the twigs causes wilting of young leaves exhibiting die back symptoms.
 Berries fail to mature forming kattekai.
 The root system decays and feeder roots die.
Causal organism: Colletotrichum coffeanum
Mode of spread and survival:
 The fungus survives on dead tissues on the bark which provides the major sources of
infection.
 Conidia dispersed by rain splash.
 Also by birds machinery etc
 Coffee pickers are also a major source of dispersal
Epidemiology:
 Dry period followed by the monsoon rain.
 Inadequate overhead shade
 Prolonged drought and
 Soil water stress favour the disease development.
Management:
 Collection and destruction infected plant debris.
 Good drainage.
 Balanced fertilizer application
 Shade should be maintained.
 Leaf mulching at the base of the plants to conserve soil moisture during dry season
  Use of resistant varieties like Blue Mountain, Geisha, Rume, Sudan
 Spraying of Bordeaux mixture 1%
Cercospora leaf spot / Brown eye spot / Berry Blotch / Fruit spot: Cercospora
coffeicola Berk. & Cooke
 The disease is severe on nursery seedlings and young crop.
 Lesions begin as small, circular chlorotic spots on the upper leaf surface
 Spots expand to become necrotic with dark brown margin and tan, gray, or white
centre
 The central portion turns light grey due to sporulation and collapses leaving shot
hole.
 Lesions are sometimes surrounded by a bright yellowish “halo,”
 Necrotic spots increase in size and become irregular in shape and cause leaf blight.
 The margins of the lesions are dark brown to reddish brown or purplish to black in
color.
 Affected leaves turn yellow and shed prematurely
 On green berries spots are initially brown, oval or irregular, slightly sunken and
necrotic with ashy centre appear.
 The spots enlarge in size and become dark brown, necrotic and cover major area of
the berries.
 Around the spots purplish halo is seen
 The tissues turn brown to black.
The affected berries shrivel, dry up and shed.
Causal organism: Cercospora coffeicola Berk. & Cooke
Stromata are slight to 50 μm in diameter, globular, and dark brown.
Conidiophores are in fascicles, 3–30 stalks, pale to medium brown, sometimes
branched, multiseptate, mildly to abruptly geniculate, 20–275 x 4–6 μm. The conidial scars
are distinct and thickened.
Conidia are hyaline, acicular to obclavate, nearly straight, needle-shaped with an
acute apex and truncate or subtruncate base with a conspicuous, thickened hilum, indistinct
multiseptate, 40–150 x 2–4 (–7) μm.
Mode of spread and survival
 Survive in debris for 35 weeks.
 Fallen leaves constitute a primary source of infection, especially at the end of the dry
season.
 Pathogen dispersal is by spores (conidia) that are windborne (mostly during the
daytime)
 Also spread by splashing rain and human contact
  Also seed borne
Epidemiology
 The pathogen sporulates readily under more humid conditions.
o o
 Germination may occur between at temperatures between 8 C and 30 C, although
o
27 C is optimum.
 the development of brown eye spot is enhanced in plants already under stress
 The highest risk for infection occurs when the temperature range is 20–28°C and
there are from 36 to 72 hours of continuous environmental wetness.
 Factors that predispose the plant to infection include
Management
 Maintain adequate plant nutrition In fact, the disease may be effectively prevented or
controlled in most locations with a proper fertility regime.
 Sanitation and crop debris management:
 Choose the planting location to avoid very high elevations and rainy locations
 Orient rows so that they are perpendicular to prevailing winds, so plant canopies and
leaves become dry more quickly after rainfall.
 Optimum planting density (number of plants per acre).
 Strive to minimize plant stresses such as drought, under-nutrition, planting on
impermeable rock outcroppings, root-knot nematodes, and root rot; these predispose
coffee plants to infection.
 Provide or ensure adequate soil drainage.
 Grow coffee under shade (35–65%), or in an agroforestry setting.
 Avoid over-irrigation
 Avoid working with coffee plants and moving through fields and nurseries when
diseased plants are wet (this minimizes potential dispersal of fungal conidia within
and among moist plants).
 Prune coffee trees to increase air circulation in the canopy.
 Harvest cherries on time, before disease progresses too far.
 Control weeds (this minimizes plant stress and relative humidity in the plant canopy).
 Avoid planting coffee transplants too deep in soils.
 Spraying of Bordeaux mixture 1% or Captan or Mancozeb 0.5% or Carbendazim
0.01% foltaf 0.4%.
Black rot / Koleroga / thread blight: Koleroga noxia Donk
It has been reported from many coffee growing countries including India.
In India it occurs in Karnataka and TN.
Symptoms:
  The striking feature of the disease is the presence of dark brown or black decaying
leaves twigs and berries. Therefore it is called as Black rot.
 Affected leaves get detached from branches and hang down by means of slimy
fungal strands.
 The fungus develops over the slimy film.
 Mycelia threads will also be seen running along the twigs.
 Numerous minute clumps of mycelium and sclerotia scattered all over the dark
patches.
 The affected leaves turn black and rot.
 On green berries blackening is seen as a narrow band.
 When the affected leaves and berries dried white fungal web can be seen.
 There will be defoliation and berry drop on the infected.
Causal organism: Koleroga noxia Donk
Basidiomycetes
Hyphae hyaline when young and turn light brown with age.
Basidia are simple, oval rounded or pyriform with sterigimata.
Basidiospore are hyaline elongated
Scelerotia are also produced hyaline at first and become brownish later scattered all
over the diseased leaves, berries and young shoots.
Mode of spread and survival
 The pathogen spreads by contact form leaf to leaf through vegetative mycelium.
 Pathogen survives as scelerotia in infected plant debris.
Epidemiology
 Usually occurs during monsoon months with high humidity and hanging mist
 Heavy rains favour the disease.
 In south India the disease is severe only in Coffea arabica
 It is influenced by south west monsoon period from June – September
 The fungus infects Canthium sp., Crotons, Jasmine, Dahlia
Management
 Uniform and medium intensity overhead shade should be maintained.
 Pruning of bushes for free passage of air and sun light.
 Removal and destroying of diseased portion by pruning.
 Removal and destruction of infected leaves.
 Provide proper drainage
 Spraying of Bordeaux mixture 1% before and during monsoon will control the
disease.
  Spray Bordeaux mixture 1% or carbendazim 0.03 % a.i. (120 g/ 200 l water) during
break in monsoon
Fusarium bark disease / Storey's bark disease: Fusarium stilbioides
It is important in South East, Asia, Southern Africa and West Indies.
Symptoms:
 The pathogen produces three types of symptom namely, ‘Storey’s bark disease’,
‘scaly bark’, and ‘collar rot’
 The pathogen infects the collar region of the stem causing collar rot.
 Produces bark scaling and canker in scaly bark’ type .
 The fungus grows beneath the bark layer which becomes flaky in texture.
 Canker is then produced which girdle the trunk and kills the tree.
 Young suckers also affected.
 The sucker have constricted bottle neck appearance at the base.
 The affected suckers liable to break after a heavy crop.
 Under storeys bark type disease cinnamon to tawny olive to brown sunken lesion
with a water-soaked margin develops near the stem base of green stems
 It expands to eventually girdle the stem.
 The lesion may bear pink spore masses in moist conditions.
 All tissues below the lesion and the cambium are killed.
 The foliage wilts and dies.
Causal organism: Fusarium stilboides
Mode of spread and survival:
 The fungus survives on dead debris.
 Infect the damaged coffee berries as secondary invader.
Epidemiology:
 Insect damage (Wood boring beetles) unfavourable cultural conditions like poor soil
management, irregular pruning and drought predispose the plant to infection.
 Management:
Good soil management practices with adequate mulching for moisture conservation.
 Proper pruning
 Improving soil fertility
 Application of captan or Captafol 0.2% to trunk bases
Coffee Berry disease / Berry blight: Colletotrichum coffeeanum var. virulans and
Colletotrichum kahawae
CBD can cause considerable yield losses of up to 75% when not adequately
controlled.
Symptoms
  Coffee berry disease also affects ripening berries causing a brown blight phase
which appears as dark, sunken anthracnose lesions on the red berry.
 The characteristic symptom of CBD is the development of small, water-soaked
lesions on young, expanding berries
 They rapidly become dark brown or black and slightly sunken.
 They enlarge to cover the whole berry, which eventually rots.
 Under humid conditions, masses of pale pink spores become visible on the surface
of lesions.
 The berries mummify and remain on the fruit branch
 These symptoms, collectively known as ‘anthracnose’, are typical of CBD.
 shedding of berries may also be seen.
 If infection occurs at a later stage of fruiting pale, corky scab like lesions may appear
on young and mature berries.
 These lesions are known as ‘scab’ lesions
Causal organism: Colletotrichum coffeeanum var. virulans and Colletotrichum
kahawae
Short conidiophores in acervali.
Conidia are small rod – shaped unicellular hyaline.
Setae either present or absent.
Mode of spread and survival
 The conidial spread is through rain splashes.
 The fungus survives on bark of the branches mummified berries and in lesions on
affected berries.
Epidemiology:
 Infection takes place in temp. between 12 – 260C with moisture.
 The disease advances with season and the rainy period.
 Long rainy period with high rain fall are suitable for the development of the diseases.
Management:
 Use of res. Var. Blue Mountain
 Spraying of copper oxide
Sooty mould: Capnoduim braziliense
 The leaves and shoots are covered with black sooty fungal growth.
 Heavy attack of the aphids and scale insects predispose for infection.
 By controlling the insects the disease is controlled.
 Spraying fish oil resin soap 1kg + starch 1kg + 200m; water.
Pink Diseases: Corticium salmonicolor
 The fungus attacks the twigs and fruits.
  The branches wither and the fruit turn black.
 The fungus occurs in several stages.
 The most common stage is the corticum stage.
 This occurs in the form of whitish or pinkish crusts on the twigs.
 Removal of affected branches by pruning.
 Application of Bordeaux paste /Spraying BM 1% as preventure method
Root diseases
Rosellina root rot/ Maya disease / Black root disease: Rosellina arcuata, R.
bundes, R. necatrix and R. pepo
The disease is called as Maya Disease in Latin America.
It is often more serious at low altitude.
Symptoms:
 Gradual yellowing of leaves, defoliation followed by death of the bush
 Accumulation of black superficial fungal growth (rhizomorph) or black wooly
mycelium on the infected roots are also seen
 On stem near the ground level, fan- shaped fungal mats with pellet like fructifications
are also seen.
 The cambium tissues at the base of the stem at soil level are affected.
 Internal discolouration of roots as thread like black line or dots
The infection spreads along main root and base of the stem also.
Casual Organism: Rosellina spp.
Perithecia are produced
Conidia – ellipsoid or ovoid, single celled, hyaline to pale brown.
Mode of spread and survival
 Survives in infected plant debris in soil as primary source of inoculums
Epidemiology
 The disease is favoured moist and warm condition.
 Soil pH of 5.2 and soil moisture of 50 – 70% Soil MHC is most optimum.
 Host mortality is increased with size of inoculum
Management
 Removal of stumps and large roots of wild trees for establishing new coffee
plantation
 Raising corn or other non host crops for two years before coffee planting
 Shade may be increased in some cases.
 Restacking of plant debris at particular interval to disturb fungal growth prevents the
spread of the diseases.
  Removal and destruction of roots of affected trees, and the holes left open for a few
months.
 Drench the soil with carbendazim 0.4 % or carboxin 75 WP 0.3% @ 3 liter/plant in
the initial stage of wilting
 Application of biocontrol agent Trichoderma in affected blocks is useful in reducing
disease incidence.
Brown root disease / Stump rot: Fomes noxius Corner
 Brown root disease also known as 'Stump Rot,'
 Mostly associated with rotting stumps of shade trees in the plantation.
 In India occurs in Karnataka and Tamil Nadu.
 Affected plants show gradual yellowing of leaves .
 Then the leaves wither and the bushes die rather suddenly.
 Stem near the ground becomes spongy.
 The roots system shows externally thick brown encrustation with adhered gravel
pitches.
 Fungal mycelium appears as brown wooly hyphae or in brown crust on root surface.
 Black charcoal – like powdery patches are seen on the encrustation.
 Inner portion of roots shows dark brown to black wavy lines of fungal hyphae.
 Spread through root contact.
 The roots become very brittle and readily snap off.
 Digging trenches of 60 cm deep and 30 cm wide.
 Affected plants should be uprooted and burnt.
Red Root rot disease: Poria hypolateritia Berk
 Aerial symptoms are similar to brown root disease.
 Root system shows red encrustation covered with soil and gravel adhering to it.
 The red encrustation is the fungal rhizomorph.
 The affected roots are washed it is deep red in colour.
 Stumps of felled trees serve as source of infection.
 Soil application of T.V 150g+15kg FYM – 10 days before and after monsoon.
 Application of lime at 1.2 kg bush after uptoory of inf. Plant.
 Whenever a shade tree is felled uproot the stump with root system to avoid disease
spread infuture.
Santavery root disease: Fusarium oxysporum f. sp. coffeae
 Sudden wilting yellowing of leaves defoliation and death of aerial parts
 T.S of infected roots shows brown to pinkish discolouration .
 Scrapping of the bark of the stem near ground level also shows internal
discolouration.
  Disease is soil borne.
 Soil drenching carbendazim 0.8% or Carboxin 0.4% @ 3-5 l / plant in the initial stage
of infection
-
DISEASES OF RUBBER

Abnormal Leaf fall: Phytophthora palmivora Butl. P. meadii Mc Rae. P.nicotianae var
parasitica and P. botryose (Chee)
Phytophthora infection occurs in several rubber growing countries including
India, Sri-Lanka, Burma, Cambodia, Vietnam, Liberia, Costa Rica, Venezuela, Malaysia and
Thailand (Edathil et al., 2000). The pathogen causes several types of symptom on the plant
of which the abnormal leaf fall symptom is most severe in many parts of south India. It
induces the shedding of leaves during June – August while general leaf fall occurs in
December. Yield loss 9 - 25 %.
Symptoms
The different types of symptoms are as follows.
On Fruits
 The fruit-pods are the first seat of infection and consequently become responsible in
spreading the disease to mature leaves and green stems
 Small lesions indicated initially by 'pin head' black globules of latex, usually at the
basal end of the pod
 They enlarge into brown water-soaked areas and correspondingly the globules of
latex become bigger and more apparent.
 The fungus produces a downy white growth on the surface of the green fruit pod.
 The Infected pods become black or grey, malformed and unopened
 The Infected pods either remain attached on the tree or drop off prematurely.
 The seeds within the pods are shriveled, distorted, unopened, unviable and rotten.
On Leaves
 The fungal growths are washed by rain down onto the leaves, petioles, young shoots
and stems where they cause further infections.
 Initially the affected leaves show circular water soaked dull grey lesions with fine
droplets of coagulated latex in concentric rings..
 In course of time the lesions enlarge and coalesce to form large, irregular necrotic
areas with various shades of black
 The infection eventually spread to petiole.
 One or more black lesion with a drop of white coagulated latex in the centre may
develop on the petiole.
  The affected leaves enormously shed prematurely either green or after turning
coppery red.
On tender shoots
 When there is severe infection, the tender shoots rot.
 The infected twigs show dark brown lesions and soon exhibit die back of green
shoots.
On stem
 The infection occurs at the tapping panel or anywhere on the stem including the
collar region
 The infection causes the bark to swell and burst.
 An amber coloured liquid oozes from the infected tissues.
 Later in the season cankerous growth develops.
 The bark rots, and a coagulated rubber pad, emanating a foul smell is seen in
between the wood and the rotting bark.
 Brownish or dark discoloration of the wood is seen below the bark.
 This infection is called patch canker or bark canker.
 In the renewed bark region, small, sunken, vertically parallel depressions are formed
due to localised rotting and drying of bark which gets pressed to the wood.
 When infected bark is removed, characteristic, distinct vertical black lines are seen
on the wood corresponding to the external depressions.
 In advanced stages of infection the bark splits open, causing gaping wounds (canker)
with foul-smelling pads of coagulated latex between the bark and wood.
 Bark rot often reduces yield.
 The renewed bark becomes highly uneven regeneration of the bark giving panel
burrs which make subsequent tapping difficult or impossible..
 This is called bark stripes or black rot or black stripes or Black thread disease.
Causal organisms: Phytophthora palmivora Butl. P.meadii McRae.
P.nicotianae var parasitica and P. botryose (Chee)
Mode of spread and survival
 The oospores and chlamydospores produced inside the bark or in soil are primary
source of infection.
 These carry the pathogen over adverse conditions.
 The sporangia and zoospores help in secondary spread through rain splash and
irrigation water.
Epidemiology:
  High atmospheric humidity, low temperature, high rainfall, and crowded canopy are
predisposing factors for the disease initiation and spread of inoculums that result in
epiphytotics.
 Disease occurs mostly during rainy season. The fungus requires high humidity for its
activity.
 The severity of the disease increases as the rain fall increases over 360 mm in a
month.
 A temperature range of 15.6 – 20.00 C most favourable for sporangial production and
spread of the disease.
 Prolonged wet weather coupled with humid atmospheric conditions favour the
disease.
 Disease incidence is less in Kanyakumari District, but increasingly heavy northwards
along the southwestern coast.
 In Sri Lanka, severe leaf fall occurs when the following weather conditions prevail for
four consecutive days in the presence of infected fruits on the trees.
1. Temperature less than 28.90C during day time.
2. RH above 80% throughout.
3. At least 2.5 mm of rain per day.
4. Less than 3 hr of sunshine per day.
5. The above periods have been named as Peries.
Management:
 Collection and destruction of infected fallen leaves and fruits.
 Prophylactic spray with Bordeaux mixture 1% or COC 0.3%.
 First spray is given prior to SW monsoon and second during the break between the
monsoons to protect new flushes.
 Aerial spraying of fycol 8 with soya oil @ 5l / ha is done in Kerala.
 Removal of bark canker affected tissues and dressing with organomercurial
fungicides or copper fungicides (Bordeaux paste).
 Susceptible clones: PB 86, PB 235, PB 260, PB 311, PB 28/59, RRIM 600, RRIM
628, RRIM 703, RRII 5, PR 255, PR 261 and Tjir 1
 Tolerant clones: RRII 105, PB 217, GT 1 and GL 1
Spray schedule developed by Rubber Research Institute of India
Prophylactic spraying of the foliage prior to the onset of south west monsoon with
Bordeaux mixture using high volume sprayers or Oil-based copper oxychloride dispersed in
diluent spray oil employing either low volume airblast sprayers from the ground or through
aerial application. For micron spraying, based on the tree spread, foliage intensity, planting
material used and age of plants, two rounds of spray using about 17 to 22 litres of fungicide
oil mixture per hectare per round (1:6 proportion) with a gap of 10 to 15 days or a single
round of spray with about 30-40 litres of fungicide oil mixture per hectare (1:5 proportion)
may be necessary. For aerial spraying 6.2 litres of 40% oil based copper oxychloride paste
in 37 litres of diluent oil or 8 kg oil dispersible copper oxychloride powder 56% in 40 litres of
oil is used per hectare. Spraying should be done as close to the monsoon as possible.
Powdery Mildew / Oidium Secondary Leaf Fall: Oiduim heveae Steinm.
The disease is more common in India and in other countries. Predominantly noticed
on newly formed tender flush during the refoliation period of January to March. The disease
is severe in Kanyakumari, Idukki and Wynad district of South India and North Eastern
States.
It causes extensive damage to rubber plantation in India.
Symptoms:
 The symptoms are more predominant on tender leaves and shoots.
 It infects mostly young shoots that refoliate after annual wintering.
 The young brown as well as light green leaves are covered with white powdery
masses.
 Diseased leaflets shrivel, curl, crinkle and their edges roll inwards.
 Soon the infected leaflets fall off leaving the petioles attached to the twigs giving a
broom stick appearance.
 The fallen leaves form a black carpet on the plantation floor.
 Sometimes petioles and young twigs are also infected.
 Later the petioles also fall off.
 On older leaves initially white patches of the fungus seen which become necrotic
lesions later.
 The inflorescence and young fruits are also covered with white powdery masses
 Infected flowers and tender fruits are shed by reducing the fruit set
 The infected tender shoots dry off and die back symptoms appear.
Causal organism: Oiduim heveae
The fungus ectophytic
Mycelium – extensively branched, hyaline septate thin walled haustoria produced.
Conidiophores – Short produced in chain
Conidia – Barrel – shaped or cylindrical basipetal
Mode of spread and survival
 The fungus survives as dormant mycelium inside the bark.
 Secondary spread by wind borne conidia
Epidemiology
  The dormant mycelium become in active cloudy days with warm weather and low
humidity.
 Cloudy days with light rains and or misty nights with dew formation during refoliation
favour serious disease outbreak.
 Under shaded condition in high elevations the disease persists throughout the year.
Management:
 Clones PB 86, GT 1, GL1, PR 107, PB 5/139, RRIM 703, RRII 208 and PB 310 show
some tolerance.
 The clones RRII 105, RRII 118, RRII 300, PB 217, PB 235, PB 280, PB 311, PB
5/51, RRIM 605 Tjir 1 and PR 261 are susceptible to the disease.
 Dusting during the refoliation period commencing from bud break in about 10% of the
trees, giving 3 to 5 rounds at weekly to fortnightly interval using 11 to 14 kg 325-
mesh fine sulphur dust per round per hectare.
 Sulphur mixed with an inert material like Talc (70:30) is commonly used.
 Wettable sulphur or Carbendazim (2.5 g /l) is also effective in nurseries and for
young plants as a spray.
 Carbendazim 0.05% a.i. (1g in 1 litre water) is more effective than sulphur for
nurseries and young rubber.
 Alternate use of Carbendazim and sulphur is recommended to avoid resistance
problem.
 Fogging with fungicide tridemorph such as Calixin 75 EC at 0.5 a.i/ha also provides a
good control of the disease.
 For efficiency, dusting may be carried out in the early morning hours when the leaves
are moist and the atmosphere calm.
 Power dusters like Skoda Micro spray power 400 or Aspee Turblow tree duster could
be used for sulphur dusting.
Colletotrichum leaf fall or Secondary leaf fall: Colletotrichum gloeosporioides (Penz.)
Sacc. Colletotrichum acutatum (Sexual stage: Glomerlla cingulata)
In North East India the disease is prevalent throughout the year except during winter.
Symptoms
 Tender leaves during the first ten days of expansion are most susceptible to
infection.
 Infection usually starts mostly at the tip of the leaves and spreads towards leaf base.
 Initially numerous minute circular brown spots are produced.
 The spots then develop a thick brown margin surrounded by yellow halo and are
erumpent.
 The central tissues turn white.
  The spots coalesce and dry up leading to defoliation.
 Sometimes the centre of the spots dry and fall off leaving shot hole.
 Infected leaves become distorted, turn black, shrivel and fall off leaving the petioles
on the plant for a short period.
 Lesions are observed on the green portions of stem also causing shoot die back.
 The fungus attacks green pods and cause rotting.
Causal organism: Colletotrichum gloeosporioides (Penz.) Sacc. Colletotrichum
acutatum (Sexual stage: Glomerlla cingulata)
Mycelium – Septate hyaline at first and light brown at later.
Conidia – Oblong, single – celled,
Perithecia – Spherical brown
Asci – Oblong, Ascospores are curved unicellular.
Mode of spreads and survival:
 The fungus survives in infected plant debrieses.
 Water disperses the conidia.
Management:
 Spraying with Bordeaux mixture 1% or chlorothalonil and propined such as Daconil
and Antracol respectively at 0.2% in water using a knapsack sprayer or a back-pack
power mist blower.
 Adequate drainage
 Application of recommended dose of fertilizers
 Spraying with Bordeaux mixture 1%, copper oxychloride 0.25%, mancozeb 0.2% or
carbendazim 0.1% at 10 - 15 day interval is also effective.
Birds eye spot – Drechslera heveae (Petch) M.B. Ellis
Symptoms:
 Common in nursery or on young plants in the field
 On tender brown leaves disease appears as dark brown water soaked spots.
 The leaves become black and get shriveled and distorted.
 Severely infected leaflets fall off leaving the petioles.
 When light green coloured leaves are infected minute yellow spots which later
develop narrow reddish brown margin and a white papery centre are observed
 This look similar to eyes of birds based on which the disease was named.
 Numerous spots are often observed on each leaflet.
 Elongated brown stripe like lesions occur on infected mid ribs, petioles and green
shoots.
 The underside of lesions develops a chocolate brown colour due to sporulation of the
fungus.
  The fungus produces minute purple spots.
Causal organism: Drechslera heveae
Conidia are curved navicular or fusiform, pale to mid golden brown or reddish brown
and smooth, 6 – 11 pseudosepta with hylum.
Mode of spread:
 The spores are disseminated by wind, rain or irrigation splashes
Management:
 Spraying with Bordeaux mixture 1% or mancozeb 0.2% or Carbendazim 0.04%
 Shading the nursery plants reduces the disease incidence.
 Maintain seedlings in vigorous condition through adequate balanced nutrition.
Corynespora leaf spot: Corynespora cassiicola (Berk & Curt)
Earlier the disease was confined to nurseries only. From 1996 onwards severe
incidence of the disease was observed in mature plantations in the Dakshin Kannnada
District of Karnataka and in the adjoining districts of Kerala. In nurseries, disease incidence
is noticed during November to May period. On mature trees, disease is observed during the
refoliation period from February to May.
Symptoms
 Minute spots (pin head lesions) develop when the leaves are very young
 The spots enlarge and become circular or irregular with a brown or papery centre
surrounded by a dark brown ring and yellow halo.
 The papery centre may fall off forming shot holes.
 Young leaflets exhibit shriveling and drying of terminal portion.
 Veins become dark brown due to toxin production by the fungus
 These appear as a fish bone or a railway track marked on a map.
 Severe infection on midrib causes leaf blight.
 The blighted leaves may remain on branches for some more time giving a burnt up
appearance.
 Severe disease incidence leads to yellowing and defoliation.
 One lesion is enough to cause defoliation, especially, if it is sited on the main vein.
Causal organism: Corynespora cassiicola
Conidia are obclavate cylindrical or slighted curved multiseptate, tapering towards
the apex
Management
 Spraying with fungicide Benlate at 0.3%.
 Repeated spraying with Bordeaux mixture 1% or Dithane (Indofil) M-45 0.2% or
Bavistin 0.02% is recommended for nursery.
 Shading the nursery reduces the disease incidence.
  Maintain seedlings in vigorous condition through adequate balanced nutrition.
 High volume spraying with mancozeb 0.2% (Dithane/Indofil M-45 2.66 g/l)
carbendazim 0.05% (Bavistin 1g/l) at 2-3 weeks interval during refoliation is effective
in mature plantation.
 Micron spraying with oil dispersible copper oxychloride 56% (8kg) or oil dispersible
mancozeb 70% (7 kg) dispersed in 40 l spray oil per ha is also effective.
Pink disease – Corticuin salmonicolor Berk & Br.
The disease is noticed during southwest monsoon period in the traditional rubber
growing areas in South India. The disease incidence is very mild in Kanyakumari District due
to the weak southwest monsoon and absence of prolonged wet conditions. Disease has
been noticed in Assam, Tripura and Meghalaya in north east. Pink disease is the most
serious stem disease of affecting mainly the young rubber trees.
Symptoms
 More damaging for plants in the age group of 2 to 12 years
 The stem with brown bark is affected anywhere from the base to branches.
 In young plants the forking region is more vulnerable.
 The early symptom is the cobweb like superficial film of silky white mycelium which
glistens in sunlight
 The mycelium grows covering all around the stem, ramifies the bark tissue and
damages it.
 When the pathogen damages the latex vessels, the latex exudes.
 Rotting, drying up and cracking of the affected bark follow
 The leaves turn yellow and dry up.
 The dried leaves remain attached to the branch.
 New sprouts develop from below the affected region.
 Light pink coloured pustules appear in parallel lines all over the bark.
 These contain the spores.
 In the advanced stage, pink encrustations appear on the lower shaded regions of the
affected branches.
 The disease gets its name from this stage.
 The pink encrustations contain the basidia on which basidiospores are produced.
Causal organism: Corticuim salmonicolor
Mode of spread
Spread – Air blown basidiospores
Rain splash dispersed conidia
Epidemiology
Wet weather and high relative humidity are favourable for disease development.
 Management
Affected plant parts should be pruned and burnt
Wound dressing with Bordeaux paste
Prophylactic: Two rounds of spraying with 1% Bordeaux mixture (during May and
August) on to the fork and branches reduces disease incidence.
Application of Bordeaux paste to the topmost brown portion of the stem with a 30 cm
wide band all around.
Curative: Application of Bordeaux paste in early stage on infected part and up to 30
cm above and below.
In advanced cases, Bordeaux paste may be initially applied and then the affected
portion scraped to remove mycelium and decayed bark, followed by a second Bordeaux
paste application.
Dried branches should be pruned after disinfection.
Thiram (10g in 1 kg) incorporated in a wound dressing compound or tridemorph 2%
(Calixin 25 ml/l) in 1% ammoniated field latex or thiride 0.75% or tridemorph 1% or
propiconazole 0.1% (Tilt 4 ml/l) in pidyvyl, china clay and water (1:2:4 by volume) is also
effective as rainwash is prevented.
Root Diseases
White root disease: Fomes lignosus
Symptoms
 The disease externally shows reduced growth rate of new shoots.
 Chlorosis of leaves followed by leaf shedding and die back.
 The fungus attacks tap root first and spreads over the root surface as white
rhizomorphs with a fan like leading edge.
 Older rhizomorphs become yellow to red.
 These rhizomorphs are seen at the base of the trunk and roots.
 A succession of annual fruiting bodies are formed on old stumps and exposed roots
or after the trees died.
C. Organism: Fomes lignosus
Fruiting bodies are bracket – shaped (7-20 cm wide) with yellow margin. They are
concentrically banded reddish brown on the upper surface with a pore – studded red –
brown lower surface.
Mode of spread and survival:
 Survives in old stumps and large roots for several years
 Spread by the contact of growing roots with rhizmorph growing in the soil.
Management:
 Old dead and infected stumps should be removed and burnt.
  The infected roots are treated with Copper Sulphate 0.2%
 Soil drenching with Brodeaux mixture 1%
Brown root disease: Phellinus noxius Corner G.H. Cunn
It occurs in most of the rubber growing countries. It is the major root disease of
rubber in India. The disease occurrence is sporadic and often noticed in replanted areas and
in sandy or light soils. Low incidence of brown root disease is noticed in Assam and Tripura
Symptoms
 The symptoms appear as loss of shiny appearance of leaves, drooping, yellowing
and buckling (curving) of leaflets
 Retardation in growth of trees.
 The leaves later turn to reddish yellow and dry up.
 Occasionally flowering and fruiting is observed.
 The trees die bark.
 On the infected roots the surrounding soil and stones from a hard and thick coating.
 Yellowish brown patches of fungal rhizomorphs are visible on the surface of roots.
 Cortex appears as brown, mottled with white patches
 Wood shows brownish discolourations and brown lines.
 On old infected stumps large, hard, brownish purple brackets of fungus with grey
underside develop.
 Infection is noticed on young nursery plants also.
 When the young trees affected they are killed.
Causal organism: Phellinus noxius Corner G.H. Cunn
Mode of spread
 The spores blown over by wind spread the disease.
 The spread is more often through root contact with infected roots.
Management:
 Completely killed and dried roots may be traced, pruned off and burnt along with any
rotting stump
 Partially affected and healthy roots washed with tridemorph 0.5% (Calixin 6.25 ml/l)
or propiconazole 0.13% (Tilt 5 ml/l) solution (Provisional recommendation).
 When the fungicide dries up, a thin coating with a wound dressing compound may be
given.
 Refill the soil and drench the base with fungicide solution.
 The dried up plants may be uprooted, root traced, collected and destroyed.
 As prophylactic, measure the bases of trees neighbouring the affected trees may
also be drenched with fungicide solution mentioned above.
Purple root disease: Helicobasidium compactum
  Purple root disease is observed more in North East India though mild scale
occurrence of the disease has also been reported from South India.
 The infection is observed both in nurseries and in the main field.
 Aerial symptoms are yellowing and drying of plants
 Infected plants are weak with sparse crowns.
 The tap root will be badly damaged and its bark often sloughs off exposing wood.
 Several adventitious roots arise with which the plant survives.
 Formation of a brown spongy fruiting body of the fungus around the collar of the infected
plants is a distinct symptom
 Removal of affected roots and plants
 Drenching of fungicides like tridemorph 0.5% (Calixin 6.25ml/L) or propiconazole 0.13%
(Tilt 5ml/L)
Poria root disease: Poria vincta (Berk.) Cooke
 The disease occurrence is sporadic
 Yellow discolouration of leaves is the only external symptom.
 The affected root shows soil encrustation as in the case of brown root disease but to
a limited extent.
 Around the root the fungus forms a complete mat of pale white in colour intermingled
with brick-red and black tinges.
Management:
 Completely killed and dried roots may be traced, pruned off and burnt along with any
rotting stump
 Partially affected and healthy roots washed with tridemorph 0.5% (Calixin 6.25 ml/l)
or propiconazole 0.13% (Tilt 5 ml/l) solution (Provisional recommendation).
 When the fungicide dries up, a thin coating with a wound dressing compound may be
given.
 Refill the soil and drench the base with fungicide solution.
 The dried up plants may be uprooted, root traced, collected and destroyed.
 As prophylactic, measure the bases of trees neighbouring the affected trees may
also be drenched with fungicide solution mentioned above.
Dry Rot, Stump Rot Collar Rot: Ustulina deusta (Hoffm.ex Fr) Lind
 Affects roots, collar, trunk and branches
 Copious exudation of latex from the lesions during the rainy season
 The fungus penetrates the wood and spreads inside.
 Later fruiting bodies of the fungus appear as soft circular to irregular, grayish white
ear lobe like structures which later join together and become grey or black and brittle.
 As a result the wood becomes soft and powdery.
  Affected trees or branches are killed or blown over.
 Black double lines formed by the fungus are seen inside the wood.
 Ustulina root infections are also noticed.
 The fungus penetrates the bark through wounds and cracks and hence the disease
incidence is more following heavy wind.
Management
 Scrape off the fructifications, affected bark and wood showing black lines.
 Apply a wound dressing compound in which Thirum 0.75% a.i (Thiride 10 g/l) is
incorporated.
 Hexaconazole 0.02% a.i (Contaf 4 ml/l) is also effective.
 Avoid accumulation of rubber at the base of the tree.
 For root infection see the treatment for brown root disease.
Red root rot: Ganoderma pseudoferrum
 The fungus attacks the root and induces wet rot.
 Reddish rhizomorphs are formed on the surface of the diseased roots and form a red
skin.
 Adventitious roots develop profusely.
 In advanced stages of decay the wood may be spongy.
 Spread thro root contact
Shrinking root disease: Sphaerostilbe repens
 The fungus invades the root system
 Defoliation occurs and the tree is killed
 The fungus spread between the bark and wood of the infected root by means of
reddish brown rhizomorph.
 Dead roots are bluish purple and emit foul odour.
 Low lying areas should be avoided for rubber planting.

DISEASES OF COCOA
White thread blight: Marasmius scandens
Horse hair blight: Marasmius equicrinis
Severe incidence was reported in 6 months old seedlings in Karnataka in 1990.
Found in severe form in the plains. White thread blight and horse hair blight are the two main
types of thread blight in cocoa
Symptoms:
 White thread blight kills the leaves by spreading a network of white mycelial threads
over leaves, petioles and branches.
 Spread longitudinally and irregularly along the surface of the stem.
  The fungus enters the leaf at the nodes along the petiole.
 On the leaves it spreads as branched fine thread and also invades cortical tissue.
 The affected leaves turn dark brown to black.
 The dead leaves detached from stem but hung by mycelial thread in a row.
 Extensive death of young branches and suspended leaves in rows
 Thick strands of mycelia are often seen on branches
 Horse hair blight forms a tangle of thin black threads through the canopy of leaves
 The dehisced leaves along with healthy leaves remain together and form a dense
mass, preventing the development of new flush
 The dead leaves with mycelial mat are easily carried by wind on to the leaves and
stems of healthy plants and initiate the disease
Mode of spread and survival
 Through mycelial threads
Epidemiology
 High humidity, less aeration and sun light.
Management:
 Removal of affected branches and leaves by pruning
 Provision of more aeration and sun light
 Spraying with Bordeaux mixture 1 % or copper oxychloride 0.4 % or Mancozeb 0.4 %
Seedling blight / Seedling die back / Black pod rot / Chupon Blight and Twig
Dieback / Trunk or Stem Canker: Phytophthora palmivora, P. megakarya, P.
citrophthora and P. capsici
Most destructive of all the fungal disease. First reported from Guyana in W. Indies in
189. In India it was first reported in 1965. Loss may be upto 10% in the world. 30-90% of the
total global crop loss is caused by this disease (Bowers et al., 2001). Most common in all the
cocoa growing areas of the world. In India most important and very serious disease of cocoa
especially during south-west monsoon
Seedling blight/Seedling die back: Phytophthora palmivora
It is severe on young seedlings during rainy season. It is observed in nurseries of
Karnataka Kerala and TN.
Symptom
 Seedling blight/seedling dieback is very common in nurseries during rainy season
 The infection starts from the tip of the stem or from cotyledonal stalk or from the collar
region.
 The disease appears as dark brown to black water soaked linear lesions.
 The lesions extend to petiole and leaves resulting in wilting and subsequent defoliation
of seedlings.
 Defoliation and die back of seedlings are noticed in advanced stages of the disease.
Black pod rot Symptoms: Phytophthora palmivora
 Pods of all ages are susceptible
 Pods or cherelles (immature pods) may be infected at any place on the surface, but
is most often initiated at the tip or stem end.
 One or more small, brown and translucent spots appear anywhere on the pod
surface
 Rapidly spreads in all direction with a line of demarcation of diseased and healthy
tissues.
 Spots soon turn to chocolate brown colour, then darken and expand rapidly with a
slightly irregular margin
 Within four to seven days of infection, the lesion enlarges and assumes an elliptical
shape
 As the lesion advances, a whitish growth of the fungus consisting of mycelia and
sporangia is produced over the dark brown pod surface (Plate4)
 Lesion increases rapidly and covers the whole pod surface (Plate5)
 Under humid conditions a white mould appears on the surface.
 The whole pod and beans are invaded by the fungus and turns black in colour, which
subsequently rots and shed in large numbers
 Infected beans are also discoloured.
 Diseased pods eventually become black and mummify.
 The pathogen also will cause a seedling blight in cacao nurseries as a result of
infection of the stem and young leaves
Chupon Blight and Twig Dieback: Phytophthora palmivora
 Water soaked lesions appear on the apex or margin of the leaves,
 They enlarge and turn dark brown to black and coalesce forming large blighted areas
leading to defoliation and dieback
 Infection spreads to petiole and extends backwards into the twigs or chupons
 The lesion spreads longitudinally in all directions and turns dark brown to black
 When the lesions girdle the stem, the portion above the point of infection wilts
showing twig dieback or chupon blight
Stem Canker: Phytophthora palmivora
 Affects both seedlings and mature plants
 Occurs on the main trunk, jorquettes and fan branches
 The canker often develops from the pods.
 The infection from the pods spreads to the peduncle and then to the cushion and
bark causing canker
  Greyish brown water soaked lesion with a broad dark brown to black margin appears
on the bark
 Reddish brown liquid oozes out from the cracks of lesions, forming a rusty deposit
 The canker at the collar region appears as dark brown, irregular, water soaked lesion
with oozing of reddish brown liquid
 Infection on the internal bark beneath the outer lesion appears as reddish brown
discolouration
 Lesions in the internal bark coalesce, leading to extensive rotting
 The infection spreads from the cortical tissues into vascular tissues reaching wood
 Wood infection appears as greyish brown to black discolouration with black streaks
 When the cankers girdle the main stem or branches, dieback symptoms occur and
the tree ultimately dies
Causal organism: Phytophthora palmivora, P. megakarya, P. citrophthora and
P. capsici
In 1976, isolates of P. palmivora from cacao were placed into one of four morphological
groups (MF1, MF2, MF3, and MF4). Further studies redefined the morphological groups.
The MF1 form was considered to be the typical P. palmivora, and the MF2 form a variant
(atypical) of P. palmivora (4). The MF3 form was described as a new species, P.
megakarya Brasier and Griffin (4), and the MF4 form considered to be P. capsici Leonian
(39,43). Recently, it has been proposed that isolates of P. capsici differing in morphological
and pathological attributes should be called P. tropicalis (2). Phytophthora palmivora is
present in most countries and is an important part of the black pod complex, while P.
megakarya is present only in several countries in West Africa (14). However, P.
megakarya appears to be more virulent than P. palmivora and is becoming the dominant
species in West Africa, moving from Nigeria and Cameroon into countries where it has not
been reported previously. In the major cacao-growing region of Bahia, Brazil, three species
have been implicated: P. palmivora, P. capsici, and P. citrophthora (Smith and Smith)
Leonian (17,22,24). Phytophthora capsici appears to be the dominant and most important
species attacking cacao in Brazil, and also has been reported to occur in other countries in
Central and South America, as well as in the West Indies, Indonesia, and India
(6). Phytophthora citrophthora is the least common species found in Brazil, but is the most
virulent (17,24). Phytophthora heveae Thompson also has been found to cause black pod in
some countries (6).
Mode of spread and survival
 The fungus survives as oospores, chlamydospores and mycelium in soil, on fallen
fruits, dried fruits and flower cushions, stem etc.
 The spread of the disease is by wind and windblown rain.
 Epidemiology:
 Continuous heavy rainfall with intermittent bright sunshine, low temperature of 22-250
C, constant high relative humidity of more than 90%, wind, cloudy weather etc. favour
the outbreak of the disease
 Closer spacing and damp locality favour the spread of the disease.
Management:
 Collect and destroy all fallen and completely infected pods at weekly intervals or
during each harvest
 Remove the piles of pod husks lying in the garden and destroy by burning
 Give proper spacing between plants.
 Prune the epiphytes and chupons frequently so as to regulate shade
 Provide adequate drainage in gardens
 Harvest the ripe pods frequently to ensure that recently infected pods are not lost
completely
 Prophylactic spray of Bordeaux mixture 1% or copper oxychloride 0.3-0.4 % with
stickers, first before the onset of heavy south west monsoon and a second and third
at 40-45 days interval, especially on pods and flower cushions
 Spray with metalaxyl or fentin acetate or Aluminium ethyl phosphonate.
Charcoal pod rot: Botryodiplodia theobromae or Lasiodiplodia theobromae
In Kerala it has become a serious disease. It is found throughout the year. But it is
severe during summer months.
Symptoms:
 Pods of all stages are susceptible to infection, especially during summer
 Pale yellow spots appear on the pods, mostly at the tip or stalk end (Plate6).
 The spots enlarge into larger lesions and cover the entire pod giving a chocolate
brown colour (Plate7).
 Severely infected pods become black in color and exhibit a sooty covering all over,
consisting of spores of the fungus (Plate8)
 Young pods become mummified and shriveled (Plate9)
 Infected pods dry up and generally remain attached to the plant
Causal organism: Botryodiplodia theobromae or Lasiodiplodia theobromae
Mode of Spread
 wound parasite
 Wind borne conidia
Management
 Collect and destroy all fallen/completely dried pods
 Regularly harvest ripened pods
  Remove the piles of pod husks and destroy by burning
 Give prophylactic spray of Bordeaux mixture 1% or copper oxychloride 0.3-0.4 % or
Mancozeb 0.3-0.4 % at 40-45 days interval, especially on pods and flower cushions
during summer months
 Spray the pod bunches twice with Contaf / Tilt 0.1% or Bavistin 0.1 % at 2-3 weeks
interval after harvesting all mature pods. Subsequently harvest only after 45 days of
spraying
 Control of mealy bug and Tea mosquitoes

Cherelle Rot / Colletotrichum Pod Rot: Colletotrichum gloeosporioides

 It is noticed especially during February-May
 The symptom mostly starts from the stalk end and proceeds towards the tip of the
pod as dark brown sunken lesion with a diffused yellow halo
 The infection also extends to the stalk and reaches the cushion
 As the infection progresses, the internal tissue of the pod becomes discoloured
 Sometimes the infection may start from anywhere on pod surface, other than stalk
region, as dark brown sunken lesion
 Such lesions coalesce and form bigger lesions with salmon / dark brown coloured
fruiting bodies of the fungus
 Ultimately, the pod turns dark brown to black and remains mummified on the tree
Management
 Collect and destroy all infected and dried cherelles
 Remove and destroy by burning, the piles of pod husks lying in the garden
 Regularly harvest the ripe pods to ensure that recently infested pods are not
completely lost
 Give prophylactic spray of Bordeaux mixture 1% or copper oxychloride 0.3-0.4 % or
Mancozeb 0.3-0.4 % at 40-45 days interval, especially on pods and flower cushions
during summer months
 Spray the pod bunches twice with Contaf / Tilt 0.1% or Bavistin 0.1 % at 2-3 weeks
interval after harvesting all mature pods. Subsequently harvest only after 45 days of
spraying
Leaf Blight and Shot Hole: Colletotrichum gloeosporioides & C.
theobromicolum
 Round to slightly irregular chlorotic spots appear on the leaves,
 Which later turn brown with a clear yellow halo around each spot.
 The spots develop anywhere on the leaf lamina but more often on the tip or margins
 The centre of the spots become necrotic, shrivel and drop off forming shot holes
 Spots enlarge or coalesce to form large blighted areas with an even margin and dark
brown to black dots representing its fruiting bodies
 Defoliation occurs, when such lesions cover a major portion of the leaf
Management
Spray 1 % Bordeaux mixture / 0.4 % copper oxychloride or 0.4 % Mancozeb (4 g/L)
Vascular Streak Dieback: Oncobasidium theobromae
 A single leaf in the second or third flush from the tip of twig becomes yellow, with
islets of green patches scattered over the yellowish lamina
 Such leaves fall off prior to the older leaves of the same branch
 Leaves above and below the first fallen ones develop similar symptoms and are lost
 This leads to a distinctive appearance where the youngest and older leaves are still
present but all the middle ones have shed
 The bark in the leaf fall region of the branch becomes rough due to swelling of the
lenticels
 The auxiliary buds of the fallen leaves sprout and then rapidly die
 At the later stage, dieback symptom appear on these branches
 Because of infection, the xylem vessels turn brownish which appear as streaks within
the vascular tissues. Hence, the disease is known as vascular streak dieback
 The disease can be easily diagnosed in the field by stripping the bark or by splitting
the affected stem longitudinally and observing the brownish streaks
Management
 Regularly prune and destroy infected branches
 Spray 0.1% Contaf or Tilt or Topas at monthly intervals in severely infected garden
Pink Disease: Corticium salmonicolor or Pellicularia salmonicolor
 Oozing of brown liquid from the fork region, the trunk and branches (Plate27)
 White, silky mycelial threads appear and spread around the branch like a “cobweb”
 Shoots wilt, leaves shed and ultimately branches dry up (Plate 28)
 As infection progresses, the trunk/branches become ringed and die (Plate29)
 Characteristic pinkish powdery coating appears on the irregular cracks
 Numerous off shoots are formed below the point of infection (Plate30)
Management
 Remove and destroy completely infected and dried shoots/branches
 Reduce overhead shade
 Prune properly to improve aeration inside the garden.
 Prune smaller infected branches and swab the cut ends with Bordeaux paste or 0.5%
Contaf / Calixin in rubber kote or coal tar (5 ml/kg)
  As a preventive measure, spray 1% Bordeaux mixture at regular intervals on forking
regions and branches during the rainy season
Witches broom: Moniliophthora perniciosa (formerly Crinipellis perniciosa
(Stahel) Singer (= Marasmius perniciosus)
 It causes abnormal growths and lesions on the shoots, branches, floral cushions and
fruits.
 It also attacks nursery seedlings.
 Basidiospores penetrate young meristematic tissues in vegetative and floral buds.
 The colonized tissues undergo several physiological and hormonal changes leading
to swelling and formation of numerous succulent vegetative branches, known as
brooms, within flower cushions and on vegetative apical or axillary buds.
 The fungus also infects pods causing green patches and necrotic lesions, uneven
ripening, and various deformations.
 Brooms and infected pods become progressively brown and dry
Frosty pod rot or Moniliophthora pod rot: Moniliophthora roreri (Ciferi & Parodi)
Evans et al.,
 Yield losses have been estimated between 25% to total loss of the crop
 It is a devastating disease of cacao pods.
 The pods are highly susceptible during the first 90 days of their growth.
 Early symptoms include discolored areas of swelling on the pods followed by a dense
formation of cream-colored powdery growth. so called frosty pod
 The area of the pod with sporulation spreads rapidly,
Root Diseases
Brown root rot - Phellinus noxius
Red root rot - Ganoderma spp.
Black root rot - Armillaria spp. & Rosellina arcuata
 Sudden premature yellowing and drying of slightly off-green leaves is a possible
indication of root diseases
 Rhizomorphs are found firmly attached to the infected roots or ramifying into a
network with soil encrustation around root
 They are brown / red / black depending on the fungus associated
 The wood of a newly-killed root has brown / black lines and is hard
 Generally, fruiting bodies of the fungi grow at the collars of diseased trees and on
decaying exposed roots or stumps
 The disease can be identified based on the fruiting bodies or rhizomorphs grown on
dead stumps or decayed roots
Management
 Remove and destroy dead/infected trees including roots.
 Treat soil with 2% CuSO4 and replant after 6 months to one year
 Prune branches, regulate shade and provide adequate spacing for improving
aeration.
 Apply organic matter @ 10-15 kg/pit and lime @ 1-2 kg/pit
 Isolate infected trees by digging trenches 1.2 m deep and 0.6 m wide
 Drench soil with 1 % Bordeaux mixture or 0.2 % copper oxychloride or Contaf/Tilt
/Bavistin
Swollen shoot – Theobroma Virus / Cocoa Swollen Shoot Virus
It is a serious disease Africa
But it has not been reported in India.
Symptoms
 Swelling develops at nodes, internodes and tips of the quick growing shoots.
 At early stage red vein banding appears on the leaves.
 The pigment is restricted to the mid rib, lateral veins and finer veins producing red
feathering symptom.
 When the leaves turn green and harden, green vein banding seen with chlorotic or
yellow translucent lesions along the major veins forming fern like pattern.
 Young unripe pods develop light and dark green mottling.
 Small abnormally shaped spherical pods
Spread
By insect vectors like mealy bug and grafting
Control:
 Removal and destruction of infected trees
 Removal of alternate hosts for virus and vector
 Control of vectors

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