Lecture Notes

Pl. Path. 5.4

Diseases of Field and Horticultural Crops
(2+1)

Prepared and Compiled by

Dr. Shivangi Kansara

Lecture notes 1 Theory syllabus and Diseases of Rice 1

 Course content
Sr. No. Name of the crop Name of the disease

1 Rice 1. Blast
2. Brown leaf spot
3. Bacterial leaf blight
4. Sheath blight
5. False smut
6. Khaira
7. Tungro
2. Maize 1. Downy mildew
2. Stalk rot
3. Leaf spots
4. Banded leaf and sheath blight
5. Late wilt
3. Sorghum 1. Smuts(Grain, Long, Loose and Head)
2. Striga
3. Anthracnose
4. Bajra 1. Downy mildew
2. Smut
3. Ergot
4. Rust

5 Groundnut 1. Early and late leaf spots

2. Collar rot
3. Rust
4. Stem and pod rot
5. Chlorosis
6. Root rot/ Charcoal rot
7. Bud necrosi
8. Afla rot disease
6. Sesamum 1. Phyllody
2. Root / Stem/ Charcoal rot
3. Leaf spot
4. Bacterial leaf blight
5. Phytopthora blight
6. Powdery mildew
7. Soybean 1. Rhizoctonia blight
2. Mosaic

Lecture notes 1 Theory syllabus and Diseases of Rice 2

8. Pigeonpea 1. Phytopthora blight
2. Wilt
3. Sterility mosaic

9. Finger millet 1. Blast

10. Black and green gram 1. Anthracnose

2. Powdery mildew
3. Leaf spot
4. Yellow mosaic
11. Castor 1. Wilt
2. Root rot

12. Tobacco 1. Damping off

2. Black shank
3. Frog eye
4. Leaf curl
5. Mosaic
6. Orobanche
13. Banana 1. Panama wilt
2. Moko wilt
3. Bunchy top
4. Sigatoka leaf spot
14. Papaya 1. Foot rot
2. Leaf curl
3. Mosaic
4. Ring spot
15. Pomegranate 1. Bacterial blight
2. Leaf spot
3. Root knot
4. Wilt
16. Brinjal 1. Phomopsis blight and friut rot
2. Little leaf
17. Tomato 1. Early and late leaf blight
2. Leaf curl
3. Buck eye rot
4. Tomato spotted wilt
18. Okra 1. Yellow vein mosaic
2. Root knot
3. Powdery mildew

Lecture notes 1 Theory syllabus and Diseases of Rice 3

19. Beans 1. Anthracnose
2. Bacterial blight
20. Coconut 1. Stem bleeding
2. Wilt
3. Bud rot
4. Ganoderma stem rot
21. Colocasia 1. Phytopthora blight

22. Tea 1. Blister blight

23. Coffee 1. Rust

24. Cluster bean 1. Powdery mildew

2. Bacterial blight
3. Bean common mosaic

25. Cotton 1. Wilt Angular leaef spot

2. Anthracnose
3. Alternaria leaf blight
4. Leaf reddening

Lecture notes 1 Theory syllabus and Diseases of Rice 4

 1. Disease of rice
1. Blast or rotten neck
2. Brown leaf spot (BLS)
3. Bacterial leaf blight (BLB)
4. False Smut or Green Smut
5. Sheath blight
6. Rice tungro
7. Zn Deficiency

1. Blast or rotten neck

Symptoms :
 The fungus attacks all aerial parts of plants at all stages of growth.
 Leaves, neck of the panicle and nodes are more commonly affected.
1. Leaf blast :
 On the leaves, symptoms originate as small specks which subsequently enlarge
into spindle-shaped spots varying in length from 0.5 cm to several centimeters.
 The centre of a well-developed spot is whitish grey with a brown margin.
2. Nodal blast :
 On nodes, blackening extends both ways up to about 1 or 2 cm.

1. Leaf Blast 2. Nodal Blast

3. Neck blast :
 The neck of the panicle is infected when the ear emerges.
 This phase is called black neck or rotten neck or neck blast.
 The neck region is blackened and shrivelled.
 Grain set in these ears are completely to partially inhibited.

Lecture notes 1 Theory syllabus and Diseases of Rice 5

  When the grains are set, the panicle breaks at the neck due to weakening of the
neck tissues.
 Such panicle hangs down and can be distinguished from a distance

3. Neck Blast
Causal Organism :
 Imperfect (anamorph/asexual) stage --Pyricularia grisea (= oryzae)
 Perfect (teleomorph/sexual) stage– Magnaporthe grisea or Ceratosphaeria grisea

 It belongs to phylum Deuteromycotina.

 The fungus produces septate, branched, hyaline to olivaceous mycelium, which
is localized in the lesions.
 Conidiophores emerge from the leaf through stomata or by rupturing the cuticle.
 They are simple, 2 to 4 septate and olivaceous in colour.
 Conidia are borne sympodially on the conidiophores.
 They are hyaline to pale olive, pyriform to obclavate or somewhat top-shaped,
usually three celled with a small basal appendage.

Disease cycle :
 The fungus overwinters in straw piles, hay slacks and seeds (PSI).

Lecture notes 1 Theory syllabus and Diseases of Rice 6

  The mycelium of the fungus survives in the infected straws for one or two years
under dry condition, but it is easily destroyed by moisture and microbial activities
when buried in soil.
 Fungus also infects several grasses as collateral host, including Panicum repens,
Digitaria marginata, Brachiaria mutica, Leersia hexandra and Dinebra
retroflexa, which occurs on field bunds in many parts of India (PSI).
 The fungus hibernates in the seeds during storage and may help to some extent
the perpetuation of the fungus during off-season.
 In the tropics, air borne conidia (SSI) are present all round the year because
susceptible hosts are always present.

Mechanism of resistance:
 Silicification of the epidermal cells of the rice plant is considered to confer
resistance against blast.
 Heavy N manuring decreases silicate accumulation in rice plant.
 The blast pathogens produces few toxins, among them α – picolinic acid,
piricularin and pyriculol.

Management:
 Field sanitation, destruction of weed host and seed treatment are precautionary
measures should be followed.
 Seed treatment with captan, thiram, carbendazim @ 2 g/kg seeds.
 Seed treatment with Trichoderma sp. 4 g/kg or Pseudomonas fluorescence @ 10
g/kg.
 Spray nursery with carbendazim 0.05 %
 Spray Blasticidin 20 ppm.
 Two sprays of carbendazim 0.05 % or 0.03 % Thiophanate methyl at boot leaf
stage and flowering stage.

2. Brown leaf spot or Helminthosporium leaf spot

History
 In India, this disease was very much in news when the Famine Inquiry
Commission (1945) concluded that this disease was one of the principle causes of
the famous “Bengal Famine” of 1942- 43.

Symptoms :
 On seedlings, the disease causes blight of seedlings
 In mature plants, leaf spotting is the most common and readily observed
symptom of the disease.

Lecture notes 1 Theory syllabus and Diseases of Rice 7

  On the leaves the spots vary in size and shape from minute dots to circular, eye-
shaped or oval spots measuring 1-14 x 0.5-3 mm.
 They are distinct and isolated, usually fairly scattered over the leaf surface.
 The smaller spots are dark brown or purplish-brown.
 The larger spots are dark brown at the edge but towards the centre they may be
pale yellow, dirty white, brown, or grey.
 Sometimes the spots are surrounded by a yellowish halo and may coalesce and
become irregular in shape.
 Badly affected leaves turn brown and dry out.
 In early and severe stage attack the heads fail to emerge from the sheath and
perish without developing fully.
 When heads emerge they are distorted in various ways.
 Lesions on the heads first appear on or near the lowest joints of the rachis.
 Black spots appear on the glumes.
 These gradually spread over the entire surface as dark brown.
 The seeds are sometimes shrivelled and discoloured.
 The presence of mycelium in infected rice has been demonstrated

On leaves On seeds coat

On seeds
Causal Organism :
 Imperfect (anamorph/asexual) stage – Drechslera (Helminthosporium) oryzae
Perfect (teleomorph/sexual) stage – Cochliobolus miyabeanus
Lecture notes 1 Theory syllabus and Diseases of Rice 8
  It belongs to phylum Deuteromycotina.
 The perfect stage of fungi has been obtained in culture, producing perithecia
containing asci and ascospores.
 The mycelium consists of inter and intra celluar hyphae and erect
conidiophores.
 The mycelium develops greyish brown to dark brown mat on the host parts and
in culture.
 The conidiophore emerge in tuft through the stomata.
 The conidia are 8 to 10 celled, elongated and slightly broader from middle.
 Conidia germinates mostly from cells of both ends.

Disease cycle :
 The pathogen is soil- and seed-borne.
 The mycelium and conidia are carried over from season to season on the seed and
in diseased crop debris left in the field (PSI).
 A few collateral hosts like Digitaria sanguinalis, Leersia hexandra, Echinochloa
colona, Pennisetum typhoides, Setaria italica and Cynodon dactylon, on which the
fungus is recorded through artificial inoculation (PSI).
 Secondary infection is caused by wind-borne conidia.
Management :
 Field sanitation
 Removal of weed host
 Proper N fertilization
 Spraying of beam (tricyclazole) 0.2 % or mancozeb @ 0.25 % or propiconazole @
0.05%
 Grow resistant varieties – Orissa T- 141 , Navagam -19

Lecture notes 1 Theory syllabus and Diseases of Rice 9

 3. Bacterial leaf blight (BLB)
Symptoms :
 The bacterium induces either wilting of plants or leaf blight.
Wilting --
 Wilting syndrome known as 'Kresek' occurs sporadically in the fields causing
serious damage.
 It commonly occurs within 3-4 weeks after transplantation of the crop.
 Kresek results either in the death of whole plant or wilting of only a few leaves.
 The Kresek-affected tillers can be confused with stem borer injury but the latter
can be easily pulled out while it is not so with Kresek-affected tillers.
Leaf blight --
 Leaf blight phase is the most predominant form of the disease occurring between
tillering and heading stages of the crop.
 The earliest symptom of the blight phase is the appearance of dull greenish water-
soaked or yellowish spots 5-10 mm in length on the leaf towards the tip or
margins, leading to tip and marginal drying.
 The infection soon extends along one or both margins, sometimes to the leaf
sheath.
 Small droplets of bacterial ooze, pale amber in colour, are found on the affected
portions.
 When dried, these droplets form minute crusts and impart a rough touch to the
leaves when passed between the fingers.
 The lesions are usually covered by saprophytic fungi, giving them a dark brown
colour.
 In severe infections, all the leaves are attacked and premature drying results.
 When the affected leaves are cut and immersed in clear water in a test tube, a
turbid ooze of the bacterium streaming from the vascular bundles, can be observed.
 The loss in grain yield due to this disease may range up to 60 per cent.

Lecture notes 1 Theory syllabus and Diseases of Rice 10

 Wilting Bacterial ooze

Leaf blight

Causal organism :
 Xanthomonas oryzae pv. oryzae
 The bacterium is rod shaped, occuring singly or in pairs, gram negative aerobic,
capsulating and non spore forming with single polar flagellum.
 Kingdom : Prokaryote
 Bacteria – have cell membrane and cell wall
 Division : Gracilicutes – Gram negative bacteria
 Class : Proteobacteria – mostly single celled
 Family : Pseudomonadaceae
 Genus : Xanthomonas
Disease cycle :
 Primary infection may result from the inoculum overwintering in the seed,
being present in the husk as well as in the endosperm.
 It also survives in soil or plant stubbles and debris, and the initial inoculum may be
built upon the nursery seedlings.

Lecture notes 1 Theory syllabus and Diseases of Rice 11

  The bacterium is reported to infect some grasses, like Leersia spp., Cyperus
rotundus, which might play a role in the spread of the disease.
 Secondary spread is brought about through wounds and stomata by bacterial
cells disseminated by wind borne rail drop splashes, by irrigation water or
rain water coming from infected fields and by contact between diseased and
healthy leaves.

Management :
 Use disease free healthy seeds.
 Soaking seeds for 8 hrs in Agrimycin @ 0.025 % followed by hot water treatment
for 10 minutes at 52 – 54 0C eradicates the bacterium from the seeds.
 Remove weed host.
 Spray streptocycline 1 g + 10 g copper oxychloride in 20 lit of water.
Use resistant varieties – TKM-6, Nauroji-1, IR-42.

4. False Smut

 Farmers consider incidence of false smut of rice as an omen of good harvest.

Symptoms :
 The disease appears on the ears, where individual ovaries are transformed
into large, velvety green masses.
 These irregular round to oval sclerotial bodies attain a size of about 8 x 10 mm.
 Only a few spikelets in the ears are affected.
 The glumes are not affected but are covered superficially by the green mass of
spores.
 They are slightly flattened, smooth, yellow to orange and are covered by a
membrane.
 The membrane bursts as a result of further growth and color of the ball becomes
yellowish green.

Lecture notes 1 Theory syllabus and Diseases of Rice 12

Causal organism :
 Imperfect (anamorph/asexual) stage – Ustilaginoidea virens
 Perfect (teleomorph/sexual) stage – Claviceps oryzae sativae
 The mycelia filling in the ovary are uniteed and fine and they develop conidia,
pseudosclerotial and sclerotial stages.
 Late in season, the conidial masses in smut balls harden and form scelerotia.
 Sclerotia germinate to produce perithecia bearing eight ascopsores.

1. Smut balls on rice earhead

a. Smut balls
b. Sclerotia
c. Cross section of stroma
containing abundant perithecia
d. Perithecia
e. Ascus with ascospores

Lecture notes 1 Theory syllabus and Diseases of Rice 13

Disease cycle :
 As the fungus has been recorded on many grasses and wild rice, it is presumed that
the spores produced on the collateral hosts become airborne and serve as the main
source of inoculum.
 Primary infection is believed to be caused mainly by ascospores produced from the
sclerotia.
 Chlamydospores play an important role in the secondary infection which is a major
part of the disease cycle.
 Chlamydospores are air-borne and are profusely present at the time heading of rice
plant.
Management :
 Dipping seeds in brine solution.
 Collect the diseased grains and destroy them as soon as possible.
 Spray copper oxychloride @ 3 g/lit of water.

5. Sheath blight
Symptoms :
 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 and irregular
blackish brown or purple brown border.
 The presence of several large lesions on a leaf sheath usually causes death of
the whole leaf.
 Plants heavily infected in the early heading and grain filling growth
stages produce poorly filled grain, especially in the lower part of the
panicle.
 The infection extends to the inner sheaths resulting in death of the entire plant.

Lecture notes 1 Theory syllabus and Diseases of Rice 14

Causal organism:
 Rhizoctonia solani (Sexual stage : Thanetophorus cucumeris)
 The fungus produces septate mycelium which are hyaline when
young and brown when old.
 It produces large number of spherical brown sclerotia.

Lecture notes 1 Theory syllabus and Diseases of Rice 15

Disease Cycle:
 The pathogen can survive as sclerotia or mycelium in soil and
initiate primary infection.
 Sclerotia are present in enormous numbers in old rice straw and
stubbles left in the field and are spread through irrigation water or
rain water.

Management :
 Deep ploughing in summer and burning of stubbles.
 Grow resistant varieties.
 Apply organic amendments viz., neem cake @ 150 kg/ha or FYM
12.5 tons/ha.
 Soil application of P. fluorescence @ 2.5 kg/ha after 30 days of
transplanting
 Avoid flow of irrigation water from infected to healthy fields.
 Spray Carbendazim @ 500 g/ha.

6. Rice tungro
Symptoms:
 Tungro is characterized by stunting of the plant and discolouration of leaves,
ranging from various shades of yellow to orange, and rusty blotches spreading
Downwards from the leaf tip.
 The young leaves show a mottled appearance and slightly twisted, whereas the
older leaves appear rusty coloured.
 In less susceptible varieties tungro virus infection delays flowering.
 lf infection of highly susceptible varieties takes place at very early stages, the
plants may die before flowering.
Lecture notes 1 Theory syllabus and Diseases of Rice 16
Causal virus :
 Tungro is a composite disease caused by two viruses: Rice Tungro Spherical
Virus (RTSV)and Rice Tungro Bacilliform Virus (RTBV)
 The RSTV is ssRNAcausing only very mild stunting of plant.
 RTBV causing main symptoms of stunting and yellowing of the plant.
 RTBV is dependent on RTSV for transmission.
 The tungro virus is transmitted only by green leaf-hopper Nephotettix verescens.

Management:
 Long fallow period.
 Neem seed cake applied at 5 kg/0.032 ha of nursery followed by spray of 5 %
neem kernel extract.
 Spray of conidial suspension of Beauveria bassiana and Paecilomyces on rice
plants kills the vectors.
 Use of resistant varieties.
7. Zn deficiency
Symptoms :
 The disease usually appears 10-15 days after transplanting.
 Leaves of diseased plants show chlorosis at the base.
 Large number of small brown or bronze spots appear on the lamina surface.
 These coalesce to form bigger spots and ultimately the entire leaf turns bronze
coloured and dries.
 The growth of diseased plants is stunted.
 Root growth is also restricted and usually the main roots turn brown.
 The finer roots are destroyed.
 In severe cases plants fail to grow further and do not produce ears but
sometimes there is natural recovery of the plants and some of them may
produce ears with few grains.

Manangement :
 The disease can be effectively managed by two sprays of a mixture of 2 kg zinc
sulphate and 1 kg of slaked lime in 400 litres of water per acre.
 The first spray is given as soon as early symptoms of the disease are noticed.
 The second spray is given 10 days later.

Lecture notes 1 Theory syllabus and Diseases of Rice 17

 Soil inhabitants Soil invaders
1. These are unspecialized parasites These are more specialized parasites
with a wide host range that are able that survive in soils in close
to survive indefinitely in the soil as association with their hosts.
saprophytes.
2. Pathogen remain in soil for more Pathogen remain in soil for 2-3 years
than 4-5 years
3. Pathogen survive in soil without Pathogen survive in diseased plant
plant debris debris in soil
4. Produced dormant structures like Not produced dormant structures
oospore, sclerotia and
chlamydospores
5. Difficult to manage as long duration Easy to manage by short crop rotation
crop rotation is required
6. Fast multiplication Slow multiplication
7. eg. Pythium, Fusarium, Sclerotium, eg. Colletotrichum, Alternaria,
Macrophomina Pyricularia etc.

Lecture notes 1 Theory syllabus and Diseases of Rice 18

 Prepared and Compiled by Dr. Shivangi S. Kansara

2. Disease of maize
1. Downy mildew / Crazy top
2. Stalk rot
3. Maydis / Southern leaf blight
4. Turcicum/ Northern leaf blight
5. Banded leaf and sheath blight
6. Late wilt

1. Downy mildew of maize or Crazy top

Symptoms :
 The most characteristic symptom is the development of chlorotic streaks on the
leaves.
 Plants exhibit a stunted and bushy appearance due to shortening of the
internodes.
 White downy growth is seen on the lower surface of leaf.
 Downy growth also occurs on bracts of green unopened male flowers in the tassel.
 Small to large leaves are noticed in the tassel.
 Proliferation of auxillary buds on the stalk of tassel and the cobs is
common (Crazy top).

Lecture notes 3 Diseases of Maize 1

 Prepared and Compiled by Dr. Shivangi S. Kansara
Pathogen :
 Perenosclerospora sorghi
 The fungus grows as white downy growth on both surface of the leaves,
consisting 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 (21-33˚C)
 High relative humidity (90 per cent) and drizzling.
 Young plants are highly susceptible.

Disease cycle :
 The primary source of infection is through oospores in soil and also dormant
mycelium present in the infected maize seeds, over wintering crop debris and
infected neighboring plants.
 Secondary spread is through airborne conidia.
 At the onset of the growing season, at soil temperatures above 20°C, oospores in
the soil germinate in response to root exudates from susceptible maize seedlings.
 Oospores are reported to survive in nature for up to 10 years.
 Once the fungus has colonised host tissue, sporangiophores (conidiophores)
emerge from stomata and produce sporangia (conidia) which are wind and
rain splash disseminated and initiate secondary infections.
 Germination of sporangia is dependent on the availability of free water on the leaf
surface.
 Conidia are produced profusely during the growing season.
 As the crop approaches senescence, oospores are produced in large numbers.

Management
 Deep ploughing.
 Crop rotation with pulses.
 Rogue out infected plants.
 Treat the seeds with metalaxyl at 6g/kg.
Lecture notes 3 Diseases of Maize 2
 Prepared and Compiled by Dr. Shivangi S. Kansara
 Spray the crop with Metalaxyl + Mancozeb @ 1kg on 20th day after sowing.
 Grow resistant varieties and hybrids.

2. Stalk rot/ maize stalk rot / stem and ear rot

Symptoms:
 Symptoms of Fusarium stalk rot are not easily distinguished from those of
Gibberella stalk rot and other stalk rot diseases.
 Rot normally begins soon after pollination and becomes more severe as the plant
matures.
 The leaves turn from a healthy green colour to a dull green.
 Wilted plants remain standing and dry, small, dark brown lesions develop on
the lowest internodes.
 When split open, the stalks may reveal a whitish-pink to salmon pink pith
discolouration often confused with the red colour of Gibberella stalk rot.
 Premature senescence and lodging due to the disintegration and shredding of
the internal stalk pith may occur; when squeezed between the thumb and index
finger at the lower nodes, the stalk often collapses.

Lecture notes 3 Diseases of Maize 3

 Prepared and Compiled by Dr. Shivangi S. Kansara

Causal Organism :
 Fusarium verticilioides= F. mondiforme (Gibberella fufikuroi)

Disease cycle:
 The fungus survives on crop residues in the soil or on the surface.
 Under favourable conditions, it may infect maize stalks either directly or through
wounds caused by hail or insects.
 Spores can be splash dispersed onto leaves and washed down the leaf into the
sheath and infect at the nodes.
 F. verticilioides is most common in warm, dry areas.
 Fusarium root and stalk rots typically occur in complexes with other root and stalk
rots such as Gibberella, Diplodia and Colletotrichum.

Management :
 Physical damage that creates wounds allowing the pathogen to enter such as insect
damage or hail storms may also predispose maize plants to stalk rot.
 Fungicide applications may be beneficial in lessening stalk rot severity

Lecture notes 3 Diseases of Maize 4

 Prepared and Compiled by Dr. Shivangi S. Kansara
3. Southern leaf blight
 The first epidemics of the Southern corn leaf blight also known as Maydis leaf
blight took place in the USA in 1970.
 The monetary value of the crop lost was 1 billion dollar.
 A highly virulent strain called Race T appeared on maize hybrids with Texas
male sterile cytoplasm.
 The disease development was related to the growing of maize with T-cytoplasm on
large areas.
 Since 1990 the use of cultivars with T male sterile cytoplasm has been forbidden in
selection.
 Presently, the cultivars with M and C types of sterility are used.

Symptoms :
 Initial symptoms observed as small (0.5 to 2.5 cm), tan lesions that may be so
numerous that they almost cover the entire leaf
 Some races of the fugus also attack the stalks, the leaf sheaths, ear husks, ears
and cobs.
 Affected kernels are covered with a black mold and cobs may rot or, if the shank is
infected early, the ear may be killed prematurely and drop.
 Seedlings from infected kernels may wilt and die within a few weeks of planting

Lecture notes 3 Diseases of Maize 5

 Prepared and Compiled by Dr. Shivangi S. Kansara

Causal organism : Cochliobolus heterostrophus

 The fungus has the anamorph Bipolaris maydis
 Facultative parasite.
 It produces a specific T-toxin causing the same symptoms of disease as those
caused by conidia.
 Conidiophores are in group, geniculate, mid dark brown, pale near the apex and
smooth.
 Conidia are fusiform, markedly curved, pale to mid dark golden brown with 5-11
septa.
Disease cycle:

Lecture notes 3 Diseases of Maize 6

 Prepared and Compiled by Dr. Shivangi S. Kansara
Favorable Conditions :
 Optimum temperature for disease development is 25-31°C.
 Relative humidity 90-100 %.
 Presence of free water on the leaf.
 Infection takes place early in the wet season.

Management :
 Use of disease resistant hybrids of maize
 Seed treatment withCaptan or Thiram at 4 g/kg
 Spray mancozeb @ 0.2 %
 Removal of infected maize residues.
 Crop rotation

4. Northern leaf blight or turcicum leaf blight

Symptoms:
 The characteristic lesions are 2 to 15 cm long cigar-shaped gray-green to tan-
colored lesions on the lower leaves.
 As the disease develops, the lesions spread to all leafy structures, including the
husks.
 The lesions may become so numerous that the leaves are eventually destroyed
causing major reductions in yield due to lack of carbohydrates available to fill the
grain.

Lecture notes 3 Diseases of Maize 7

 Prepared and Compiled by Dr. Shivangi S. Kansara
Causal organism: Cochliobolus carborum
 Anamorph – Bipolaris zeicola
 Race 1 of Cochliobolus carborum produces the host specific HC toxin, which is
toxin only on specific maize lines.
 Mycelium is localized in the infected lesion.
 Conidiophores emerge through stomata and are simple, olivaceous, septate and
geniculate.
 Conidia are olivaceous brown, 3-8 septate

Disease Cycle
 The fungus overwinters as mycelia and conidia on com residues left on the soil
surface.
 The conidia are transformed into thick-walled resting spores called
chlamydospores.
 New conidia are produced on the old corn residue, and the conidia are carried by
the wind or rain to lower leaves of young corn plants.
 Secondary spread within fields occurs by conidia produced on the leaf tissues.

Management
 Planting resistant hybrids.
 Seed treatment with Thiram or Captan @ 2.5 g/kg seed.
 A one to two year rotation away from corn.
 Destruction of old corn residues by tillage.
 Spray Mancozeb @ 0.2%, if required repeat after 15 days.

5. Banded leaf and sheath blight/rot

Symptoms:
 Symptoms of BLSB are conspicuous and characterized with presence of peculiar
bands on leaf sheath and sclerotial bodies on affected parts of the plants.
 Symptoms appear on all aerial plant parts except tassel.
 The disease manifests itself on leaf, leaf sheath, stalks and ears as leaf and sheath
blight, stalk lesions or rind spotting and stalks breakage, clumping and cracking of
styles (silk fibers) and horseshoe shaped lesions with banding of caryopses
resulting in ear rots.

Lecture notes 3 Diseases of Maize 8

 Prepared and Compiled by Dr. Shivangi S. Kansara
 The symptoms appeared within 4–5 days after inoculation, which are irregular,
water-soaked, straw-coloured lesions on leaf bases and sheaths.
 The lesions enlarge rapidly resulting in discolored areas alternating with dark
bands, apparent on lower leaves after 7–8 days.
 However, lower leaf sheath and the ears are more quickly attacked by the
pathogen.

Lecture notes 3 Diseases of Maize 9

 Prepared and Compiled by Dr. Shivangi S. Kansara
Causal Oragasnism:
 Rhizoctonia solani f. sp. Sasakii
 BLSB disease caused by R. solani f. sp. sasakii = Hypochonus sasakii
[Thanatephorus cucumeris (Frank) Donk] is one of the most widespread,
destructive, and versatile pathogen prevalent in most parts of the world with a wide
host range including maize causing seed decay, damping-off, stem canker, root rot,
aerial blight, and seed or cob decay.
 R. solani f. sp. sasakii is morphologically characterized by pale to brown colour of
mycelium, branching near the distal septum in young growing hyphae, presence of
a constriction and formation of a septum in branch near the point of origin, absence
of clamp connections, sclerotia of undifferentiated texture.
 The colonies produced by the pathogen are fast growing and form silky white
colonies on PDA medium at 28 ± 10C losing their luster gradually and becoming
dull in appearance.

Disease Cycle
 The primary source of inoculum include sclerotia in soil or in infected host debris
and the active mycelium on the other grass hosts that grow in the vicinity of maize
plant in fields.
 Sclerotia which survive on plant debris often come up on the soil surface during
field preparation and other operations.
 They come in contact with newly planted seedlings/plants and cause infection.
 Secondary spread is due to contact of healthy plants with infected leaves/sheaths
and is responsible for the distribution of the pathogen during the main growing
season of the crop.
 The infection continues to mid-dough stage covering the entire plant including the
ear but not the tassel.
 Seeds are not considered to be a source of inoculum and may not play a major role
in severe disease outbreaks.
 If ear infection occurs at the late stage, germination of the seed is adversely
affected resulting in

Management:
 Selection of a well-drained field and planting on raised beds.
 Cultural practices like stripping of the second and third leaf sheaths from the
ground level at the age of 35–40 days old crop is effective.
Lecture notes 3 Diseases of Maize 10
 Prepared and Compiled by Dr. Shivangi S. Kansara
 Inter-cropping of maize with legumes especially with soybean.
 Application of P. fluorescens and T. harzianum reduce BLSB incidence in field
besides improving plant growth.
 Seed dressing fungicides (Bavistin 50WP @ 2.5 g/kg of seed, Vitavax Power @
Carboxin 37.5 % + Thiram 37.5 % @2.5 g/kg of seed and Thiram 50WP @ 2.5
g/kg of seed has been found effective for the management of BLSB.

6. Late wilt
Symptoms:

 Leaves appear streaked as tissue between the veins becomes dull green and then
chlorotic before eventually rolling inward and appearing scorched while
retaining somewhat of a green color.
 Yellow to reddish brown streaks appear on the basal internodes of the stalk.
 Stalks dry and have a shrunken and hollow appearance with dark yellow to
brownish macerated pith and brownish-black vascular bundles.
 Lower parts of infected stalks become dry, shrunken and hollow.
 Fewer ears are produced, and kernels that form are poorly developed and may be
infected with the pathogen.
 Seed-borne infection results in seed rot and damping-off of seedlings or
seedlings with stunted roots.

Causal organism:
 Harpophora maydis

Lecture notes 3 Diseases of Maize 11

Prepared and Compiled by Dr. Shivangi S. Kansara

Lecture notes 3 Diseases of Maize 12

 Prepared and Compiled by Dr. Shivangi S. Kansara
Disease cycle:

Management:
 Disease-free seed
 Soil solarization, balanced soil fertility, and flood fallowing
 Sanitation measures such as deep tillage may have a significant impact on disease
 Hot water seed treatment (60 0C for 10-15 minutes) can reduce seed transmission
 late summer planting reduced disease severity
 Moisture stress is a major predisposing factor for late wilt, frequent watering or
saturated soils reduced late wilt.
 Captan, carbendazim, carboxin and thiram seed treatments significantly reduced
late wilt
 Balanced fertility can reduce disease severity, although it does not provide
complete control.
 Low levels of nitrogen fertilization (60 kg/ha) increased wilt

Lecture notes 3 Diseases of Maize 13

 Prepared and Compiled by Dr. Shivangi S. Kansara

Sr. Northern leaf blight Southern leaf blight

No.
1 It is also known as turcicum leaf blight It is also known as maydis leaf blight
2 Lesions are 2 to 15 cm long cigar- Symptoms observed as small (0.5 to 2.5
shaped gray-green to tan-colored cm), tan lesions, numerous that cover the
lesions on the lower leaves. entire leaf
3 Causal organism Causal organism
Telomorph : Cochliobolus carborum Telomorph : Cochliobolus
Anamorph – Bipolaris zeicola heterostrophus
Anamorph : Bipolaris maydis
4 It produces the host specific HC toxin, It produces a specific T-toxin causing the
which is toxin only on specific maize same symptoms of disease as those
lines. caused by conidia.

Lecture notes 3 Diseases of Maize 14

 3. Diseases of Sorghum
1. Smuts
2. Striga
3. Anthracnose/ Colletotrichum leaf spot

Smuts
 There are seven smut diseases of Sorghum, four of which occur in India :
Covered/kernel/short or grain smut : Sphacelotheca sorghi (Sporisorium
sorghi)
Loose smut : Sphacelotheca cruenta (Sporisorium cruentum)
Long smut : Tolyposporium ehrenbergii
Head smut : Sphacelotheca reiliana (Sporisorium reiliana)

1. Covered/kernel/short or grain smut

Symptoms :
 The disease becomes appears only at the time of grain formation in the ear at which
time the smut sori formed in the place of healthy grains.
 The size of the sori varies with the variety, but generally they are larger than the
normal grain.
 They are oval to cyclindrical, 4-15 mm in length and 3-5 mm broad and dirty grey.
 Most of the grains of an infected ear are replaced by the smut sori.
 Ratoon crops exhibit higher incidence of disease.

Lecture note 3 Diseases of Sorghum 1

Causal organism :
 Sphacelotheca sorghi / Sporisorium sorghi
 The pathogen forms teliospores (overwintering stage) and sporidia.
 Teliospores are spherical or roundish, sporidia are oblong.

Disease cycle :
 The pathogen is externally seed borne. The spores are borne on the surface.
Lecture note 3 Diseases of Sorghum 2
  They germinate with the seed and infect the seedling by penetrating through the
radicle or mesocotyl establish systemic infection that develops along the
meristematic tissues.
 At time of flowering, the fungal hyphae get converted into spores, replacing the
ovari with the sori.
 If the diseased ears are harvested with the healthy ones and thresh together, the
healthy grains become contaminated with the smut spores released from the
bursting of the sori.
 The spores remain dormant on the seed untill next season.
 The smut sproes remain viable indefinitely, depending on how they are stored.
 In some cases they may be viable even after 10 years.
 The fungus can also be brought into artificial culture on agar media, producing a
yeast-like growth.
 Only when two compatible strains of opposite sex unite can the fungus infect the
host.

Management :
 Use disease free seeds.
 Grow resistant varieties.
 Remove diseased plant from the field.
 Follow crop rotation
 Treat seeds with Sulphur @ 4-6 gm/ kg or captan / thiram 4 g/ kg seed.
 Solar enery treatment: seeds were soaked in water at ordinary temperature during
sumeer for 4 hrs and then spread out in the hot sun.

2. Loose smut / Kernel smut of sorghum

Symptoms :
 The affected plants are stunted, produce thinner stalks, more tillers and earlier
flowering than the healthy plants.
 All spikelets of an infected ear are malformed and hypertrophied.
 The sorus replaces the pistil and stamens, and is borne on glumes and pedicel.
 The size of the sori ranges from 3 -18 mm in length and 2-4 mm in thickness.
 The sori are surrounded by a thin, grey membrane, which ruptures exposing
masses of the spores.
 A conical curved columella remains after the discharge of the spores.

Lecture note 3 Diseases of Sorghum 3

Causal organism :
 Sphacelotheca cruenta / Sporisorium cruentum
 The spores are dark brown, sporidia are spindle shaped or oblong.
 The sorus is covered by a thin membrane which ruptures very early, exposing the
spores.
 In the centre of each sorus is a long conidoal columella as in grain smut but longer
and curved.

Disease cycle :
 It is externally seed borne and soil borne to some extent in dry soil.
 The fungus enters the seedling through the radical, mesocotyl or epicotyl and then
becomes systemic causing smutting of ovaries at the time of ear formation.
 Since it is systemic, ratoon crops from infested main crops are also infected.
 The optimum temperature for spore germination is around 30 0C.

Favourable condition:
 Soil temperature – 18-23 0C
 Soil humidity 15-20 %

Management :
 Use healthy seeds.
Lecture note 3 Diseases of Sorghum 4
  Crop rotation and field sanitation.
 Remove diseased plant from the field.
 Treat seed with sulphur @ 4-6 g/kg seed or systemic fungicides carboxin and
carbendazim @ 3 – 4 g/ kg

3. Long smut
Symptoms :
 Only close examination of the ears in the field reveals the presence of long smut.
 Usually a few smut sori are scattered sporadically through out the ear.
 The sorus is covered by a whitish to dull yellow, fairly thick membrane and is
much longer than those of the other two smuts.
 It is cylindrical , measuring 4 cm in length and 6-8 mm in width.
 Usually the membrane remains intact until broken mechanically releasing the black
spore mass.

Causal organism :
 Tolyposporium ehrenbergii
 The spore mass is granular, black, intermixed with shreds of host tissue.

Disease cycle :
 The fungus is air borne and seed borne. The infection takes place by means of
sporidia which enters the floral parts, producing sori about 12 – 15 days later.

Lecture note 3 Diseases of Sorghum 5

  The spores in the soil germinate to produce clusters of sporidia which become air
borne and cause primary infection.
 Secondary infection may also take place through the spores released from the
smutted ear in the field.

Management :
 Grow resistant varieties.
 Remove diseased plant from the field.
 Cropr rotation
 Field sanitation.
 Early sowing of the crop.

4. Head Smut
Symptoms :
 The disease becomes apparent only at the time of flowering.
 In the place of a normal inflorescence, a sorus fully covered with a greyish-white
membrane emerges from the boot leaf.
 The cylindrical sorus is usually 8-10 cm long and 2.5-5.0 cm wide.
 When it has fully emerged, the fungal wall ruptures, exposing large mass of black,
powdery spores.
 If the wind is blowing at the time of sorus emergence, the air-borne spores resemble
a smoky cloud around the head.
 When the spores are blown off, a network structure of dark, filamentous vascular
tissues of the host is exposed.

Lecture note 3 Diseases of Sorghum 6

Causal organism :
 Sphacelotheca reiliana /Sporisorium reilianum
 The pathogen forms both teliospores (Hibernating stage of the pathogen)
and sporidia in its life cycle.

Disease cycle :
 The pathogen is externally seed borne and major source of infection is soil boren
inoculum.
 The fungus in soil infects young seedlings.
 It becomes systemic, growing along with the apical tissues, covering the entire
floral tissues and converting it into a sorus while still in the boot leaf.
 When the sorus opens, it releases large masses of smut spores, which may
eventually reach the soil.
 In dry soil, the spores remain viable for a considerable period, at least until the
following crop season.
 With rain or irrigation water they germinate, and if young seedlings are present in
the vicinity, they infect the host plant.
Favourable condition:
 Temperature 14 to 36 0C
 Soil temperature 18-23 0C and soil humidity 15-20 %

Management :
 Collecting smutted heads in cloth bags and dipping in boiling water.
 Follow suitable crop rotation.
 Treat the seeds before sowing.
 Sanitation
 DFeep ploughing

Lecture note 3 Diseases of Sorghum 7

 Comparison of the characters of four smuts of sorghum found in India
Character Grain smut Loose smut Long smut Head smut
Organism S. sorghi S. cruenta T. ehrenbergi S. reiliana
Ear infection All or most All or most Only about 2 Entire head
grains smutted grains smutted per cent of smutted into a
grains are single sorus
infected
Sori small, 5-15 x small, 3-18 x 2- long, 40 mm x 7.5-10 cm x
3-5 mm 4 mm 6-8 mm 2.5-5 cm
Collumella short columella long columella columella columella
present present absent, but 8 – absent, but a
10 vascular network of
strands present vascular tissues
present
Spores in single, in single, always in balls, loosely bound
round to oval, spherical or globose or in balls,
olive brown, elliptical, dark angular, spherical or
smooth walled, brown, spore brownish angular, dull
5-9 µ in wall pitted, 5-9 green, warty brown, 10 – 16
diameter µ in diameter spore wall, 12- µ in diameter
16 µ in
diameter
Viability of over 10 years about 4 years about 2 years up to 2 years
spores
In culture yeast like in colonies in colonies with in colonies
growth with with sporidia masses of germ tubes and
sporidia and resting sporidia sporidia
spores
Spread Externally Externally air-borne soil-borne and
seed-borne seed-borne seed-borne

Lecture note 3 Diseases of Sorghum 8

 2. Striga

 Striga is well known semi root parasite.

 There are about 30 – 35 species of striga.
 The most important species found in India are Striga asiatica, S. densiflora, S.
euphrasioides and S. lutea.
Symptoms :
 Affected plants remain stunted, wilt and turn yellowish.
 Infected roots bear a large number of striga haustoria, which are attached to the
root and feed on it.
 The infected plants are stunted in growth and may die prior to seed setting.

Parasite :
 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.

Lecture note 3 Diseases of Sorghum 9

  The parasite then slowly attach to the root of the host by haustoria, 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.
 The disease spread in the field in a circular pattern.
 The seeds are spread by wind/ by water/ by contaminated tools and equipment or by
contaminated soil carried on farm machinery.

Management :
 Field is to be kept free from weed host plants.
 The shoots of parasites should be pulled out before seed setting and destroyed.
 2, 4, D weedicide
 Regular weeding and interculture operation.
 Trap crop like legume may be used to stimulate the germination of seeds

3. Anthracnose/ red rot/ Colletotrichum leaf spot

Symptoms :
 Fungus causes small, red purple or brown spots with whitish or purple centres.
 The spots are elliptical or spindle shaped, 2 – 4 mm long and 1 – 2 mm broad.
Lecture note 3 Diseases of Sorghum 10
  The infection is found mostly on the basal and older leaves, the young ones usually
being free from infection.
 Under conditions of high humidity or high rainfall, the spots increase in number
and coalesce to cover more leaf area.
 On centre of lesions, few or numerous small, black dots are develop; these are the
fruiting bodies (Acervuli) of the fungus.
With time infection spread to the stem, causing reddish streaks.

Causal organism :
 Colletotrichum graminicola (Imperfect stage), Glomerella graminicola (Perfect
stage)
 Acervuli with setae arise through epidermis.
 Conidia are hyaline and single celled.

Lecture note 3 Diseases of Sorghum 11

Disease cycle :
 The fungus can survive as mycelium in host residue, wild sorghum species or on
some weeds and as conidia or mycelium on seed.
 It can persist upto 18 months in disease residues.
 Secondary spread through wind or rain splashes

Management :
 Grow resistant varieties.
 Follow crop rotation with non host crop
 Clean cultivation, Elimination of grasses
 Treat seeds with thiram or captan or sulphur 4 – 6 g/kg seeds.
 Three sprays of zineb 0.2 % or mancozeb 0.2 % at 15 days interval from 45 days
after sowing.

Lecture note 3 Diseases of Sorghum 12

 4. Diseases of Bajra
1. Ergot
2. Downy mildew
3. Smut
4. Rust
1. Ergot or sugary disease
Symptoms :
 The disease occurs only at the time of flowering.
 The symptom is seen by exudation of small droplets of light pinkish or brownish
sticky fluid (honey dew) from the infected spikelets.
 A few to many such spikelets may be found in a group, which darken with age.
 This attracts several insects.
 In the later stage, small grayish or dark brown sclerotia are formed.
 This sclerotia replace the ovary or grain and are about 0.5 – 1 cm in length, 1-
2 mm in diameter and are hard and woody.

Causal organism:
 Claviceps fusiformis and rarely by Claviceps microcephala
 The honey dew produced on the ears is full of conidia.
 In the initial stages macroconidia are formed and later microconidia
 The honey dew stage is followed by the development of sclerotia which
are elongated to round, light to dark brown.
 Sclerotia germinate by producing long stalk bearing perithecial stroma.

Compiled and Prepared by Dr. Shivangi S. Kansara Lecture Notes 4 Bajra Diseases
Disease cycle :

 The fungus spread from plant to plant in the conidial stage.

 The honey dew mixed with the inoculum attracts insects, which help in the
dissemination of the conidia and spread of the disease.
 The sclerotial body helps the fungus to perpetuate from season to season.
Compiled and Prepared by Dr. Shivangi S. Kansara Lecture Notes 4 Bajra Diseases
  They remain in the soil or plant debris and germinate during the next season to
produce the ascus stage, which can cause infection of the spike, producing the
conidial stage.
 The sclerotia are viable longer when buried deep in the soil.

Management :
 Use certified/clean seed.
 Immerse the seeds in 10 per cent comman salt solution and remove the floating
sclerotia.
 Spray with carbendazim 500 g or mancozeb 1.25 kg or ziram 1 kg/ha when 5-10 %
of flowers have opened and again at 50 % flowering stage.
 Long crop rotation
 Repeated deep ploughing reduce sclerotia/ primary source
 Immediately sowing after on set of monsoon.

2. Downy mildew or Green ear

Symptoms :
 Green ear disease of bajra caused by Sclerospora graminicola reported by E. J.
Butler in 1907 from India.
 The infected plants tiller excessively and are dwarfed.
 The foliage becomes pale and chlorotic, and broad streaks are prominent.
 As the disease advances, the streaks turn brown.
 On close examination, downy fungal growth can be seen on the lower surface of
the leaf and even on the upper surface, in severe case.
 This surface growth is more profuse during rainy and humid seasons.
 In many affected plants, ears fails to form or if formed, they are malformed into
green leafy structures; hence the name “Green ear” .
 Mostly the entire ear is transformed into leafy structures, but at times a part of the
ear alone is affected, the other part producing normal grains.
 The infection converts the various floral parts, including glumes, palea,
stamens and pistil into green leafy structures.
 As the disease advances, the green leafy structures become brown and dry.

Compiled and Prepared by Dr. Shivangi S. Kansara Lecture Notes 4 Bajra Diseases
Causal organism:
 Sclerospora graminicola
 The mycelium is intercellular, non septate and systemic
 Short hyaline sporangiophores arise through stomata and branch irregularly bearing
sporangia.
 Sporangia are hyaline, thoin walled.
 Oopsores are round in shape, thick and smooth.

Disease cycle :
 The oospore remain viable in soil for five years or more giving rise to primary
infection of the host seedlings, which takes place by direct penetration of root
hairs and the coleoptile by germ tubes.
 Secondary spread starts from sporangia (zoospore), which are the most active
during the rainy season.
 The zoospores enter the leaf stomata to initiate infection.
 Very high humidity (90 %), presence of water on the leaves and temperatures
of 15 -25 0C favours the formation of sporangiosphore.

Management :
 Avoidance of low lying and water logging fields for sowing.
 Crop rotation for more than 5 years should be followed.
 Seed treatment with metalaxyl (Apron)@ 6 g/kg or metalaxyl MZ (Ridomil MZ)
@ 8 g/kg followed by two sprays of metalaxyl MZ 0.2 % at 25 and 35 days after
sowing.
Compiled and Prepared by Dr. Shivangi S. Kansara Lecture Notes 4 Bajra Diseases
  Roughing of infected plants
 Grow resistant varieties.
 Immediately sowing after onset of monsoon. Late sowing is avoided.

3. Grain smut / Smut of bajra

Symptoms :
 The disease become apparent at the time of grain setting.
 A few grains, sporadically distributed on the ear, may be replaced by oval to top
shaped sori, which are generally two or three times the size of the normal grain.
 They are bright green to dirty black in colour and often rupture to expose a
black spore mass.

Causal organism:
 Tolyposporium penicillariae
 The pathogen is mostly confined to the sorus
 The sori contain round spores in group and are not easy to separate.

Disease cycle :
 The infection starts mainly from air born spores, which germinate to produce the
sporidia that enter the spikelets and infect the ovary.
 The spore balls remain in the soil to germinate during the next season, producing
masses of sporidia, which become air borne and infect the ear.

Compiled and Prepared by Dr. Shivangi S. Kansara Lecture Notes 4 Bajra Diseases
Management :
 Removal and destruction of infected ear heads.
 Immediately sowing after on set of monsoon. Late sowing is avoided.
 Crop rotation and field sanitation to reduce the source of primary inoculum.
 Spraying the crop with Vitavax @ 0.1 % at boot leaf stage.

4. Rust

Symptoms :
 The minute, round uredosori occur in groups on both the surfaces of leaves,
particularly towards the distal end of the blade on leaf sheath and stem.
 The telia which appear later in the season, are black, elliptical and sub
epidermal and are also distributed over the leaf blade, leaf sheath and stem.
 In severe infections, the plants appears unhealthy and slightly stunted.

Causal organism:
 Puccinia penniseti
 Uredospores are oval, teliospores are dark brown in colour, two celled.

Disease cycle :
 The fungus is macrocyclic, heterociuos, producing uredial and telial stages on
bajra and aeacial and pycnidial stages on several species of Solanum,
including brinjal.
 Since bajra is grown through the main season and brinjal all the year round.
 Moreover, some species of Solanum are perennial weeds which can harbour the
pathogen and thereby help to spread the disease.

Compiled and Prepared by Dr. Shivangi S. Kansara Lecture Notes 4 Bajra Diseases
Favourable condition:
 Closer planting
 Low temperature 10-12 0 C

Management :
 Grow resistant varieties
 Two sprays of mancozeb or zineb @ 0.2 % at 15 days interval starting from the
initiation of disease.
 Destroy alternate host
 Immediate sowing after onset of monsoon.

Compiled and Prepared by Dr. Shivangi S. Kansara Lecture Notes 4 Bajra Diseases
 Page |1

Diseases of groundnut
Major diseases :
1. Tikka diseases or leaf spot
2. Rust
3. Collar rot or seedling blight
4. Root rot
5. Stem rot/Sclerotial rot
6. Bud necrosis
7. Chlorosis
8. Root knot nematode
Minor diseases :
1. Anthracnose – Colletotrichum dematium and C.capsici
2. Rosette – Groundnut rosette virus

1. Tikka diseases or leaf spot

Symptoms :
 The disease is caused by two different pathogens, namely, Cercospora
arachidicola and Cercospora personatum (Phaeoisariopsis personatum).
 The two pathogens mostly occur on the same leaves.
 The Cercospora arachidicola appears about a month earlier than the
Phaeoisariopsis personatum.
 The two pathogens cause symptoms differing each other.
Early leaf spot
 Lesions are sub-circular in shape and from 1 to over 10 mm in diameter.
 They are dark brown in colour on the upper leaflet surface where most sporulation
occurs and a lighter shade of brown on the lower leaflet surface.
 The early leaf spot usually has a light to dark brown centre and a yellow halo.
 Distribution of fruiting structures is random on upper leaflet surface.
 Lesions are also produced on petioles, stems and pegs.
 These are oval to elongate in shape and have more distinct margins than the leaflet
lesions.

Compiled and Prepared by Dr. S. S. Kansara Lecture notes 5 Diseases of Groundnut

 Page |2

 On severity of the diseases, leaflets become chlorotic, then necrotic, lesions

coalesce and leaflets are shed.

Late leaf spot

 Lesions circular to sub-circular in shape with 1 to 6 mm diameter.
 All lesions are dark brown to black in colour.
 On the lower leaflet surface where most sporulation occurs the lesions are black in
colour and slightly rough in appearance.
 Fruiting structures are in concentric rings on the lower leaflet surface.
 Lesions on other parts and effects on disease severity are similar to that of early
leaf spot.

Compiled and Prepared by Dr. S. S. Kansara Lecture notes 5 Diseases of Groundnut

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Comparison of early and late leaf spots

Characteristics Early Leaf Spot Late Leaf Spot

Seasonal development Early Late

Shape of spot Circular to irregular, Usually circular
spots are
surrounded by yellow
Yellow halo Present Absent
Leaf surface where first Upper Lower
and most spores produced
Colour of spot on upper Light brown to black Brown to black tending
leaf surface tending toward brown toward black
Colour of spot on lower Brown Black
leaf surface
Haustoria Not produced Produced
Causal organism:
 The fungal mycelium is confined to the leaf spot and is present both inter-intra-
cellularly.
 The hyphae develop into the hymenial layer in the sub epidermal region and short
conidiophores are produced in bunches from the hymenial layer on which hyaline,
whip like conidia are bornwe singly.
 The perfect stages of the two fungi have been frond on the dead host tissues.
 Magnesium deficiency increases susceptibility to the disease.

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Disease cycle :
 The fungus spreads mostly by air-borne inoculum, but primary infection originates
with the fungus getting carried over on plant debris or by the seed.
 The role of the perfect stage perpetuating the disease in India is unknown.

Favorable Conditions :
 Warm and moist weather.
 Optimum temperature, 24-28°C.
 High relative humidity, 90% for a period of 3 days.
 Heavy doses of nitrogen and phosphorus fertilizers.
 Deficiency of magnesium in soil.

Management
 Grow tolerant varieties.
 Seed dressing with Benlate and Vitavax (2 gm/kg of seed).
 Intercropping pearl millet or sorghum with groundnut (1:3).
 Crop rotation with non-host crops preferably cereals.
 Deep burying of crop residues in the soil, and removal of volunl groundnut plants.
 Foliar application of aqueous Neem leaf extract (2-5%) or 5% Neem
seed kernel extract at 2 week's interval 3 times starting from 4 weeks
after planting.
 Foliage spray with Bordeaux Mixture (4:4:50), Mancozeb (0.2%) Carbendazim
(0.1%), if required repeat after 15 days.

2. RUST
Symptoms :
 The disease attacks all aerial parts of the plant
 The disease is usually found when the plants are about 6 weeks old.
 Rust can be readily recognized as orange coloured pustules (uredinia)
that appear on the lower leaflet surface and rupture to expose masses
reddish brown urediniospores.
 Pustules appear first on the lower surface and in highly susceptible cultivars the
original pustules maybe surrounded by colonies of secondary pustules.
 Pustules may also appear on the upper surface of the leaflet
 The pustules are usually circular and range from 0.5 to 1.4 mm in diameter.

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Pathogen
 Puccinia arachidis
 The pathogen produces both uredial and telial stages.
 Uredial stages are produced in abundant
 The production of telia is limited.
 Teliospores are dark brown with two cells.
 Pycnial and aecial stages have not been recorded.
 There is no information available about the role of alternate host

Disease Cycle
 The pathogen survives as uredospores on volunter groundnut plants or 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.
 Rains plash and implements also help in dissemination.

Favourable Conditions
 Low temperature, 20-25°C.
 High relative humidity above 85 per cent.
 Heavy rainfall.

Management
 Crop rotation and field sanitation.
 Use resistant/tolerant varieties.
 Avoid monoculturing of groundnut.
 Remove volunteer groundnut plants and reservoir hosts.
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 Early sowing in the first fortnight of June to avoid disease incidence.

 Intercropping pearl millet or sorghum with groundnut (1:3).
 Destroy Volunteer (self sown) groundnut plants and crop debris.
 Foliar application of aqueous Neem leaf extract @ 2-5%.
 Spray Mancozeb 2 kg or Wettable Sulphur 3 kg or Tridemorph 500ml or
Chlorothalonil 2 kg/ha.

3. Collar rot or seedling blight

Symptoms
 The pathogen causes both pre-emergence and post-emergence infection.
 Seeds may be killed in pre-emergence rotting.
 The seeds are covered with black masses of spores and internal tissues of seed
become soft and watery.
 Post-emergence infection causes death and rapid decay of seedlings.
 Young plants collapse and die soon after emergence due to rotting of elongated
hypocotyls.
 Collar region become dark brown & shredded.
 In mature plants large lesions develop on stem just below the soil surface & then
spread upward along the branches causing wilting & death.

Pathogen
 Aspergillus niger and A. pulverulentum
 The mycelium of the pathogen is hyaline to sub-hyaline.
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 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

Disease Cycle
 The pathogen survive in plant debris in the soil. The pathogen is also seed born in
nature.
 Soil-born conidia cause disease carry over from season to season.
 The other primary source is the infected seeds.

Favorable Conditions
 High soil temperature 30-35° C.
 Low soil moisture.
 Deep sowing of seeds.

Management :
 Seed treatment with Trichoderma viride/T.harizanum @ 4 g/kg seed.
 Soil application of Trichoderma viride/T.harizanum @ 2.5 to 5 kg/ha, preferably in
conjunction with neem cake or mustard cake @ 500 kg/ ha.
 Destruction of plant debris.
 Remove and destroy previous season's infested crop debris in the field.
 Crop rotation.

4. Root rot/ Charcoal rot

Symptoms
 The disease may appear at any stage of the crop growth.
 Water soaked necrotic spots appear on the stem just above the ground level.
 The lesions darken as the infection spreads upward to the aerial parts and down
into the roots.
 The entire stem becomes shredded and with the development of sclerotia
 becomes black and sooty in appearance.
 Roots, pegs and pods also rot and become covered with sclerotia.
 Roots are commonly attacked in association with stem rots and wilt.
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 Occasionally only the roots are attacked, when the tap root turns black and later
becomes rotten and shredded.
 The kernels turn black with abundant sclerotia internally and externally on the
testas and shells.
 The symptoms of the leaf infection are characterized by marginal zonate and
irregular spots.
 Minute spots are also quite common and expand into bigger wavy spots.

Pathogen
 Macrophomina phaseolina
 The pathogen produces hyaline to dull brown mycelium.
 Sclerotia are black, smooth, hard and 0.1-1 mm diameter, and occur within roots,
stems, leaves and fruits.
 Conidiomata are pycnidial, dark-brown, and either solitary or gregarious on leaves
and stems.
 Conidiophores are hyaline, short and cylindrical
 Conidia are hyaline, ellipsoid to obovoid.
 R. bataticola or M. phaseolina was detected in the seed coat, cotyledons and
embryo of groundnut.

Disease Cycle
 The pathogen remains dormant as sclerotia for a long period in infected plant
debris and in the soil.
 The primary infection is through soil-borne and seed-borne sclerotia.
 The secondary spread of sclerotia or conidia is aided by irrigation water,
implements and human agency etc.

Favorable Conditions
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 Temperature 18-20°C.
 Prolonged rain at seedling stage.
 Low lying areas.

Management
 Seed treatment with Carbendazim 2 g/kg seed or Captan 3 g/ kg seed or Thiram @
3-5 g/kg seed or Trichoderma viride at 4g/kg.
 Spot drench with Carbendazim at 0.5 g/lit.
 Adequate fertilization and irrigation.

5. Stem rot/ Sclerotial rot

Symptoms
 The first symptom is the sudden wilting of a branch which is completely or
partially in contact with the soil.
 The leaves turn brown and wilt but remain attached to the plant.
 At the junction of the branch with the stem near soil a white coating of fungus
mycelium is formed.
 As the disease advances a white mycelium web spreads over the soil and the basal
canopy of the plant.
 The sclerotia, the size and colour of mustard seeds, appear on the infected areas as
the disease develops and spreads.

Causal organism :
 Sclerotium rolfsii
 Perfect stage – Athelia rolfsii

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Disease cycle :
 Primary source of inoculum : Soil borne/seed borne/sclerotia present in soil/
multiplying in fallen plant debris.
 Sclerotia remain viable for 8 years in soil.
 Secondary source of infection : water irrigation/rain and farm equipment.

Favourable condition :
 Frequent rain/ irrigation favours the disease
 Moderate to high temperature
 Fluctuation in temperature and moisture
 In sandy and sandy loam well aerated soil, disease development take place more
rapidly.
 High P2O5 increase disease, gypsum increase disease.

Management :
 Crop rotation with maize, whaet, cotton and sorghum
 Filed sanitation
 Deep ploughing
 Application of T. harzianum mixed with well decomposed FYM or castor cake @
1.5 kg in 300 kg can be applied just before sowing.
 Soil solarization

6. Bud necrosis
Symptoms
 Chlorotic rings are present on leaves of infected plants.
 A prominent symptom is necrosis of terminal bud.
 Plants infected early in the season are stunted, and shoots bear small leaves that are
distorted and mottled.
 Mature plants show less stunting and Chlorotic rings and mottle on young leaflets
often occur about 40 days after planting.
 Necrosis of the bud may spread to the petioles and stem, sometimes leading to
death of the plant.
 Later formed leaves are smaller than normal and show a wide range of symptoms,
including distortion, mosaic mottling and general chlorosis.
 Pod size and number are greatly reduced. In late infections, pod size is reduced.
 Seeds are often shrivelled and have mottled and discoloured testa.
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Pathogen
 Although the disease was earlier reported to be caused by tomato spotted wilt virus
(TSWV), now referred to as peanut bud necrosis virus (PBNV).
 The virus particles are spherical, 30 nm in diameter and enveloped.
 ssRNA with multipartite genome.

Transmission
 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 palmi, T. tabaci and Frankliniella sp.

Management
 Early sowing.
 Grow resistant varieties
 Cultivars like Kadiri 3 and ICGS 11 which are tolerant to this disease should be
used.
 Remove and destroy infected plants up to 6 weeks after sowing.
 Application of Monocrotophos 500 ml/ha, 30 days after sowing.
 Plant density can be increased to decrease the proportion of infected plants.
 Intercropping of cereal crops such as pearl millet.

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7. Chlorosis
 Plant grown on soils of high pH (7.6 to 8.3) value frequently show iron deficiency
symptoms.
 In gujarat, highly calcarious soil results in chlorosis of groundnut leaves.
 Young leaves turn yellow and then white, and the plants become dwarf.
 Under such induced iron deficiency, chlorotic symptom appear more rapidly under
low light intensity.
 Iron is mainly concerned with the process of photosynthesis.
 It is catalyst of chlorophyll synthesis and part of many enzymes.
 A solution of 100 g ferrous sulphate and 10 g citric in 10 liters of water sprayed at
10 days interval for 2-3 times.
 Chelated iron 2 % sprayed at 10 days interval for 2-3 times.

8. Afla disease
 Aspergillus flavus is responsible for the disease of peanuts and corn commonly
known as yellow mould.
 This disease does not reduce the yield, but the the quality of the produce is very
poor.
 In the early 1960s, aflatoxin, a toxic metabolite of A. flavus was found in peanut
meal.
 Feed prepared with this meal caused the death of 100 000 turkeys in Great Britain.
 A very small amount (10-20 ppb) can produce fatal liver cancer in young animals.
 Yellow mould is more severe in the tropics, with symptoms appearing both early in
the growth of the peanut seedlings, and near harvest time on pods and seeds in the
soil.
Symptoms:
 Symptoms first appear as spots on the cotyledons of the seedlings.
 Seedlings and un germinated seeds shrivel to become a dried brown to black mass
covered by yellow or green spores.
 Plants that survive germination and emergence appear chlorotic due to the presence
of aflatoxin throughout the plant.
 The roots are stunted and lack a secondary root system, a condition known as
aflaroot.
 The leaves are small and pointed with a thick and leathery texture.

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 Following harvest, further infections may develop, with fungal growth covering
the seed surface and invading the seed itself.
 A yellow to brown discolouration, and weight loss occurs as a result.
 Seed infection results in reduced quality and viability and the production of
aflatoxin.

Pathogen:
 Aspergillus flavus produces hyphae that are colourless, septate and branched.
 A vesicle is borne at the end of each long conidiophore.
 On this vesicle, rows of sterigmata develop, that bear chains of yellow-green to
blue-green conidia.
 The conidial heads, each containing a mass of conidial chains.
 A. flavus may also produce sclerotia.

Epidemiology:
 The extent of yellow mould damage and aflatoxin production is dependent on the
environmental conditions and production, harvesting and storage practices.
 The pathogen is seedborne and soilborne, and active in high humidity (90-98%)
and low soil moisture.
 Temperatures conducive to growth are 17-42°C with aflatoxin production between
25-35°C.

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Diseases of sesame
1. Phyllody
2. Root rot or stem rot or charcoal rot
3. Cercospora Leaf spot
4. Powdery mildew
5. Phytopthora blight
6. Bacterial blight

1. Phyllody
Symptoms:
 Phyllody manifests itself mostly in the flowering stage, when the floral parts are
transformed into green leafy structures, which grow profusely.
 The sepals are transformed into leaf like structures and the corolla, stamens and
carpels, turn green and leafy.
 The veins of the phyllody structure are thick and prominent.
 The entire floral part appears leafy and the flower is sterile.
 The ovary is also malformed into elongated structures, resembling a shoot.
 Thus, the phyllody structure is a leafy outgrowth of every floral part.
 The leaves of diseased plants are reduced in size and chlorotic, with vein-
clearing symptoms.
 The internodes are shortened, the plant is stunted, and branching is abnormal,
resulting in a plant malformed beyond recognition.

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Causal organism :
 The diseased is caused by a mycoplasma/phytoplasmas
 Prokaryotic cells without cross walls, a few of them have a helical structure and
are called spiroplasmas. Most, however, are round to elongate are now called
phytoplasmas.
 Phytoplasmas cannot be grown on artificial nutrient media and, so far, no plant
disease has been reproduced on healthy plants inoculated directly with
phytoplasmas obtained from diseased plants.
 They lack cell walls, are bounded by a "unit" membrane, and have cytoplasm,
ribosomes, and strands of nuclear material.
 The size of their chromosomes varies from 530 kilobases of DNA to 1130
kilobases.
 Their shape is usually spheroidal to ovoid or irregularly tubular to filamentous,
 Phytoplasmas are generally present in the sap of a small number of phloem sieve
tubes.
 Most plant mollicutes are transmitted from plant to plant by leafhoppers, but
some are transmitted by psyllids and plant hoppers.
 Plant mollicutes also grow in the alimentary canal, hemolymph, salivary glands,
and intracellularly in various body organs of their insect vectors.
 The mycoplasma is transmissible to Crotalaria spp., Cicer arietinum
L., Trifolium .pp Brassica spp., Melilotus indica and a few other hosts.
 It is possible that the mycoplasma survives on these hosts and is passed on to
sesamum from them.

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Management :
 Phyllody can be controlled by spraying the plants with an effective insecticide to
prevent transmission of the mycoplasma. Spray Dimethoate at 500 ml/ha.
 Soil treatment with phorate 10 @ 11 kg/ha or thimet 10 g@ 10 kg/ha at the time
of sowing.
 Late sowing also reduces the disease.
 All the known varieties of sesamum are susceptible.
 Thus more work is needed to breed mycoplasma-resistant sesamum varieties,
using wild species as a source of resistance.
 Rouge out the infected plants periodically.
 Avoid growing sesame near cotton, groundnut and grain legumes.

2. Root rot or stem rot or charcoal rot

Symptoms:
 This disease is also known as root & stem rot and charcoal rot of sesamum.
 The characteristic symptoms of the disease are observed usually on the roots,
stems, capsules and seeds of the infected plants.
 Roots and the collar regions of the stems show brown discolouration that
extends upwards, resulting in discolouration of most of the parts of stem.
 Severely infected plants foil to produce seeds.
 If seeds are formed they remain light in weight, small in size and shriveled in
appearance.

Causal organism:
 Macrophomina phaseolina
 The pathogen remains dormant as sclerotia in infected plant debris as well as in
soil.
 The infected plant debris also carries pycnidia.
 The pathogen mainly spreads through infected seeds which carry sclerotia and
pycnidia.

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 The pathogen also spreads through soil borne sclerotia.

 The secondary spreads is also through movement of workers, animals, water and
equipments used in field.

Disease cycle:
 The pathogen remains dormant as sclerotia in infected plant debris as well as in
soil.
 The infected plant debris also carries pycnidia.
 The pathogen mainly spreads through infected seeds which carry sclerotia and
pycnidia.
 The secondary spread is through the conidia transmitted by rain water, workers,
animals and equipments.

Favourable condition:
 Day temperature 30 0C and above.
 Prolonged drought followed by plentiful irrigation.

Management :
 Seed treatment with Carbendazim + Thiram (1:1) @ 2 g/kg seed.
 Seed treatment with Trichoderma viride @ 4g/kg seed.
 Apply neem cake 150 kg/ha.
 Spot drench with Carbendazim (0.1%).

3. Cercospora Leaf spot

Symptoms:
 The disease first manifests itself on the leaves as minute water-soaked lesions,
which enlarge to form round to irregular spots 5-15 mm in diameter on both leaf
surfaces.
 The spotted area is light brown to white in the beginning which later becomes
dark grey.
 Several spots may occur on a single blade, enlarging to coalesce and blight a
large portion of the leaf.
 Blighting occurs if the disease comes on as early as a month after sowing.
 When the fungus attacks mature plants, leaf blight and defoliation occur.
 Often infection takes place on the leaf petiole, stem and pods, producing linear,
dark coloured, deep-seated lesions.
 The damage to plant growth and grain yield depend on the severity of infection
on the stem and pods and the stage at which the infection takes place.

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Causal organism:
 Cercospora sesami
 The hyphae of the mycelium in the host are irregularly septate, light brown
coloured and thick walled.
 They produce conidiophores in clusters, which emerge through the stomata and
bear the conidia on the surface.
 The conidiophores are light brown coloured at the base, more or less hyaline at
the tip, 0-3 septate.
 The conidia are whip-like, hyaline to light yellow, thin walled, 7 to 10 septate
and measure 90-136 x 3-4 µ.

Disease cycle:
 The fungus is seed-borne, both internally and externally, but
can also survive in the plant debris.
 Thus, primary infection in the field may be
from seed and infested plant debris and secondary spread may be through wind-
borne conidia.

Favourable condition:
 Warm and humid weather.

Management:
 The externally seed-borne fungus can be eradicated by chemical seed treatment,
whereas the internal infection can be eradicated only by treating the seeds with
hot water for about 30 minutes at 53°C.
 Secondary infection can be checked by fortnightly spray with 1 per cent
Bordeaux mixture.
 Nothing is known about resistance of sesamum varieties to this serious disease.
 Seed treatment with Carbendazim or Thiram at 2 g/kg seed.

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 Seed treatment with Pseudomonas fluorescens @ 4g/kg.

 Spray with Mancozeb @ 0.2 %

4. Powdery Mildew

Symptoms:
 Initially greyish-white powdery growth appears on the upper surface of leaves.
 When several spots coalesce, the entire leaf surface covered with powdery
coating.
 The infection may be seen on the flowers and young capsules in severe cases,
leading to premature shedding.
 The severally affected leaves may be twisted, malformed, started drying and fall
off.
 The seed produced from diseased plants are small and wrinkled.

Causal organsim:
 Erysiphe cichoracearum
 The Pathogen produces hyaline, septate mycelium which is extophytic and sends
haustoria into the host epidermis.
 Conidiophores arise from the mycelium and are short, non septate bearing
conidia in long chains.
 The conidia are single celled, ellipsoid or barrel-shaped 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.

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 In the later stages of infection, the mycelial growth changes to dark or black
because of development of cleistothecia.

Disease Cycle :
 The Pathogen is an obligate parasite.
 The 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.
 The pathogen has a wide host range and is always present in nature.

Favorable Conditions
 Low relative humidity.
 Dry humid weather.

Management
 Remove the infected plant debris and destroy.
 Spray wettable Sulphur (0.25%) or Karathane (0.1 %), if required, repeat after
15 days.

5. Stem/Phytopthora blight
Symptoms:
 At first, 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.
 Water-soaked patches appear on the leaves and spread till the leaves wither.
 Infection may be seen on flowers and capsules.
 Infected capsules are poorly developed with shriveled seeds.

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Causal organism:
 Phytopthora parasitica var. sesame
 The pathogen produces non-septate, hyaline mycelium
 The sporangiophores are hyaline, branched and bear sporangia.
 The sporangia are spherical and hyaline
 The oospores are spherical, smooth and thick walled.

Favourable condition:
 Low temperature 250C
 High relative humidity – above 90 %
 Prolonged rainfall

Disease cycle:
 The pathogen can survive in the soil through dormant mycelium and oospores.
 The primary infection is through seeds carrying the fungus as dormant
mycelium.
 Secondary spread of the disease is through sporangia and zoospores.

Management:
 Field sanitation
 Seed treatment with captan or thiram @ 2 g/kg or metalaxyl @ 4 g/kg seed
 Avoid monocropping, rotation with non host crops
 Spray Metalaxyl @ 0.2 %

6. Bacterial Leaf blight

Symptoms:
 At first water soaked spots appear on the undersurface of the leaf and then on
the upper surface.
 They increase in size and become angular and restricted by veins and dark
brown in color.
 Several spots coalesce together forming irregular brown patches and cause
drying of the leaves.
 The reddish brown lesions may also occur on petioles, stem and capsules.
 Bacterial ooze comes out from the infected parts under favourable conditions.

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Causal organism:
 Xanthomonas campestris pv. sesame
 The bacteria are Gram negative, rod shaped and with monotrichous flagella.

Disease cycle:
 The bacteria survive in seed and in infected plant debris
 The seed to plant transmission in both systemic and local.
 The secondary spread of the disease is through air borne inoculum and rain
splashes.

Favourable condition:
 High humidity
 Temperature 20-26 0C
 Higher dose of nitogen

Management:
 Remove and burn infected plant debris
 Spray Streptomycn sulphate or streptocycline @ 100g/ha

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Diseases of soybean
1. Rhizoctonia blight / charcoal rot
2. Mosaic

1. Rhizoctonia blight / charcoal rot

Symptoms:
 Infected seedlings can show reddish brown discoloration at the emerging portion
of the hypocotyl.
 The discoloured area turn dark brown to black and infected seedlings may die in
hot and dry weather.
 In older plants, the charcoal rot phase appears.
 It is characterized by light brown discoloration of the sub epidermal tissues in
the taproot and lower part of the stem.
 Leaves turn yellow and wilt, but remain attached to the plant.
 Superficial stem lesions may extend from the soil line upward.
 When the epidermis is removed, black sclerotia of the fungus may be so
numerous as to give a greyish black colour to tissue.
 When split open the taproot and the base of the stem show black streaks in the
wood tissues.

Lecture note 7 Soybean diseases Page 1

 Prepared and Compiled by Dr. S. S. Kansara

Causal organism:
 The disease is caused by the pycnidial fungus Macrophomina phaseolina.
 Its synonyms are M. phaseli, Rhizoctonia bataticola, Sclerotium bataticola and
Botryodiplodia phaseoli.
 In nature and in cultures Sclerotial form is most common.
 Mycelium is superficial, hyaline to branched and septate.
 On the host sclerotia are formed within the roots, stems, leaves and fruits.
 Sclerotia are jet black, smooth, hard and round to irregular in shape.

Disease cycle:
 Sclerotia of the fungus can survive free or embedded in host tissues in soil or in
seeds for more than a year.
 Secondary spread of the disease is through rain water, irrigation water and farm
implements.

Management:
 Crowding of the seedlings should be avoided.
 The field may be flooded for 3-4 weeks before planting.
 Application of organic matter in the soil.
 Long term crop rotation
 Application of neem seed cake @ 150kg/ha anf FYM @ 10 t/ha
 Application of T. viride.
 Soil solarization.
 Soil application of benomyl or captan.

2. Mosaic/yellow mosaic of soybean

Symptoms:
 Two types of symptoms are seen: Yellow mosaic and Necrotic mottle.
 The visible sign of diseases is the appearance of yellow spots on lamina surface.
 The leaves show yellow patches alternating with green areas.
 Such yellow leaves gradually change to whitish shade and ultimately become
necrotic.
 In case of necrotic mottle, the center of yellow spots develops necrosis.
 The virus becomes systemic in plant.
 Number and size of the pods per plant and seeds per pods are gradually reduced.
 The pods are deformed and contain shriveled, undersized seeds.

Lecture note 7 Soybean diseases Page 2

 Prepared and Compiled by Dr. S. S. Kansara

Causal virus:
 Four viruses causing yellow mosaic diseases: Mungbean yellow mosaic virus,
Mungbean yellow mosaic India virus, Horsegram yellow mosaic, Dolichos
yellow mosaic virus.
 It is identified as bipartite begomovirus.
 Transmission by Bemisia tabaci (Whitefly).

Management:
 Grow resistant varieties.
 Spray 0.1 % metasystox, starting when the crop is a month old.
 Soil application of granular insecticides.

Lecture note 7 Soybean diseases Page 3

 Prepared and Compiled by Dr. S. S. Kansara

Diseases of Pigeon pea

1. Wilt
2. Sterility mosaic
3. Phytopthora blight
1. Wilt
Symptoms :
 The plants show signs of gradual wilting, as if affected by drought about five to six
weeks after sowing.
 The leaves of affected plants turn yellow prematurely, the foliage droops and
within three or four days the plants wilt.
 Within six weeks plants of all ages may be affected.

 The disease first appears sporadically on a few plants, later spreading in

concentric circles to nearby plants.
 In severe cases large patches of wilted plants can be found, frequently resulting in
more than 50 per cent dead plants in a field.

Lecture note 8 Pigeon pea diseases Page 1

 Prepared and Compiled by Dr. S. S. Kansara

 When diseased plants are pulled out and examined in the field, black lesions of
varying size but mostly linear with irregular margin may be seen on the stem and
tap roots.

Normal

Diseased

 The lesions and discolouration are deep seated and this becomes clear if the bark is
peeled off, revealing the stem and root tissues in the affected portions as deeply
black.
 The symptoms spread upwards along the stem to several inches above ground level
and downwards along the tap and lateral roots, causing dry rot.
 Often only one side of the stem and root system is affected, in which case the
lesions are found only on that side of the plant.
 This type of infection clearly reflects the vascular nature of the disease.

Lecture note 8 Pigeon pea diseases Page 2

 Prepared and Compiled by Dr. S. S. Kansara

Causal organism :
 Fusarium oxysporum f. sp. udum
 The fungus is mainly confined to vascular tissues and is present both inter- and
intra-cellularly.
 If a diseased stem or root, particularly from near the soil surface, is examined in
transverse section under a microscope, the large number of fungal hyphae can be
seen mostly in the vascular bundles.
 Also, the host cells can be found to be discoloured brown.
 The fungus can be cultured on simple media, growing profusely to produce both
micro- and macro-conidia.

Disease cycle :
 The fungus is a facultative parasite remaining in the soil saprophytically for long
periods of time.
 It attacks the roots with germ tubes arising from micro- or macro-conidia or
chlamydospores, reaching the vascular tissues to establish and multiply rapidly,
causing wilting of parts or all of the plant.
 There is evidence that the infection is primarily through the fine root.

Lecture note 8 Pigeon pea diseases Page 3

 Prepared and Compiled by Dr. S. S. Kansara

 Once the fungus is established in the vascular bundles, it is provided with plenty of
nutrients for rapid activity, killing the plant within a few days.
 When the crop is harvested the plants are cut at the stem base, leaving the entire
root system and stubble to infest the soil.
 As a saprophyte, the organism continues to multiply in soil and remains there until
the next crop is sown.
 If a crop is sown every year in the same field the fungus builds up, increasing the
disease incidence.
 The fungus withstands adverse conditions, including a pH range of 4.0-9.0, at soil
temperature as high as 35°C.
 The fungus produces one or more toxins, especially fusaric acid, which destroy
the vascular tissues causing the plants to wilt.
 Drooping of leaves (epinasty) is due to ethylene produced by the infected plants.
 It is also possible that wilting results when the disintegrated cell walls of the
vascular bundles by pectinolytic and cellulolytic enzymes release large fragments
of chemicals which block free movement of food materials and water.

Lecture note 8 Pigeon pea diseases Page 4

 Prepared and Compiled by Dr. S. S. Kansara

Management :
 Long crop rotations which avoid red gram for 3-4 years help to starve the fungus
and reduce its virulence.
 The disease is less severe when red gram follows tobacco in the same field.
 Deep ploughing in summer.
 Green manuaring
 Seed dressing with thiram or carbendazim @ 3 g/kg
 Bio control agent like Trichoderma viridae, T.harzianum
 Use resistant varieties.

2. Pigeon pea sterility mosaic

Symptoms :
 The diseased plants are characterized by malformed leaves, which are crinkled
and small.
 The leaves are crowded and the axillary buds stimulated, resulting in a bushy
growth.
 The entire plant is stunted with shortened internodes.
 The diseased plants are invariably sterile, causing severe losses in grain yield.

Causal organism :
 This disease is transmitted by the eriophid mite Aceria cajani.

Lecture note 8 Pigeon pea diseases Page 5

 Prepared and Compiled by Dr. S. S. Kansara

 There is some evidence that it is soil-borne and transmitted by ectoparasitic

nematodes.

Disease cycle :
 The old and self sown plants may act as source of infection for the virus.
 The virus is not sap transmissible but can be transmitted by eriophid mite and
grafting.

Management :
 Self sown crop removing around the fresh crop.
 Spray acaricide properguide 57 % EC @ 2 ml/lit.
 Frequent and careful roughing.

3. Phytopthora blight
Symptoms:
 Infection of seedlings is visible as water-soaked lesions in the primary and
trifoliate leaves and within 3 days the lesions become necrotic.
 On stems, brown to dark brown lesions, are formed near the ground level.
 They enlarge in size and girdle the stem.
 Girdling of stem is often seen 1 to 1.5 meters up the stem.
 Similar lesions develop on the branches.
 Wind easily breaks the stems at the point of infection.
 The stem lesions late develop into cankerous structures at the edges.
 Sometimes the affected area cracks and shred.

Lecture note 8 Pigeon pea diseases Page 6

 Prepared and Compiled by Dr. S. S. Kansara

Causal organism:
 Phytopthora drechsleri f. sp. Cajani
 Mycelium is cottony, hyaline and coenocytic.
 The sporangiophores are develops into sporangium.
 The sporangia contains zoospores.
 Zoospores are biflagellated,hyaline and reniform.
 Oospores are smooth, hayaline, spherical and thick walled.

Disease cycle:
 The pathogen is capable of surviving in soil and also in infected debris for at least
one year.
 Oospores and chlamydospores are the main structure of survival.
 At the onset of rainy season oopores germinate by sporangia and infecting the
young seedlings.
 Secondary inoculum is disseminated by water, movement of soil and rain splashes.

Favourable condition:
 High humidity and temperature range of 28-32 0C

Lecture note 8 Pigeon pea diseases Page 7

 Prepared and Compiled by Dr. S. S. Kansara

 Darkness, humidity and temperature during night favour the disease.

 Addition of nitrogen as ammonium sulphate increase the disease and addition of
potassium in form of potassium sulphate reduces the disease.

Management:
 Avoid running water from infected field and low lying field.
 Crop rotation, wide inter row spacing.
 Interculture with legumes like urdbean and mungbean.
 Grow resistant varieties
 Seed treatment with biocontrol agents.
 Seed treatment with metalaxyl+mancozeb.

Lecture note 8 Pigeon pea diseases Page 8

 Prepared and compiled by Dr. S. S. Kansara

Diseases of Finger millet

1. Blast
 The disease was reported for the first time in India, from Tanjore delta of Tamil
Nadu by Mc Rae (1920).
 The average loss due to finger millet blast has been reported to be around 28% and
has been reported as high as 80-90 % in endemic areas.

Symptoms :
 The plant is susceptible to the diseases during all stages of its growth, from seedling
to grain formation stage.
 The young seedlings are affected both in the nursery and in the field. The lesion are
generally of spindle shaped.
 In the beginning the spots have yellowish margin and greyish centre, later the centre
becomes whitish grey.
 This fungal growth comprises of conidiophores and conidia. The distal portion of
the leaves beyond the lesion may hang or drop off.
 Stem infection causes blackening of the nodal region, penetrating in to the tissues.
 The neck region turns black and shrinks.
 Olive grey fungal growth is also seen on the affected area.
 During the severe infection the ears hang down from the stalk and sometimes may
also break away.
 Generally the infected ears becomes chaffy and only a few shrivelled grains may be
found.
 The affected portion of the ear head turn black.

Lecture note 9 Finger millet diseases Page 1

 Prepared and compiled by Dr. S. S. Kansara

Causal Organism :
 Pyricularia grisea
 The fungus produces septate, branched, hyaline to olivaceous mycelium, which is
localized in the lesions.
 Conidiophores emerge from the leaf through stomata or by rupturing the cuticle.
 They are simple, 2 to 4 septate and olivaceous in colour.
 Conidia are borne sympodially on the conidiophores.
 They are hyaline to pale olive, pyriform to obclavate or somewhat top-shaped,
usually three celled with a small basal appendage.

Disease cycle :-
 PSI : Seed borne conidia.
 SSI : Air borne conidia.

Favourable condition :-
 Temp. 25 – 30 ºC
 Relative humidity - 90%

Management
 To give seed treatment with Tricyclazole (8g/kg seeds).
 During the later stages of the crop two sprays of Ediphenphos or Kitazin or
Propiconazole (0.1%) or Carbendazim or Tricyclazole (0.05%), first at the time of
ear emergence and second after 10 days.
 Use of resistant varieties like VL 149, GPU 26, GPU 28, GPU 45, CO 13.
 Seed treatment with Trichoderma harzanium and one spray of Pseudomonas
fluorescens at the time of flowering and second spray 10 days later can also control
all three blast diseases.
 Allitin (0.1%), a synthetic product of garlic oil and neem oil were also found
effective against blast pathogen under in vitro conditions.

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 Compiled and Prepared by Dr. S. S. Kansara
Diseases of black & green gram
1. Anthracnose
2. Cercospora leaf spot
3. Powdery mildew
4. Yellow mosaic

1. Anthracnose
Symptoms
 The pathogen can attack all aerial parts at any stage of plan growth.
 Main symptoms are circular, black, sunken spots with dark center and bright red
orange margins on leaves and pods.
 In severe infections the affected parts wither off.
 Seedling gets destroyed due to infection soon after seed germination.

Causal organism:
 Colletotrichum lindemuthianum
 The pathogen mycelium is septate, hyaline and branched.
 The conidiophores are hyaline and short and bear cylindrical or oblong, hyaline,
thin walled, single celled conidia with oil globules
 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 perfect stage of the fungus produces perithecia with limited number of asci.
 The asci contain typically 8 ascospores which are one or two celled with a central
oil globule.
Lecture note 10 Black and green gram diseases Page 1
 Compiled and Prepared by Dr. S. S. Kansara

Disease Cycle
 The pathogen is seed-borne and cause primary infection through seed.
 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.

Favorable Conditions
 Cool and wet seasons.
 Temperatures 13-26°C.
 Relative humidity above 92%.

Management
 Use disease free seed.
 Hot water treatment at 54°C for 10 min.
 Treat the seeds with Carbendazim @2 g/kg
 Follow crop rotation.
 Remove and destroy infected plant debris in soil.
 Spray Carbendazim (0.1 %) or Mancozeb (0.2%) soon after the appearance of
disease and repeat after 15 days.

2. Cercospora Leaf Spot

Symptoms:
 Small circular spots develop on the leaves with grey center and brown margin.
 Several spots coalesce to form brown irregular lesions.

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 Compiled and Prepared by Dr. S. S. Kansara
 Sometimes in severe cases defoliation occurs.
 The brown lesions may be seen on petioles and stem in severe cases.
 Severe leaf spotting and defoliation occurs at the time of flowering and pod
formation under favorable environmental conditions.

Causal organism:
 Cercospora canescens
 The pathogen produces clusters of dark brown septate conidiophores.
 The conidia are hyaline, linear; thin walled and 5-6 septate.

Disease Cycle
 The pathogen survives on diseased plant debris and on seeds.
 The secondary spread is by air-borne conidia.

Favorable Conditions
 High Humidity, temperature-18-30°C.

A: Conidiophores, B: Conidia, C: Infected leaf

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 Compiled and Prepared by Dr. S. S. Kansara
Management:
 Field sanitation
 Use disease free seed and resistant varieties.
 Intercrop the moong with tall growing cereals and millets.
 Maintain low crop population density and wide row planting.
 Spray Mancozeb (0.2%) or Carbendazim (0.1 %) solution.

3. Powdery mildew
Symptoms:
 The disease appears on all the above ground part of the plant.
 Initial symptoms are marked by faint, slightly dark area on the leaves.
 This area develops into small, white powdery spots.
 They enlarge and coalesce to form a complete coating of white powder on
leaves, stems and pods.
 The powdery mass consisting of mycelium and conidia eventually turn dry
white.
 In case of severe infection, defoliation takes place.

Causal organism:
 Erysiphe polygoni, the fungus is ectophytic and obligate parasite.
 Conidiophore arises vertically from the leaf surface, bearing conidia in short
chain.
 Conidia are hyaline, thin walled, barrel shaped or cylindrical or elliptical and
single celled.
 Cleistothecia appear as black, globose with myceloid appendages.

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 Compiled and Prepared by Dr. S. S. Kansara
 Each cleistothecium contains 4 – 8 asci.
 Each ascus contain 3 – 8 ascospores
 It is spreading on the surface of the host and sending haustoria to epidermal
cells to get nutrients.

Disease cycle:
 PSI –ascospores from cleistothecia on host tissue
 SSI - Air borne conidia or through rain splash

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 Compiled and Prepared by Dr. S. S. Kansara
Management:
 Crop debris collected and burnt
 Resistant variety
 Spray with wettable sulphur (0.2 %) or tridemorph (0.05 %) and repeat at 15
days interval.

4. Mungbean yellow mosaic

Symptoms:
 The initial symptoms appear as yellow spots on the young leaves.
 The yellow patches coalesce to form large patches.
 Eventually the entire leaf may turn yellow.
 Maturity is delayed in diseased plant and flower and pods production are
severely reduced.

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 Compiled and Prepared by Dr. S. S. Kansara
Causal virus:
 The disease caused by mungbean yellow mosaic virus (MYMV), a whitefly
(Bemisia tabaci) transmitted geminivirus and also by grafting.
 Geminate virus particle, ssDNA, bipartite genome with two genomic
components DNA- A and DNA-B.
 Host range mungbean, urdbean, soybean, pigeon pea

Management:
 Manipulation in date of sowing
 Foliar application of metasystox at weekly intervals.
 Resistant varieties.
 Seed treatment with Thiomethoxam 70 WS or Imidacloprid 70 WS @ 4 g/kg
 Remove the weed hosts periodically

Lecture note 10 Black and green gram diseases Page 7

 Compiled and prepared by Dr. S. S. Kansara

Diseases of castor
1. Wilt
2. Root rot

1. Wilt
Symptoms:
 Leaves drop off leaving behind only stem.
 Diseased plants are sickly in appearance.
 Wilting of plants, root degeneration, collar rot, drooping of leaves and
necrosis of affected tissue and finally leading to death of plants.
 Necrosis of leaves starts from margins spreading to intervenial areas and finally
to the whole leaf.
 Split open stem shows brownish discoloration and white cottony growth of
mycelia much prominently in the pith of the stem.

Causal organism:
 Fusarium oxysporum f. sp. ricini
Lecture note 11 Castor diseases Page 1
 Compiled and prepared by Dr. S. S. Kansara

Disease Cycle:
 The fungus is soil-borne and remains in the soil as saprophyte for 2-3 years.
 The disease is primarily transmitted through infected seed.
 The secondary spread is aided by rain and irrigation water.

Favorable Conditions
 High day temperature 30-35°C.
 Low humidity 50-60%.
 Low soil moisture

Management
 Selection of disease free seeds.
 Grow tolerant and resistant varieties like Jyothi, Jwala, GCH-4, DCH-30 and
SHB -145.
 Multiplication of 2 kg of T. viride formulation by mixing in 50kg farm yard
manure. Sprinkling water and covering with polythene sheet for 15days and
then applying between rows of the crops is helpful in reducing the incidence.
 Seed treatment with Thiram @ 2g/ kg or Carbendazim @ 2g/ kg seed.
 Seed treatment with 4g of Trichoderma viride talc formulation.

2. Stem rot / Root rot

Symptoms:
 Small brown depressed lesions on and around nodes.
 Lesion often coalesces and girdles the stem causing leaf drop.
 Drying and death starts from apex and progress.
 Infected capsules discoloured and drop easily.
 Sudden wilting of plants in patches under high moisture stress coupled with
high soil temperature.
 At ground level black lesions are formed on stem.
 Young leaves curl inwards with black margins and drop off.
 Entire plant and top of the plant withers.

Lecture note 11 Castor diseases Page 2

 Compiled and prepared by Dr. S. S. Kansara

Causal organism:
 Macrophomina phaseolina
 Pathogen produces dark brown, septate mycelium with constriction at hyphal
branches.
 Minute, dark, round sclerotia are produced.
 The pathogen also produces dark brown, globose pycnidia.
 Pycniospores are thin walled, hyaline and single celled.

Disease cycle:
 The pathogen over seasons as sclerotia and resting mycelium in dry soils and in
plant residues.
 Primary spread is seed borne and soil borne sclerotia.
 Secondary spread is through pycnidiospores.

Favourable condition:
 Day temperature 300C
 Prolonged dry season

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 Compiled and prepared by Dr. S. S. Kansara

Management:
 Healthy seeds
 Grow resistant varieties
 Seed treatment with Thiram @ 2 g/kg or Carbendazim @ 2 g/kg or
Trichoderma viride @ 4g/kg.
 Destruction of crop debris.
 Soil drenching

Wilt Root Rot

Loss of turgidity, leaf collapse and leaf Disintegration of tissue as a result of

fall are the symptoms of wilt disease action of invading organisms, usually
bacteria or fungi are known as rot disease
Wilt pathogen colonise the vascular Rot pathogens secrete cell wall degrading
system, infection of collar and root enzyme
cortex
Wilt disease are caused by several Rot are caused by several fungal and
fungal and bacterial genera such as – bacterial genera such as – Erwinia,
Fusarium, Verticillium, Pythium, Rhizoctonia, Macrophomina etc.
Erwinia, Ralstonia etc.
Example – Bacterial wilt of potato Example –Dry root rot of gram caused by
caused by Ralstonia solanacearum Rhizoctonia bataticola

Lecture note 11 Castor diseases Page 4

 Prepared and compiled by Dr. S. S. Kansara
Diseases of Tobacco
1. Damping off
2. Black shank
3. Frog eye spot
4. Wild fire
5. Mosaic
6. Leaf curl

1. Damping off
Symptoms:
 The pathogen attack the seedlings at any stage in the nursery
 Disease occurs in two stages : Pre emergence and Post emergence Damping off
Pre-emergence damping-on
 Failure of seedling to emerge after sowing.
 Recovered seed has a watery rot; if the shoot or root emerges it has dark necrosis.
 A number of other pathogens can cause similar symptoms, so pathogen isolation
and identification is needed to confirm diagnosis.
Post-emergence damping-off
 Post emergence damping- off is the most destructive phase.
 The tiny two leaved seedlings may disappear due to wet rotting of stems and the
seedlings stand diminishes daily.
 Generally damping-off occurs in patches which spread quickly if unchecked.
 The older seedlings show shriveling and brown discoloration of the stems near
the soils and start rotting under wet soil conditions.
 The decayed stems collapse and seedlings topple over leaving parchment like
brown crest over the soil.
 The wet rotting and sudden collapse of seedlings starts in circular patches and
under wet weather conditions may extend over the whole seedbed causing near
total loss.
Post-harvest
 Water-soaked lesions or a watery rot of the tissue.
 Under conditions of higher humidity a cottony white mycelium may be observed
on the tissue.

Lecture note 12 Tobacco diseases Page 1

 Prepared and compiled by Dr. S. S. Kansara

Causal organism:
 Pythium aphanidermatum
 The pathogen produces thick, hyaline, thin walled, non-septate mycelium.
 It produces irregularly lobed sporangia which germinate to produce vesicle
containing zoospores.
 The zoospores are biflagellate and kidney shaped.
 Oospores spherical, light to deep yellow or yellowish brown colored measuring
17-19 (am in diameter.

Favourable Conditions
 Low temperature -below 24°C.
 Low soil temperature - about 20°C.
 High atmospheric humidity 90-100 per cent.

Lecture note 12 Tobacco diseases Page 2

 Prepared and compiled by Dr. S. S. Kansara
 Overcrowding of seedling.
 Ill drained nursery beds.
 Heavy shade in nursery.
 High soil moisture.

Disease Cycle
 The pathogen survives in the soil as oospores and Chlamydospore.
 The primary infection is from the soil-borne fungal spores.
 The secondary spread through sporangia and zoospores transmitted by wind and
irrigation water.
 When sexual reproduction starts, resulting in the formation of oospores which
help to survive adverse environmental conditions.
 Thus the fungus is capable of living for many years in soil, completing its life
cycle both saprophytic ally and as a facultative parasite.

Management
 Preparation of raised seed beds 15 cm high with channels around to provide
drainage.
 Drench the seed bed with 1 per cent Bordeaux mixture or 0.2 per cent Copper
oxychloride, two days before sowing.

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 Prepared and compiled by Dr. S. S. Kansara
 Avoid overcrowding of seedlings by using recommended seed rate (1 to
1.5g/2.5m2).
 Provide light, but frequent irrigation. Provide better drainage system.
 Spray the nursery beds two weeks after sowing with 0.2 per cent Mancozeb or
0.3 per cent Copper ox chloride and repeat subsequently at 5 days interval under
dry weather and at 2 days interval under wet cloudy weather or spray 0.2 per cent
Metalaxyl at 10 days interval commencing 2O days after germination.

2. Black shank
Symptoms:
 The pathogen may affect the crop at any stage of its growth.
 Although, all parts are affected, the disease infects primarily the roots and base of
the stem.
 In nursery the affected seedlings show blackening of roots and stem near soil.
 Under wet weather conditions the conidial infection spreads to leaves, which show
black or brown water soaked lesions resulting in leaf blight and collapse.
 The disease appears in scattered patches in the field.
 In the field blackening starts at the collar region and spreads both downwards and
upwards causing rotting and necrosis of the whole stem including basal leaves.
 First sign of infection seen in the vigorously growing plants is yellowing of leaves,
sudden wilting and ultimately death of plants under warm weather.
 The stems of such plants when split open show brown to black dried pith in disc like
plates characteristic of black shank.

Lecture note 12 Tobacco diseases Page 4

 Prepared and compiled by Dr. S. S. Kansara

Causal organism:
 Phytopthora parasitica pv. nicotianae
 The pathogen 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 generally biciliate and kidney
shaped.
 The fungus also produces thick walled Chlamydospore.
 Oospores are thick walled, smooth, globose, and light yellow colored.

Disease Cycle
 The pathogen is present in the soil as dormant mycelium, oospores and
Chlamydospore for more than 2 years.
 The pathogen lives as a saprophyte on organic wastes and infected crop residues in
soil.
 The primary infection is by means of oospores and Chlamydospore in the soil.
 Secondary spread is by wind-borne sporangia.
 The pathogen in the soil spreads through irrigation water, farm implements and
animals.

Favorable Conditions
 Frequent rainfall.
 High soil moisture.

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Management
 Grow resistant varieties
 Provide adequate drainage in the nursery.
 Drench the nursery beds with Bordeaux mixture 11%) or Copper oxychloride (0.3%)
solution, two days before sowing.
 Spray the beds IS days after sowing with Metalaxyl (0.2%) or Copper oxychloride
(0.3%) or Bordeaux mixture (0.3%) solution and repeat after 10 days.
 Select healthy, disease free seedlings for transplanting.
 At the time of transplanting, seedlings with blackened stem should be discarded to
prevent spread of disease to field.
 Remove and destroy the affected plants in the field.
 Spray Mancozeb (0.25%) or Copper oxychloride (0.3%).
 Spot drench with Bordeaux mixture (0.4%) or Copper oxychloride (0.3%) solution.

3. Frog Eye Spot

Symptoms
 The disease symptoms appear mainly on the lower leaves.
 They are usually circular, brown or tan with dark-brown and pale ashy or white
parchment like centre resembling frog's eye at early stages.
 During wet weather they may not be typical as above, as the outline may be angular
and the white centre may be absent and they may enlarge from 0.25 cm to 1.5 cm in
diameter.
 During frequent rains large necrotic areas appear which destroy much of the leaf.
 During hot dry weather, frog eye-spot may be only pin point in size.
 In flue-cured tobacco the same pathogen causing infection at the harvesting time
when cured results in innumerable* small, uniform, dark-brown to black spots
popularly known as “ Barnspots” which affect the market value of the leaf.

Pathogen
 Cercospora nicotianae
 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 slender, slightly curved, thin walled hyaline and 2-12 septate.

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Disease Cycle
 The pathogen is seed-borne and also persists on crop residues in the soil.
 The primary infection is from the seed and soil-borne inoculum, m
 The secondary spread is through wind-borne conidia.

Favorable Conditions
 Temperature 20-30°C.
 High humidity 80-90 per cent.
 Close spacing.
 Application of frequent irrigation.
 Excess application of nitrogenous fertilizers.

Management
 The nurseries should be located away from barns.
 Remove and burn plant debris in the soil.
 Adopt optimum spacing.
 Spray the crop with Bordeaux mixture (0.4%) or Thiophanate Methyl (0.1%) or
Carbendazim (0.1%) and repeat after 15 days.
 Avoid excess nitrogenous fertilization.
 Regulate irrigation frequency.

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4. Tobacco mosaic Virus
Symptoms
 The symptom begins 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 associated more with the veins, turning into irregular blisters.
 The early infected plants in the season are usually 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".

Causal virus:
 Tobacco mosaic virus
 Tobacco mosaic virus has a rod-like appearance.
 Its capsid is made from 2130 molecules of coat protein and one molecule of
genomic single strand RNA, 6400 bases long.
 The coat protein self-assembles into the rod like helical structure around the RNA
which forms a hairpin loop structure.
 The protein monomer consists of 158 amino acids which are assembled into four
main alpha-helices, which are joined by a prominent loop proximal \ to the axis of
the virion.
 Virions are ~300 nm in length and ~ 18 nm in diameter.
 The RNA is located at a radius of -6 nm and is protected from the action of cellular
enzymes by the coat protein.

Disease Cycle
 TMV does not have a distinct overwintering structure.

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 Rather, it will over-winter in infected tobacco stalks and leaves in the soil, on the
surface of contaminated farm implements.
 The virus spreads most rapidly by contact, sap, farm implements and operators.
 The virus has a wide host range, affecting nearly 50 plant species belonging to nine
different families.
 The virus is not seed-transmitted in tobacco but tomato seeds transmit the virus.
 With the direct contact with host plants through its vectors (normally insects such as
aphids and leaf hoppers), TMV will go through the infection process and then the
replication process.

Infection
 After its multiplication, it enters the neighboring cells through plasmodesmata.
 For its smooth entry, TMV produces a 30 kDa movement protein called P30 which
enlarge the plasmodesmata.
 TMV most likely moves from cell-to-cell as a complex of the RNA, P30, and
replicase proteins.
 It can also spread through phloem for longer distance movement within the plant.
 Moreover, TMV can be transmitted from one plant to another by direct contact.
 Although TMV does not have defined transmission vectors, the virus can be easily
transmitted from the infected hosts to the healthy plants, by human handling.

Favorable Conditions
 As long as the surrounding temperature remains below approximately 40°C, TMV
can sustain its stable form.

Management
 Grow resistant varieties like TMV, RR 2a, TMV RR2, and TMV RR3.
 Remove and destroy infected plants.
 Adopt crop rotation by growing non-host plants for two seasons.
 Keep the field free of weeds which harbour the virus.
Lecture note 12 Tobacco diseases Page 9
 Prepared and compiled by Dr. S. S. Kansara
 Wash hands with soap and running water before or after handling the plants or after
weeding.
 Spray the nursery and main field with botanical leaf extract!
 Bougainvillea @ 1 litre of extract in 150 litres of water, two to three times at 7 days
intervals.

5. Leaf Curl
Symptoms
 The infections may occur at any stage.
 When young plants are infected the entire plant remains very much dwarfed.
 Curling of leaves with clearing and thickening of veins; twisting of petioles;
puckering of leaves; rugose and brittle and development of enations.
 Three forms of leaf curl expression are observed.
 First the leaf margins curl downward towards the dorsal side and show thickening of
veins with enation on the lower surface.
 Second 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.
 Third the transparent symptom shows the curling of leaves towards the ventral side
with clearing of the veins and enations are absent.

Pathogen
 Tobacco leaf curl virus (TLCV)
 The disease is caused by Tobacco leaf curl geminivirus.
 Virions are geminate, non- enveloped, 18 nm diameter, circular ssDNA genome.

Disease cycle
 The virus is not transmissible through sap or seed.
 The virus has a narrow host range in eight plant families.

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 Due to wide host range of the virus many other plants are acting as source of
inoculums.

Management
 Remove and destroy the infected plants.
 Rogue out the reservoir weed hosts which harbour the virus and whiteflies.
 Planting tobacco crop during the crop periods when the vector population is low.
 Spray Methyldemeton @ 0.2 per cent to control the vectors.

6. Phanerogamic parasite Broom Rape

Symptoms
 The infected plants are stunted and show withering and drooping of leaves to
wilting.
 These indicate 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.
 Generally, it appears on clusters of 50-100 shoots around the single tobacco plant.
 The quality and yield of leaves are reduced.

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Parasite
 Orobanche cernua var. desertorum
 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.

Development of Disease
 Broomrapes overwinter as seeds, which may survive in the soil for more than 10
years.
 Seeds germinate only when roots of certain plants grow near them, although not all
these plants are susceptible to the pathogen.
 On germination the seed produces a radicle, which grows toward the root of the host
plant, becomes attached to it, and produces a shallow cup-like appressorium that
surrounds the root.
 From the appressorium, a mass of undifferentiated cells penetrate the host, extend to
and, occasionally, into the xylem, and absorb nutrients and water from it.
 Some of these cells differentiate into parasite xylem vessel elements and connect the
host xylem with the main vascular system of the parasite.
 Other undifferentiated cells become attached to phloem cells and obtain nutrients
from them, which they transport back to the parasite.
 Soon the parasite begins to develop a stem, which appears above the soil line and
looks like an asparagus shoot.
 Meanwhile, the original root produces secondary roots that grow outward until they
come in contact with other host roots to which they become attached and
subsequently infect.
 From these points of contact, new roots and stems of the parasite are produced and
result in the appearance of the typical clusters of broomrape plants arising from the
soil around infected host plants.
 Several such broomrapes may be growing concurrently on the roots of the same host
plant.
 The broomrape stems continue to grow and produce flowers and seeds, which
mature and are scattered over the ground in less than two months from the
emergence of the stems.

Management
 Rogue out the tender shoots of the parasite before flowering and seed set.

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 Spray the soil with 25 per cent copper sulphate.
 Apply few drops of kerosene directly on the shoot.
 Grow decoy or trap crops like sorghum, cowpea, chilli or moth bean to stimulate
seed germination and kill the parasite.
 Spray 0.1 per cent Allyl alcohol.

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 Prepared and compiled by Dr. S. S. Kansara

Diseases of Banana
1. Panama wilt
2. Bunchy top
3. Bacterial wilt
4. Sigatoka leaf spot

1. Panama wilt
Symptoms:
 The wilt symptoms appear on 3 to 5 months old plants.
 The earliest signs are faint yellow streaks on the petiole of oldest leaf.
 There is progressive yellowing of the old leaves and eventual collapse of the
petiole.
 Often all the leaves, except the youngest, collapse and the heart alone remains
upright.
 About 4-6 weeks after the appearance of streaks on the petiole, only the dead
trunk of the pseudo stem is left.

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 Prepared and compiled by Dr. S. S. Kansara

Causal organism:
 Fusarium oxysporum f. sp. cubense
 The mycelium is intra cellular, typically found in the xylem vessels.
 This mycelium produces microconidia in host tissue.
 The macroconidia are pedicellate, sickle shaped and 3 septate.
 Chlamydospores are oval or spherical.

A. Culture grown on PDA. B. Sporodochia on leaves. C. Macroconidia. D. Microconidia. E. Thick-

walled chlamydospores. F. Monophialides produce microconidia and macroconidia. G. False head

Disease cycle:
 It is soil borne through its thick walled chlamydospores.
 Germination of chlamydospores occurs in response to host root exudates.

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 The infection always occurs through injured lateral roots.

 Nematodes help in exposing the roots to infection.
 The disease spreads mainly by contact of the root system of adjacent healthy
plants with spores released by diseased plants.
 Floods help in local dispersal of the pathogen.

Management:
 Use disease free suckers for planting.
 Dipping of suckers in carbendazim (0.1%) before planting
 Corm injection of 3 ml of 2% carbendazim
 Infected plants should be eradicated
 Resistant Cultivar
 Avoid ill drained soils, and prefer slightly alkaline soils for cultivation.
 Flood fallowing for 6 to 24 months or crop rotation with rice.
 Application of lime 1-2 kg/pit to the infected pits.

2. Banana bunchy top

Symptoms:
 Dark broken bands of green tissues on the veins, leaves and petioles.
 Plants are extremely stunted.
 Leaves are reduced in size, marginal chlorosis and curling.
 Leaves become upright and brittle.
 Many leaves are crowded at the top.
 Branches size will very small.
 If plants infected earlier, no bunch will be produced.

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Transmission:
 The virus is not transmitted by mechanical inoculation.
 The virus transmitted by insect vector Banana aphid Pentalonia nigronervosa.
 The aphid acquires the virus in a feeding period of 24 hours and transmits the
virus in to healthy plants.
 The aphid retains the virus for a period of 13 days.
 The virus perpetuates through infected plant suckers.

Management:
 Adaption of strict quarantine measures.
 Eradication of all infected suckers by spraying with kerosene.
 Certified virus free suckers should be used.
 Control vector by spraying methyl-o-demoton (1ml/lit.) or phosphamidon
(1ml/lit.)

3. Bacterial wilt (Moko Disease)

Symptoms:
 Moko wilt which may be confused with panama wilt of banana.
 The symptoms start on rapidly growing young plants.
 The youngest three leaves turn pale green or yellow and collapse near the
junction of lamina and petiole.
 Most leaves collapse within 3-7 days.
 The characteristics symptoms occur on young suckers, these are blackened,
stunted and may be twisted.
 Vascular discolouration in plants is concentrated near the centre of the
pseudostem.
 A firm brown dry rot is found within fruits of infected plants.

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 If the symptoms on fruits are not present than the disease may be Fusarium wilt.

Causal organism:
 It is caused by bacterium Ralstonia solanacearum earlier known as
Pseudomonas solanacearum.
 It is a Gram negative bacterium with rod shaped and having 1-4 polar flagella.

Disease cycle:
 The bacteria survive through infected rhizomes and also in the soil for 6 months
to 2 years.
 There spread is through use of infected rhizome, cutting tools and through
insects.
 The bacteria multiply rapidly in the xylem.
 The production of ethylene by bacterium and diseased plants.
 The pre mature ripening of fruit finger ends is attributing to ethylene.

Management:
 Grow resistant varieties.
 Use disease free suckers for planting.
Lecture note 13 Banana diseases Page 5
 Prepared and compiled by Dr. S. S. Kansara

 Eradicate infected plants and adjacent healthy plants.

 A long fallow or flooding during off season.
 Crop rotation of banana with sugarcane and rice.
 Summer ploughing
 Disinfection of tools with formaldehyde with water 1:3 ratio.
 Fumigation of infected site with Methyl bromide or chloropicrin.
 Bio control with Pseudomonas fluorescence.

4 Sigatoka leaf spot

Symptoms:
 The symptoms appears on third and fourth leaves from the top.
 The leaves show small, indistinct, longitudinal, light yellow spots parallel to the
side veins.
 A few days later, the spots become 1-2 cm long; turn brown with light grey
centres.
 Adjacent spots coalesce to form large dead areas on the leaf.
 In severe infections, the entire leaves die within a few days.
 As a result of the loss of leaves the immature fruits bunches fail to fill out and
ripen and fall out.
 Individual bananas appear undersized and angular in shape; their flash develops
a buff pinkish colour.

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Causal organism:
 Cercospora musae
 Mycosphaerella musicola
 Conidia are produced on sporodochia on both sides of the leaf but more on
upper leaves.
 The conidia are slender, long, septate and hyaline.
 Perithecia are dark brown to black.
 Asci contain ascospores which are hyaline, two celled.

Disease cycle:
 Pathogen survives on dry infected leaves on the field soil and primary infection
takes place through ascospores in infected plant debris.
 Secondary spread through wind borne conidia.
 Infection takes place through stomata on lower surface of young leaves.

Favourable condition:
 High humidity, heavy dew and rainy weather with temperature above 21 0 C.
 Soil with poor drainage and low fertility favours the disease.
 Thick planting, presence of weeds and increased numbers of suckers promote
the disease.

Management:
 Removal and destruction of the affected leaves.
 Prevent water accumulation around the plant and go for periodical weeding.
 Spray mancozeb (0.25 %) or copper oxychloride (0.3%) in mineral oil.
 Spray chlorothalonil (0.2%) or carbendazim or thiophanate methyl (0.1%).

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 Prepared and compiled by Dr. S. S. Kansara

Diseases of Papaya
1. Stem rot /foot rot
2. Ring spot
3. Leaf curl

1. Stem rot/ Foot rot

Symptoms:
 Spongy water soaked spot in the stem at the ground level which enlarge and
girdle the stem.
 The diseased area turn brown or black and rot.
 Rotting generally spreads above and below on the stem down to the roots
which also begin to rot.
 Terminal leaves turn yellow droop off.
 Due to disintegration of parenchymatous tissues at the base of the stem, the
entire plant topples over and dies.
 If the bark is removed, the internal tissues appear dry, brown and give
honeycomb appearance.
 Damping off of papaya seedlings is also caused by the same pathogen.
 Seedlings raised in infected nurseries carry the disease when transplanted in
the main field.

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 Prepared and compiled by Dr. S. S. Kansara

Causal organism:
 Pythium aphanidermatum
 Mycelium is hyaline, coenocytic.
 Sporangia terminal or intercalary produce vesicle at the end of the hyphae.
 Zoospores are biflagellate and reniform.
Disease cycle:
 The pathogen perennates in soil through oospores or mycelium in infected
plant debris and serves as primary source of infection.
 The oospores or zoospores or mycelium comes in contact with ground plant
parts and cause infection.
 The zoospores produced as a result of primary infection get disseminated by
water currents.

Favourable condition:
 Excessive rains and relatively high temperature
 Appears from June to August
 Young seedlings are more susceptible

Management:
 Seedlings should be raised in well drained nursery area.
 Uproot the diseased seedlings and burn.
 Water logging in the field should be avoided.
 Affected pit should not be used for replanting.
 Drench the base of the stem with copper oxychloride @ 0.25% or metalaxyl @
0.1% of Bordeaux mixture @ 1.0%

2. Ring spot/ Mosaic

Symptoms:
 Vein clearing and puckering of the infected leaves.

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 Prepared and compiled by Dr. S. S. Kansara

 Margin and distal parts of the leaves roll downward and inwards, mosaic
mottling, dark green blisters, leaf distortion which result in shoe string
symptoms and stunting of the plants.
 On fruits, circular concentric rings are produced. If the fruits are affected
earlier then no fruit formation taken place.

Causal virus:
 Papaya Ring spot virus
 The virus particle is rod shaped and thermal inactivation point of the virus lies
between 54 to 600C.

Mode of spread
 Vector – aphid (Aphis gossypii, A. craccivora)
Lecture note 14 Papaya diseases Page 3
 Prepared and compiled by Dr. S. S. Kansara

 Disease spreads to cucurbits

Management:
 Raise papaya seedlings under insect proof conditions
 Disease free seedlings
 Raise sorghum / maize as barrier crop
 Rouge out affected plants immediately on noticing symptoms
 Do not raise cucurbits around the field.
 Spray with 2% groundnut oil emulsion weekly

3. Leaf curl
Symptoms:
 Curling, crinkling and distortion of leaves, reduction of leaf lamina, rolling of
leaf margins inward and downward, thickening of veins.
 Leaves become leathery, brittle and distorted. Plants stunted.
 Affected plants do not produce flowers and fruits.
 Spread by whitefly Bemisia tabaci

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Survival and spread:

 Primary infection: Infected plant parts
 Secondary infection: Whitefly (Bemisia tabaci) and grafting
 Virus also infects tobacco, tomato, sunhemp, chilli, petunia etc.

Management:
 Disease free seedlings
 Rouging and destruction of diseased plants
 Vector control with Monocrotophos @ 0.05% or Dimethoate @ 0.2% or
Metasystox @ 0.1%

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 Prepared and complied by Dr. S. S. Kansara

Diseases of Pomegranate
1. Bacterial blight
2. Cercospora leaf and fruit spot
3. Root knot
4. Wilt

1. Bacterial blight
Symptoms:
 Small irregular water soaked spots, 2-5 mm in diameter appear on the leaves.
 Leaves distorted and malformed
 Severely infected young leaves shed.
 The bacterium attacks stem, branches and fruit also.
 On the stem, the disease starts as brown to black spots around the nodes and finally
girdling and cracking of nodes.
 Branches break down
 Brown to black raised spots on the fruit with L or Y shaped cracks.

Causal organism:
Xanthomonas axonopodis pv. punicae
 Prepared and complied by Dr. S. S. Kansara

Disease cycle:
 Primary infection : Infected cuttings
 Secondary infection: Wind splashed rains
 The bacteria infect through wounds and stomata openings.

Management:
 Clean cultivation and strict sanitation in orchard
 Spray Carbendazim (1%) along with antibiotic.

2. Cercospora leaf and fruit spot

Symptoms:
 Light zonate brown spots appear on the leaves and fruits
 The affected area in the twigs become flattened and depressed with raised edges.
 The affected fruits showed small irregular black spots, which later on coalesce,
into big spots.
 In severe cases the whole plant dies.

Causal organism:
 Cercospora sp.
 Prepared and complied by Dr. S. S. Kansara

Disease cycle:
 Primary infection : Diseased plant debris
 Secondary infection: Wind borne conidia

Management:
 The diseased fruits should be collected and destroyed
 Two to three spray with mancozeb (0.25%) at 15 days interval.

3. Root knot

 Meloidogyne: a Greek word; melo= apple, oid = resembling; gyne= female;

meaning apple-like; the shape the female of this genus acquires on maturity.
 Its common name root-knot nematode is given for the characteristic symptom of
knots or galls produced by this nematode on the roots of host plants.
 Although over 90 species of Meloidogyne have been described to date, four species
viz., M. incognita, M. javanica, M. arenaria and M. hapla with their cosmopolitan
distribution and widest host range are of particular economic importance to
vegetable production.

Symptoms:
 Aboveground symptoms are reduced growth and fewer, small, pale green or
yellowish leaves that tend to wilt in warm weather.
 Blossoms and fruits are few and of poor quality.
 Affected plants usually linger through the growing season and are seldom killed
prematurely.
 Characteristic symptoms of the disease appear on the underground parts of
the plants.
 Infected roots develop the typical root-knot galls that are two to several times
as large in diameter as the healthy root.
 Several infections along the root give the root a rough, clubbed appearance.
 Roots infected by certain species of the nematode also develop a bushy root
system.
 Usually, however, infected roots remain smaller and show necrosis and rotting,
particularly late in the season.
 When tubers or other fleshy underground organs, such as carrots, potatoes,
peanuts, and yam, are attacked, they produce small swellings over their
surface, which become quite prominent and cause distortion or cracking.
 Roots of trees are also attacked by the root-knot nematodes and develop galls
roughly proportional in size to the length of time since infection.

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The Pathogen: Meloidogyne spp.

 The male and female root-knot nematodes are easily distinguishable
morphologically.
 The males are wormlike and about 1.2 to 1.5 millimeters long by 30 to 36
micrometers in diameter.
 The females are pear shaped and about 0.40 to 1.30 millimeters long by 0.27 to
0.75 millimeters wide.
 Each female lays approximately 500 eggs in a gelatinous substance.
 The first and second stage juveniles are wormlike and develop inside each egg.
 The second stage juvenile emerges from the egg into the soil.
 Second stage juvenile is the only infective stage of the nematode.
 Prepared and complied by Dr. S. S. Kansara

 If it reaches a susceptible host, the juvenile enters the root, becomes sedentary, and
grows thick like a sausage.
 The nematode feeds on the cells around its head by inserting its stylet and
secreting saliva into the cells.
 The saliva stimulates cell enlargement and also liquefies part of the contents of the
cells, which are then withdrawn by the nematode through its stylet.
 The nematode then undergoes a second molt and gives rise to the third-stage
juvenile, which is stouter and goes through the third molt and gives rise to the
fourth-stage juvenile, which can be distinguished as either male or female.
 These undergo the fourth and final molt and the male emerges from the root
as the worm-like adult male, which becomes free-living in the soil, while the
female continues to grow in thickness and somewhat in length and appears
pear shaped.
 The female continues to swell and, with or without fertilization by a male,
produces eggs that are laid in a gelatinous protective coat inside or outside the root
tissues, depending on the position of the female.
 Eggs may hatch immediately or a few of them may overwinter and hatch in the
spring.
 A life cycle is completed in 25 days at 27°C, but it takes longer at lower or higher
temperatures.
 When the eggs hatch, the infective second-stage juveniles migrate to adjacent parts
of the root and cause new infections in the same root or infect other roots of the
same plants or roots of other plants.
 Most root-knot nematodes are found in the root zone from 5 to 25 centimeters
below the surface.
 Root-knot nematodes are spread primarily by water or by soil clinging to
farm equipment or on infected propagating stock transported into uninfected
areas.
 Prepared and complied by Dr. S. S. Kansara

Development of Disease:
 Second-stage juveniles enter roots behind the root tip and keep moving until
they reach positions behind the growing point.
 There, they settle with their head in the developing vascular cylinder.
 Cells near the path of the juveniles begin to enlarge.
 Two or 3 days after the juvenile has become established, some of the cells around
its head begin to enlarge.
 Their nuclei divide, but no cell walls are laid down.
 The existing walls between some of the cells break down and disappear, giving
rise to “giant cells”.
 Each gall usually contains three to six giant cells, which are due to substances
contained in the saliva secreted by the nematode in the giant cells during
feeding.
 The giant cells attract nutrients from surrounding cells and serve as feeder
cells for the nematode.
 Swelling of the root results from excessive enlargement and division of all types of
cells surrounding the giant cells and from enlargement of the nematode.
 As the females enlarge and produce their egg sacs, they push outward, split the
cortex, and may become exposed on the surface of the root or remain completely
covered, depending on the position of the nematode in relation to the root surface.
 Prepared and complied by Dr. S. S. Kansara

 Moreover, some fungi, e.g., Fusarium, Rhizoctonia, and the oomycete Pythium,
grow and reproduce much faster in the galls than in other areas of the root, thus
inducing an earlier breakdown of the root tissues.

Management of root-knot nematode

 Fallowing
 Root destruction: Since root-knot can survive and reproduce on the roots left in
the soil after harvest, galled roots should be uprooted and destroyed.
 Soil Tillage: Repeated tilling and turning of the soil at regular intervals for 30 days
during hot and dry seasons between crops reduce root-knot nematode densities in
the upper horizons due to desiccation of eggs and juveniles.
 Organic amendments: Incorporation of large amounts of organic material (5
quintals/hectare) into the soil reduces root knot densities. Oil cakes, coffee husks,
neem, marigold leaves, crustacean skeletons, sawdust, urea, chicken manure and
bagasse comprise a few examples of organic amendments.
 Control may be due to:
 toxic compounds present in the organic material as in neem;
 toxic metabolites produced during microbial degradation;
 enhancement of nematode antagonists.
 Neem-based oil cakes and related products have been studied intensely in
India for control of root knot nematodes.
 Soil Solarization: The lethal temperature for control of plant parasitic nematodes
is considered to be around 45°C.
 Use of healthy planting material: Nematode-free seedlings should be selected for
transplanting.
 Non host crops: Cruciferous crops which are either moderately resistant or
tolerant to root knot nematodes are successfully rotated with a smaller number of
highly susceptible vegetable crops.
 A rotation of cauliflower, garlic and brown sarson (Brassica campestris sub. sp.
oleifera) is effective in reducing root-knot densities.
 A rotation of sesame, maize, groundnut, sorghum, cabbage, velvet bean and then
resistant sweet potato is effective in controlling M. incognita.
 Trap crops: Lettuce and radish are used as trap crops for root knot management
programs at some places. Lettuce is harvested with the shoot and root system intact
before the completion of nematode life cycle which usually completes within a
month.
 Antagonistic crops: Antagonistic plants are those which produce nematicidal
compounds.
 Marigold, sunhemp, castor-bean, asparagus and sesame are some of
important antagonistic crops used for nematode control activity.

Lecture note 15 Pomegranate diseases Page 7

 Prepared and complied by Dr. S. S. Kansara

 The best studied antagonistic plant is marigold (Tagetes) known to produce

terthienyl and derivatives of bithienyl that are toxic to root knot nematode.
 Resistance: Resistant cultivars should not be grown continuously for years to
avoid the emergence of resistance breaking biotypes of the nematode.
 Chemicals: Use of nematicides should be preferably confined to nurseries only at
recommended doses.
 Under unavoidable circumstances they may be used under field conditions.
 A number of granular nematicides (phorate @ 1 Kg a.i. /ha, carbofuran @ 3 Kg a.i.
/ha, oxamyl, thionazin, terbufos, isazophos, aldoxycarb, ethoprophos, fenamiphos,
cadusafos and avermectins) are effective against root-knot nematodes on vegetable
crops under field and green house conditions.
 Granular nematicides are either broadcast over the soil surface and incorporated
into the soil before planting or banded into or over the plant furrow.
 Liquid formulations allow application by surface and drip irrigation.
 Application through drip irrigation places the material directly in the rhizosphere
and allows treatment at will or treatment when necessary during the growing
season.
 It also allows splitting or extending application over specific time intervals to
coincide with optimum control.
 For example, oxamyl applied to tomato by drip irrigation is more effective than
granular nematicides applied at transplanting in controlling root-knot nematodes.
 Dip treatment or treatment of transplants in nurseries is more practical.
 For example, dip treatment of seedlings of eggplant and tomato with fenamiphos,
fensulfothion or carbosulfan @500ppm for 30 minutes or 1000ppm for one hour
significantly reduced M. incognita galling.
 Biological control:
 Application of fungal pathogens, parasites or predatory fungi that infect eggs,
juveniles or adults in the soil or on the root surface.
 Paecilomyces lilacinus and Pochonia chlamydosporia which are oviparasitic fungi
are effective when their commercial formulations are applied @ 50g/m2 along
with sufficient quantity of FYM/vermicompost at the time of nursery preparation.
 FYM/ vermicompost helps in colonization of these fungi.
 Field inoculation and management by using the obligate bacterial parasite
Pasteuria penetrans- an obligate parasite of Meloidogyne spp. @ 50g/m2 in
nursery or 20kg/ ha in field conditions.
 The spores formed, can resist both drought and exposure to non-fumigant
nematicides. The parasite seems to be more effective on warm soils and soils low
in organic matter, which characterizes most tropical soils where root knot is a
problem.

Lecture note 15 Pomegranate diseases Page 8

 Prepared and complied by Dr. S. S. Kansara

 Promotion of the naturally occurring antagonistic potential in soils with

amendments or crop rotation.
 Biological enhancement of transplants or planting material with plant health-
promoting rhizosphere- or endorhiza-associated bacteria or fungi.
 Quarantine: Quarantine, if practiced, can add greatly by preventing introduction
of a pest into a country or local region.
 In order to protect local production, effective quarantine laws and of course border
inspections are needed for nematodes.
 At the national level, monitoring systems can be used to prevent local spread of
nematodes by close scrutiny of commercial vegetable nurseries.
 Integrated Nematode Management: Seedlings may be raised in solarized nursery
beds treated with carbofuran @ 0.3 g a.i. /h (10 g/m2 ) + neem cake @ 500 Kg/ha
in nematode infested soil ten days before transplanting.
 Soil solarization combined with dazomet gives good control of root knot and
increased tomato yield.
 Similarly, solarization together with carbofuran increased tomato yields by 96%
and solarization with neem cake by 52%, coupled with a significant reduction in
nematode population.
 Solarization for 2–4 weeks, combined with fenamiphos is considered a sustainable
control measure in greenhouse tomato.
 Crop rotation and soil incorporation of T. erecta resulted in significant reductions
in M. incognita root galling and increased yield.

4. Wilt

Symptoms:
 Initially yellowing of foliage of one or few branches of a tree occurs
 Later this spreads over the whole tree and leads to complete defoliation.
 Wilt progresses from lower leaves to the top.
 Vertical stem cracking is common.
 Cross and vertical section of affected plant parts generally reveals dark greyish
brown streaks in the vascular tissue.

Causal organism:
 Ceratocystis fimbriata

Disease cycle:
 Spores of the fungus survive as resting structure or active mycelium in infected
plant parts in soil for 4 months.
 Above ground plant parts are infected through wounds

Lecture note 15 Pomegranate diseases Page 9

 Prepared and complied by Dr. S. S. Kansara

 The spores are spreads by infected seedling, irrigation and rain water, insects etc.
 After entering the host, mycelium and spores moves through through the vascular
tissue of tree, causing reddish brown to purple staining in the xylem

Management:
 Soil application of Trichoderma sp. combined with Paecilomyces sp. at 25 g/2 kg
well decomposed organic manure around the trunk of the tree.
 Soil application of neem, karanj, mahua and castor cake
 Soil application of propiconazole (0.1%) + boric acid (0.5%) + phosphoric acid
(0.5%)
 Remove and destroy infected plant material
 Disinfect pruning and grafting tools before and after use.
 Ensure sufficient space among trees.
 Prepared and compiled by Dr. S. S. Kansara

Diseases of brinjal
1. Phomopsis blight and fruit rot
2. Little leaf

1. Phomopsis blight and fruit rot

Symptoms:
 The plants are attacked at all the stages of growth.
 On leaves, circular to irregular, greyish brown having light center appears.
 The diseased leaves become yellowish in color and may drop off.
 Several black pycnidia can be seen on older spots.
 The lesions on the stem are dark brown, round to oval and have greyish center
where pycnidia develop.
 At the base of the stem, the fungus cause characteristic constrictions leading to
canker development and toppling of the plant.
 On fruits, small pale sunken spots appear which on enlargement cover entire
fruit surface.
 These spots become watery leading to soft rot phase of the disease.
 A large number of dot like pycnidia also develop on such spots.
 The infection of fruit through calyx leads to development of dry rot and fruits
appear black.

Lecture notes 16 Brinjal diseases Page 1

 Prepared and compiled by Dr. S. S. Kansara

Causal organism:
 Phomopsis vexans
 Diaporthe vexans
 Mycelium is septate and hyaline becoming dark with age.
 Pycnidia are submerged. Conidia are produced on simple to branched
conidiophores.
 Two types of conidia: Alpha conidia, which are sub cylindrical and beta
conidia, which are filiform and curved.
 The perfect stage produces perithecia in which asci with 8 hyaline, bicelled
ascospores are produced

Disease cycle:
 The pathogen is seed borne and also survives in plant debris as mycelium and
pycnidia.
 The pathogen is locally disseminated as water borne pycniospores.
 The spores exude out through the ostiole and can easily be thrown away by
rain drops.
 They can also disseminated by tools and insects.
 Inoculum present in the form of mycelium and pycnidia results in diseased
seedlings.

Management:
 Use of disease free seed.
 Crop rotation and summer ploughing
 Hot water treatment of seed at 500C for 30 minutes.
 Seed treatment with Thiophanate methyl @ 1 g/kg seed.

Lecture notes 16 Brinjal diseases Page 2

 Prepared and compiled by Dr. S. S. Kansara

 Spray twice with Thiophanate methyl or carbendazim @ 0.1 % at 20 days

interval.
 Removal and destruction of infected crop debris.

2. Little leaf
Symptoms:
 Small or little leaves.
 The petiole is so short that the leaves appear to be sticking to the stem.
 Affected plants have narrow, soft, smooth and yellow shorter leaves.
 Newly formed leaves and internodes are much shorter.
 Mostly there is no flowering but if flowers are formed they remains green
 Fruiting is rare, if fruit formed, it becomes hard, tough and fails to mature.


Pathogen:
 Phytoplasmas
 They are having ovoid to spherical body which is concentrated in the phloem
sieve tubes.

Disease Cycle:
 The disease is transmitted by grafting and by leaf hopper Hishimonas phycitis
 Collateral host : Datura, Chilli, Tobacco and Tomato

Management:
 Grow resistant varieties
 Destruction of infected plants

Lecture notes 16 Brinjal diseases Page 3

 Prepared and compiled by Dr. S. S. Kansara

 Eradication of solanaceous weed hosts

 Spray Malathion 3ml/lit or soil application of Phorate.

Lecture notes 16 Brinjal diseases Page 4

 Prepared and compiled by Dr. S. S. Kansara

Diseases of tomato
1. Early blight
2. Late blight
3. Leaf curl
4. Buck eye rot
5. Tomato spotted wilt

1. Early blight of tomato

Symptoms:
 The disease first become visible as small, isolated, scattered, pale brown spots
on the leaflets.
 Lowest leaves are attacked first and the disease progresses upwards.
 In the necrotic tissues concentric rings develops to produce a target board effect,
the most characteristics symptoms of the disease.
 There is a narrow chlorotic zones around the spot.
 When these leaf lesions involve larger veins, chlorosis extends well beyond the
necrotic spots.
 This is due to a toxin alternaric acid produced by the fungus and trans located
through the veins.
 The leaves shrivel and fall down.
 Stems may also be attacked, these lesions may lead to collapse of the branches
or of entire above ground plant parts and exposed the fruits to sun scald.
 On fruits, elongated and sunken lesions can develop.

Lecture notes 17 Tomato diseases Page 1

 Prepared and compiled by Dr. S. S. Kansara

Causal organism:
 Alternaria solani
 Mycelium consists of septate, branched and dark brown.
 Conidiophores emerge through the stomata from the dead center of the spot.
 Conidia are beaked, muriform and dark coloured.

Disease cycle:
 The disease spreads through infected seeds.
 Mycelium and conidia survive in soil on diseased plant debris to cause primary
source of infection.
 Infection on lower leaves first takes place through conidia formed on crop
debris on soil.
 Secondary spread of the disease occurs through conidia.
 These conidia are disseminated by wind, water and insects.
 Disease intensity is influenced by frequency of rains, humidity, duration of dew
deposits on leaves, photoperiod and temperature.

Lecture notes 17 Tomato diseases Page 2

 Prepared and compiled by Dr. S. S. Kansara

Management:
 Crop rotation and field sanitation
 Five sprayings of Dithane z-78 or Dithane M-45 (0.2%).
 Spray with Blitox(0.25%), difolatan, daconil, Antracol and Captan at intervals
of 10-21 days.
 Grow resistant varieties

2. Late blight of tomato

Symptoms:
 Brown dead spots or extended dead areas appear at the tip or margins of the
leaves and spread downward.
 If moist weather prevails, the entire leaf may be killed in 1-4 days.
 Primary lesions appearing on petioles, stems as well as on leaves.
 When spots are examined in early morning hours on the lower sides of the leaf a
whitish or greyish mildew growth appears.
 On tomato fruits, dark olivaceous, greasy appearing spots are formed.
 These may expand until the entire fruit is involved.

Lecture notes 17 Tomato diseases Page 3

 Prepared and compiled by Dr. S. S. Kansara

 The tissue remains firm at first with varying depth of discoloured tissues under
the skin.
 In very moist weather, especially when there are cracks on the skin, a white weft
of fungal growth develops over parts of the invaded area.

Causal organism:
 Phytopthora infestans
 The mycelium is coenocytic and hyaline
 Sporangiophores are hyaline, branched intermediate and thick walled.
 Sporangia are hyaline oval or pear shaped.
 Zoopsores are biflagellate

Lecture notes 17 Tomato diseases Page 4

 Prepared and compiled by Dr. S. S. Kansara

Favourable condition:
 High relative humidity (>90%)
 Optimum temperature 13-240C
 Rainfall

Management:
 Select healthy seedling for transplanting
 Grow resistant varieties
 Two sprays of metalaxyl+mancozeb @ 0.25 % at 15 days interval
 Recommended dose of nitrogen
 Avoid low lying areas
 Use biocontrol agents

3. Leaf curl
Symptoms:
 The leaf curl is characterised by severe stunting of the plants with downwards
rolling and crinckling of the leaves.
 The newly formed leaves show chlorosis.
 The older curled leaves become leathery and brittle.
Lecture notes 17 Tomato diseases Page 5
 Prepared and compiled by Dr. S. S. Kansara

 Stunting of the plants is due to shortening of the intednodes.

 The diseased plants look pale and produce more lateral branches resulting in a
bushy growth.
 There is partial or complete sterility of the plant.

Causal virus:
 Tobacco leaf curl virus (Geminivirus)
 In addition to tomato other natural hosts of the virus are tobacco, papaya and
chilli.
 The virus is neither seed nor sap transmissible.
 Dodder transmission has been reported.
 The main agency of its transmission is whitefly Bemisia tabaci.
 The virus is reported to be transmitted by the vector after 30 min of acquisition.
 The virus is persistent in the body of the vector and is retained for more than 12
days or for whole life

Management:
 Spray Methyl parathion (0.02%) and dimethoate (0.05%).
 Soil application of carbofuran @ 1.5 kg/ha at nursery beds
Lecture notes 17 Tomato diseases Page 6
 Prepared and compiled by Dr. S. S. Kansara

 Two to three sprays of Dimethoate or metasystox 0.02 % at 10 days interval

 Spray Mineral oils 2% after fruit formation
 Infected plant should be removed
 Grow border or barrier crops like maize and sorghum
 Yellow sticky traps.

4. Buck eye rot

Symptoms:
 Spots on immature tomato fruits are marked with pale brown, concentric rings
resembling slightly the markings on a buck eye nut.
 These spots may be small or they may cover a major portion of the fruit surface.
 There is no rotting of the skin but internal flesh may be discoloured up to the
core.
 Green fruits show brownish circular spots at the blossom end, shrink and are
mummified.
 Concentric rings are formed in spots.

Causal organism:
 Phytopthora nicotianae
 Mycelium is hyaline and non septate
 Sporangia are borne on sporangiophores
 Oospores are thick walled.
Lecture notes 17 Tomato diseases Page 7
 Prepared and compiled by Dr. S. S. Kansara

Disease cycle:
 The fungus survives in the soil in the form of Oospores (resting spores) from
one season to other season.
 The pathogen is soil and internally seed borne.
 Secondary spread by rain splash.
 Fruits in contact with the soil which has been saturated with water for about 12
hours readily catch infection.

Management:
 Crop rotation, destruction of weeds, good drainage, selection of light soil
 Staking of plants to prevent contact between leaves or fruits and soil and
removal of lower leaves and fruits up to 30 cm.
 Four sprays of 0.3% Difolatan, Dithane M – 45 at 10 days interval.
 Spray with captafol, macozeb and copper ocxychloride

5. Tomato spotted wilt virus

Symptoms:
 The symptoms of tospoviruses vary greatly with the host affected, plant organ
affected, and age of plant or organ at the time of infection.
 In general, however, tospovirus symptoms appear as chlorotic or necrotic rings,
lines, or spots on leaves, stems, and fruits; necrotic streaks on stems; bronzing,
curling, and wilting of leaves; rings, necrotic spots, and malformations on fruits;
stunting and necrosis of parts or whole plants; and, generally, greatly reduced
yields.

Causal virus:
 Tomato spotted wilt virus
 It contains three linear ssRNA

Lecture notes 17 Tomato diseases Page 8

 Prepared and compiled by Dr. S. S. Kansara

Disease transmission:
 Tospoviruses are transmitted by at least seven species of thrips.
 These include the western flower thrips (Frankliniella occidentalis), tobacco
thrips (F. fusca), common blossom thrips (F. schultzei), onion thrips (Thrips
tabaci), and melon thrips (T. palmi).
 Tospoviruses can be acquired from infected plants by thrips larvae but not by
adult thrips.
 Once a larva acquires the virus, however, usually after feeding on an infected
leaf for 30 minutes or more, it then retains the virus through molting, pupation,
and emergence so that the emerging adult thrips is viruliferous and can transmit
the virus to healthy plants for the rest of its life.
 Inoculation feeding periods must be 30 minutes or longer.
 Fortunately, adult thrips, once alighting, do not move from plant to plant as
much as aphids do and so transmission of tospoviruses is not as explosive as
some of the aphid-borne viruses.
 Tospoviruses overseason in their perennial or biennial hosts from which their
thrips vectors transmit them to healthy plants.
 The virus spreads into phloem and parenchyma cells and multiplies in their
cytoplasm.

Lecture notes 17 Tomato diseases Page 9

 Prepared and compiled by Dr. S. S. Kansara

Management:
 Crops susceptible to tospoviruses should not be planted near other susceptible
crops.
 Only tospovirus-free transplants should be planted.
 Roguing of infected plants may help.
 Plants should be monitored for thrips vectors and should be treated with
insecticides to keep thrips populations to a minimum.

Lecture notes 17 Tomato diseases Page 10

 Compiled and prepared by Dr. S. S. Kansara

Diseases of okra
1. Yellow vein mosaic
2. Root knot nematode
3. Powdery mildew

1. Yellow vein mosaic

Symptoms:
 The main symptoms of the disease are vein clearing and veinal chlorosis of
leaves.
 The yellow network of the veins is very conspicuous and veins and veinlets are
thickened.
 In severe cases the chlorosis extends to interveinal areas and complete leaf turn
yellow
 Fruits are dwarfed, malformed and yellowish – green in colour.

Causal virus:
 Yellow vein mosaic virus
 It is not sap transmissible but transmitted by grafting

Lecture notes 18 Okra diseases Page 1

 Compiled and prepared by Dr. S. S. Kansara

 In nature the virus is transmitted by whitefly, Bemisia tabaci and okra leaf
hopper, Empoasca devastans.

Disease cycle:
 It is not seed borne.
 It maintained a continuous cycle through its wild or cultivated hosts.
 The insect transmit the virus to the main crop.

Management:
 Spraying with 0.3% Follidol.
 Four to six sprayings of Ekkatox, Metasystox, Rogor, Demicron.
 Destroy the weed hosts
 Spraying Monocrotophos 1.5ml/liter or chlorpyriphos 2.5 ml+neem oil 2 ml/lit of
water

2. Powdery mildew
Symptoms:
 The fungus produces greyish powdery growth on the under as well as on the
upper surface of the leaf causing severe reduction in fruit yield.

Causal organism:
 Erysiphe cichoracearum
 Conidia are single celled, hyaline, barrel shaped and in long chains
 Cleistothecia are globose and dark brown myceloid appendages
 The number of ascospores is usually 2 rarely 3 per ascus
 The ascospores are single celled, hyaline and oval to cylindrical.

Lecture notes 18 Okra diseases Page 2

 Compiled and prepared by Dr. S. S. Kansara

Disease cycle:
 PSI –ascospores from cleistothecia on host tissue
 SSI - Air borne conidia or through rain splash
Management:
 Crop debris collected and burnt
 Resistant variety
 Spray with wettable sulphur (0.2 %) or tridemorph (0.05 %) and repeat at 15 days
interval.

3. Root knot
Same as per given in Pomegranate

Lecture notes 18 Okra diseases Page 3

 Compiled and prepared by Dr. S. S. Kansara

Diseases of beans
1. Anthracnose
2. Bacterial blight
1. Anthracnose
Symptoms:
 In soil infected seeds generally undergo rot and show distinct pinkish fungal spores on seed coat.
 On seedlings, the cotyledons show small to large, brown to black, sunken spots.
 On growing plants the leaves show small, angular and brown lesions mostly adjacent to veins.
 On pods the spots appear as black sunken cankers with light or grey centered area
 The center portions of these spots show pinkish mass of spores especially in wet weather.
 Mature seeds from diseased pods may or may not be stained.
 If stained, the color is various shades of brown.
 On stems of adult plants, the spots are eye shaped and longitudinal along the stem.

Causal organism:
 Colletotrichum lindemuthianum
 Perfect stage – Glomerella cingulata f.sp. phaseoli
 Mycelium is septate, branched and hyaline becoming dark with age
 Acervuli develop beneath the cuticle.
 Conidia are borne on short conidiophores
 Setae are brown and hyaline. The fungus also produce perithecia

Disease cycle:
 The fungus overwinters in infected seeds and in plant debris
 Conidia or dormant mycelium in infected seeds germinate, become active and infect the young
seedlings.
 Secondary spread is through wind, water, rain splashes and insects

Favourable condition:
 90 % RH
 Rainfall
 Compiled and prepared by Dr. S. S. Kansara

Management:
 Grow disease free seeds
 Field sanitation
 Soil should be well drained and good spacing
 Seed treatment with thiram, carbendazim, carbendazim+ thiram, mancozeb @ 2.5 g/kg seeds
 Two to three sprays of mancozeb or carbendazim at 15 days interval.
 Biological control with Pseudomonas sp.

2. Bacterial blight
Symptoms
 The symptoms appear first on the lower sides of the leaves as small, water-soaked spots.
 The spots enlarge, coalesce, and form large areas that later become necrotic.
 Bacteria may also enter the vascular tissues of the leaf and spread into the stem.
 In common blight and in bacterial brown spot, the infected area, which is surrounded by a
narrow zone of bright yellow tissue, turns brown and becomes rapidly necrotic.
 Several small spots coalesce and produce large dead areas of various shapes.
 In halo blight, a much wider halo-like zone of yellowish tissue 10 millimeters or more in width
forms outside the water-soaked area, giving the leaves a yellowish appearance.
 All diseases produce identical symptoms on the stems, pods, and seeds, but when a bacterial
exudate is produced on them, it is yellow in common blight (Xanthomonas) and light cream or
silver colored in halo blight and in bacterial brown spot (Pseudomonas).
 On the stem, water-soaked, sometimes sunken lesions form that gradually enlarges
longitudinally and turns brown, often splitting at the surface and emitting a bacterial exudate.
 Compiled and prepared by Dr. S. S. Kansara
 Such lesions are most common in the vicinity of the first node, where they girdle the stem,
usually at about the time the pods are half mature.
 The weighted plant often breaks at the lesion.
 On the pods, water-soaked spots also develop that enlarge and turn reddish with age.
 Often the vascular systems of the pod become infected, resulting in infection of the seed through
its connection with the pod.
 Seeds may rot or may show various degrees of shriveling and discoloration depending on the
timing and degree of infection.
 Similar symptoms are caused on pea and soybean by two different species of Pseudomonas.

Causal organism:
 Three blights of bean are caused by bacteria:
 Common blight, caused by Xanthomonas campestris pv. phaseoli,
 Halo blight caused by Pseudomonas syringae pv. phaseolicola, and
 Bacterial brown spot caused by P. syringae pv. syringae.
 All three diseases occur wherever beans are grown and cause similar symptoms.
 In the field, the three diseases affect the leaves, pods, stems, and seeds in a similar way and are
usually impossible to distinguish from one another on the basis of symptoms.
 Common blight seems to be more prevalent in relatively warm weather, whereas the other two
blights are more prevalent in relatively cool weather.

Development of Disease:
 In all three bacterial blights, bacteria overwinter in infected seed and infected bean stems.
 Compiled and prepared by Dr. S. S. Kansara
 From the seed, bacteria infect the cotyledons, and from these they spread to the leaves or enter
the vascular system and cause systemic infection, producing stem and leaf lesions.
 Internally, bacteria move between cells; however, the latter collapse, are invaded and then
digested, and cavities form.
 When in the xylem, bacteria multiply rapidly and move up or down in the vessels and out into
the parenchyma.
 They may ooze out through splits in the tissue and may reenter stems or leaves through stomata
or wounds.

Management:
 Use of disease-free seed,
 Three year crop rotation,
 Sprays with streptocycline or tetracycline
 Avoid overhead irrigation
 Compiled and prepared by Dr. S. S. Kansara

Diseases of coconut
1. Wilt
2. Stem bleeding
3. Bud rot
4. Ganoderma stem rot/ basal stem rot/ Thanjavur wilt/ bole rot

1. Wilt
Symptoms:
 Leaves of the middle whorl wilted and extends to the outer whorl
 The leaflets are bent abnormally and this called “ribbing” of leaflets.
 Gradually these leaves turn yellow and exhibit marginal necrosis.
 In fruit bearing trees, the buttons and tender nuts shed in large numbers.
 The affected trees produce less number of the flowers and nuts are reduced in size and of
poor quality.
 The root system of affected palms starts decaying

Causal organism:
 The exact cause of the disease is not known
 From the roots of the infected plants, fungi such as Botryodiplodia theobromae, Rhizoctonia
solani and R. bataticola were isolated.
 Bacterial species such as Pseudomonas and Enterobacter, nematode like Rhadopholus similis
were isolated.
 The disease is particularly noted on the palms growing along the waterways.
Control:
 Removal of severely diseased plants
 Grow high yielding hybrids
 Application of 25-50 kg FYM
 Mixed and intercropping
 Cultivation of fodder crops
 Compiled and prepared by Dr. S. S. Kansara

2. Stem bleeding
Symptoms:
 Exudation of reddish brown fluid from the cracks of the stem
 The fluid trickles down to several feet on the stem and exudates dries up forming a black
crust
 The tissue below the cracks turns yellow and decay.
 The vigour of the tree is affected and nut yield is reduced.
 In extreme cases, the trees may become barren and die.

Causal organism:
 Ceratocystis paradoxa / Ophiostoma paradoxa
 The fungus produce two types of conidia
 Macroconidia are produced on conidiophores, either singly or in chains
 They are dark green in colour
 Microconidia are produced endogenously inside the long cells of conidiophores.
 The pathogen produces hyaline perithecia with asci and ascospores

Disease cycle:
 PSI: Through perithecia and chlamydospores in cracks and cavities of infected stem
 SSI: Through conidia dispersed by irrigation water, insects and wind

Favourable condition:
 Heavy rainfall followed by drought
 Cracks and insect wounds on stem
 Poor fertilization and poor maintenance of orchard
 Damage by beetles

Management:
 Avoid mechanical injuries to the stem
 Provide proper drainage during rainy season
 Chisel out affected tissues and dress the wound with hot coal tar or Bordeaux mixture
 Along with 50 kg of organic manure, apply 5 kg neem cake containing Trichoderma to the
basin during September.
 Compiled and prepared by Dr. S. S. Kansara

 Coconut stem borer insects should be controlled by applying Carbaryl 50% WP on the trunk
at 3 g per liter.
3. Bud rot
Symptoms:
 Severe on young palms
 Yellowish green discolouration of the heart leaf or crown leaf
 The basal tissues of the leaf rot quickly and can be easily separated from the crown
 Spindle withers and droop down
 The leaves and sheath in the central spindle fall of leaving an outer whorl of green leaves
 The withered central shoot can be pulled out very easily from the crown
 Young nuts fail to mature and fall

Causal organism:
 Phytopthora palmivora
 The fungus produces intercellular, non septate and hyaline mycelium
 Sporangiophores are hyaline and simple or branched
 Sporangiophores bears hyaline, thin walled, pear shaped sporangia
 Sporangia releases reniform, biflagellate zoospores
 The fungus produces thick walled spherical oospores

Disease cycle:
 PSI: Through dormant mycelium or oospores or chlamydospores
 SSI: Through sporangia with numerous zoospores which spread rapidly in the rain water or
wind or insects
 Compiled and prepared by Dr. S. S. Kansara

Favourable condition:
 High rainfall
 High atmospheric humidity
 Low temperature
 Wounds caused by Rhinoceros beetles

Management:
 Cutting and burning of badly infected palms
 Remove the infected portions and protect with Bordeaux paste.
 Spray copper fungicides after onset of monsoon
 Give prophylactic spray with 1 % Bordeaux mixture

4. Ganoderma stem rot/ basal stem rot/ Thanjavur wilt/ bole rot
Symptoms:
 The younger leaves turn yellowish brown
 The new leaves formed were smaller and yellowish in color.
 The wilting plants also show bleeding patches near the base of the trunk
 A brown gummy liquid oozes out from the cracks in the tree which slowly results in the death
of outer tissue
 The decay of the basal portion occurs slowly

Causal organism:
 Ganoderma lucidum
 The fungus produces a semicircular basidiocarp (bracket) which is attached to the tree with a
stalk
 The bracket is about 10-12 cm diameter and woody
 The upper surface is tough, shining, and light to dark brown with concentric furrow.
 The lower surface is white and soft with numerous minute pores
 These pores represents the opening of the hymenial tubes which are lined with basidia and
basidiospores
 Basidiospores are oval, brown and thick walled

Favourable condition:
 Trees grown in sandy loam and sandy soils, water logging and damages caused by weevils
and beetles
 Compiled and prepared by Dr. S. S. Kansara

Disease cycle:
 The fungus is soil borne and survives in the soil for long time
 The primary infection is through basidiospores in the soil, which attack roots
 The irrigation water and rain water also help in the spread of the fungus

Management:
 Remove and burn severely infected trees
 Isolate the diseased trees by digging a trench all around to check the spread
 Apply heavy dose of FYM or compost or green manure at 50 kg / tree/ year along with 5 kg
neem cake
 Drench the soil near the tree with 40 liter of 1 per cent Bordeaux mixture at quarterly interval
for 3 years and repeat after 2-3 years
 Apply Aureofunginsol 2 g+ Copper sulphate 1 g in 100 ml of water or Tridemorph 2ml/ 100
ml of water through stem injection or root feeding at quarterly intervals.
 Compiled and prepared by Dr. S. S. Kansara

1. Blister blight
Symptoms:
 Small, pale or pinkish round spots on young leaves.
 The spots enlarge and protrude out enough to give a blister like appearance.
 The pinkish colour turns to deep red, old spots turn powdery and whitish
 Often the upper surface depressed to form a blister on the lower surface, over which the
powdery fungal growth is prominent.
 The disease occurs on leaf petioles and tender stems
 Severely infected older leaves drop off.

Causal organism:
 Exobasidium vexans
 Fungus is inter and tra cellular
 Basidia is cylindrical, hyaline and thin walled
 Basidiospores are oblong and hyaline

Disease cycle:
 The pathogen can exist endemically in plantation all the year round.
 It becomes more active and multiplies rapidly during humid weather accompanied by
bright sun
 The life span from spore to spore is about three to six weeks, during which it builds up
large masses of basidiospores, spreads rapidly to cause secondary infection

Management:
 Spray with 1% Bordeaux mixture
 Mist spraying with Cuprous oxide or copper oxychloride at the rate of 25 to 40 gm in
100 litres and repeated after every picking
 Picking and destroying the infected older leaves, Protective spray after the plucking

Lecture notes on tea diseases Page 1

 Compiled and prepared by Dr. S. S. Kansara

1. Phytopthora blight
Symptoms:
 The disease first appears as small, dark, roundish spots on leaf.
 These spots rapidly enlarge and become circular, oval or irregular.
 Gradually, a very large part of the lamina gets involved.
 Later the affected portions drop out leaving shot holes in the leaf.
 The periphery of the spots is zoned in different shades of brown, green and
yellow.
 Unusually wet weather the corms may rot completely.

Causal organism:
 Phytopthora coiocasiae
 The mycelium is coenocytic, intercellular, producing haustoria.
 Sporangiophores are formed on the surface of the leaf, bearing single, pear
shaped or elongated sporangia.
 Each sporangia contains 12 reniform biflagellate zoospores.
 Oospores are spherical.

Disease cycle:
 The pathogen perpetuates through oospores in diseased leaf debris in soil and
through infected corms
 Secondary spread is through zoospores disseminated through irrigation water
and rainwater.

Management:
Lecture notes 22 Colocasia diseases Page 1
 Compiled and prepared by Dr. S. S. Kansara

 Select disease free corms

 Field sanitation.
 Spray Bordeaux mixture (2:2:50), Blitox 50 (2.5 kg/.ha), metalaxyl and Dithane
Z-78 (2kg/ha) at 10-15 days interval.
 Grow resistant varieties.

Lecture notes 22 Colocasia diseases Page 2

 Compiled and prepared by Dr. S. S. Kansara

1. Rust
Symptoms:
 The disease was first reported from Ceylon in 1868
 Small yellowish spots develop on under surface of leaf.
 Soon the spots enlarge to 10 to 15 mm
 The colour turns orange brown and powdery masses of spores are seen on the
surface.
 Characteristic chlorotic lesions can be seen on the upper surface corresponding
to the rusted spots on the lower surface
 As the disease advances the orange red colour fades to become white.
 The host tissues become dark brown, black and dries up.

Causal organism:
 Hemileia vastatrix
 Pycnidial and aecial stages of the pathogen have not seen
 Urediospores are reniform, have one flat and the other convex side
 Teliospores are one celled, pedicellate, round or turnip shaped and have no
dormancy
 Basidiopores do not infect coffee and no alternate host are known

Disease cycle:
 The coffee rust fungus exists primarily as mycelium, uredia and urediospores
on infected leaves
 The urediospores are mainly disseminated by wind, rain, contaminated
planting materials, movement of workers and insects.
 The disease is favoured by high temperature and high moisture

Lecture notes on coffee diseases Page 1

 Compiled and prepared by Dr. S. S. Kansara

Management:
 Field sanitation
 Spraying of carboxin or oxycarboxin 20 EC @ 0.1%
 Biological control with Verticillium lecanii, V. leptobactrum, Cladosporium
hemileiae etc

Lecture notes on coffee diseases Page 2

 Compiled and Prepared by Dr. S. S. Kansara

Diseases of cotton
1. Wilt
2. Bacterial blight/Black arm/ Angular leaf spot/ Boll rot
3. Anthracnose
4. Alternaria leaf blight
5. Leaf reddening

1. Wilt
Symptoms:
 The disease affects the crop at all stages
Seedling stage:
 Cotyledons of the seedling turn yellow and then brown.
 The base of the petiole shows brown ring, followed by wilting and
drying of the seedlings
Mature plant stage:
 Initial symptoms are yellowing of edges of leaves and area around the
veins from older leaves and progress toward the top.
 Discolouration starts from the margin and spreads towards the midrib.
 The leaves lose their turgidity, gradually turn brown and finally drop
off.
 The defoliation or wilting may be complete leaving the stem alone
standing in field
 Sometimes partial wilting occurs, where only one portion of the plant
is affected, the other remains healthy.
 In transverse section, Brown or black discoloured rings is seen.
 In severe cases, discolouration may extend throughout the plant
starting from roots extending to stem, leaves and even bolls

Lecture notes 24 Cotton diseases Page 1

 Compiled and Prepared by Dr. S. S. Kansara

Causal organism:
 Fusarium oxysporum f. sp. vasinfectum
 Colourless mycelium forming macro and micro conidia and
chlamydospores
 Macroconidia are 1 to 5 septate, thin walled and hyaline

Lecture notes 24 Cotton diseases Page 2

 Compiled and Prepared by Dr. S. S. Kansara

 Microconidia are hyaline, spherical and single or two celled.

Disease cycle:
 The pathogen can survive in soil as saprophytes and as
chlamydospores for many years
 The pathogen is both externally and internally seed- borne.
 The primary infection is mainly from dormant hyphae and
chlamydospores in the soil
 The secondary spread is through conidia and chlamydospores which
are disseminated by wind and irrigation water.

Favourable condition:
 Soil temperature 20-300C
 Soil humidity 40 to 70 %
 pH = 5.3
 Hot and dry periods followed by rains
 Heavy black soils with alkaline reaction
 Heavy Nitrogen fertilizers

Management:
 Deep summer ploughing during June-July
 Grow resistant varieties
 Treat the acid delinted seed with Carboxin or carbendazim @ 2 g/kg
 Remove and burn infected plant debris
 Apply FYM or other organic manures
 Follow mixed cropping
 Spot drench with Carbendazim 1 g/liter
 Delay planting to the end of October

2. Bacterial blight/Black arm/ Angular leaf spot/ Boll rot

Symptoms:
 The pathogen attacks all stages from seed to harvest.

Lecture notes 24 Cotton diseases Page 3

 Compiled and Prepared by Dr. S. S. Kansara

 Dark green, water soaked, angular lesions 1 to 5 mm on leaves and

bracts, especially on undersurface of leaves. Hence called angular leaf
spot
 Sometimes extensive dark green, water soaked lesions along the veins
known as vein blight.
 Lesions dry and darken with age and leaves may be shed prematurely
resulting in extensive defoliation
 Black lesions on the stem which girdle and spread along the stem or
branch and leaf veins turn brown known as black arm
 Dark green water soaked, greasy, circular lesions of 2 to 10 mm
across the bolls, especially at the base of the boll.
 As the boll matures the lesions dry out and prevent normal boll
opening known as Boll rot
 The bacterium spreads inside the boll and lint gets stained yellow
because of bacterial ooze and loses its market value.
 The pathogen also infect seed and causes reduction in size and
viability of seeds

Lecture notes 24 Cotton diseases Page 4

 Compiled and Prepared by Dr. S. S. Kansara

Causal organism:
 Xanthomonas axonopodis pv malvacearum
 Gram negative
 Rod shaped with single polar flagella
 Non spore forming

Disease cycle:
 Pathogen inoculum may either be present in field on infected crop
residue from previous season or within infected seeds
 Secondary spread is through rain splashes, irrigation water

Favourable condition:
 High temperature 30-400C
 RH 85 %

Lecture notes 24 Cotton diseases Page 5

 Compiled and Prepared by Dr. S. S. Kansara

 Early sowing
 Poor tillage
 Delayed thinning

Management:
 Grow resistant varieties
 Delint the seeds with concentrated sulphuric acid at 100 ml/kg seed
 Soak seeds in streptomycin sulphate (0.1%) overnight.
 Spray with streptomycin sulphate + Tetracycline 100 g along with
copper oxychloride at 1.25 kg/ha

3. Anthracnose
Symptoms:
 The pathogen infects the seedling and produces small reddish circular
spots on cotyledons and primary leaves
 The lesions develop on the collar region, stem may be girdled, causing
seedling to wilt and die
 In mature plants, small reddish circular spots on leaves, the fungus
attacks the stem, leading to stem splitting and shredding of the bark
 Small water soaked, circular, reddish brown depressed spots appears
on bolls
 The lint is stained to brown, becomes solid brittle mass of fiber

Lecture notes 24 Cotton diseases Page 6

 Compiled and Prepared by Dr. S. S. Kansara

Causal organism:
 Colletotrichum capsici
 The pathogen forms large number of acervuli on infected parts
 The conidiophores are slightly curved, short and club shaped.
 The conidia are hyaline and borne single on conidiophores

Disease cycle:
 The pathogen survive as dormant mycelium in seed or as conidia on
the surface of seeds
 The pathogens also perpetuates on rotten bolls and other plant debris
in soil
 The secondary spread is by air borne conidia

Favourable condition:
 Prolonged rainfall at the time of boll formation
 Close planting

Management:
 Remove and burn infected plant debris and bolls in the soil
 Rouge out the weed hosts
 Treat the delinted seeds with carbendazim or Thiram or captan @ 2
g/kg seed
 Spray the crop at boll formation stage with mancozeb (0.2%) or
copper oxychloride (0.3%) or carbendazim (0.1%)

4. Alternaria leaf blight

Symptoms:
 Small, circular, brown, gray brown to tan spots with purple margins
varying from 1 to 10 mm in diameter.
 They often exhibit concentric zonation and have dry, grey center
which often cracks and fall out (shot hole).
 Older spots may coalesce producing irregular dead areas

Lecture notes 24 Cotton diseases Page 7

 Compiled and Prepared by Dr. S. S. Kansara

 Stem lesions begin as small sunken spots which develop into a canker,
the tissue splitting and cracking.
 Flowers and bolls may be shed, the bolls become mummified and the
fiber attacked.

Causal organism:
 Alternaria macrospora
 The pathogen produces dark brown, short, 1-8 septate, irregularly
bend conidiophores
 The conidia are 3-9 transversely septate and 4 longitudinally septate,
with a beak, light to dark brown in colour

Disease cycle:
 The pathogen survives in dead leaves as dormant mycelium
 The primary spread is through irrigation water
 The secondary spread is mainly by air borne conidia

Favourable condition:
 Temperature 25-280C
 High humidity
 Intermittent rains
 Nutritional stress

Lecture notes 24 Cotton diseases Page 8

 Compiled and Prepared by Dr. S. S. Kansara

Management:
 Remove and destroy the infected plant residue
 Spray mancozeb (0.2%) or copper oxychloride (0.3%)
 At the initiation of the disease, repeat the spray at 15 days intervals

5. Leaf reddening

Symptoms:
 The actual reddening of the leaves can vary slightly depending on the
cause and the crop stage.
 In most cases, leaf margins turn red first and the discoloration late
spreads to the rest of the blade.
 Other symptoms may include wilting, reddening of stems, poor or no
ball development, leaf and fruit shed and stunted plants.
 During senescence, the discolouration is a natural process that can
usually be observed throughout the whole field.
 Besides nitrogen and Magnesium deficiencies, leaf reddening can also
be caused by over exposure to direct sunlight, cold temperature and
wing damage.

Lecture notes 24 Cotton diseases Page 9

 Compiled and Prepared by Dr. S. S. Kansara

Cause of disease
 Deficiencies of Nitrogen and Magnesium, sometimes due to
deficiencies of phosphorus and potassium.
 Increase in red pigment anthocyanin
 Temperature stress, poor soil fertility, over exposure of temperature
and cold temperature

Management:
 Correct mineral deficiencies
 Use cotton varieties resistant to abiotic stress.
 Judicious irrigation
 Monitor soil nutrients

Lecture notes 24 Cotton diseases Page 10

 Compiled and Prepared by Dr. S. S. Kansara

Disease of Cluster bean

1. Powdery mildew
2. Bacterial blight
3. Bean common mosaic

1. Powdery mildew
Symptoms:
 The disease first appears on the leaves and on other green parts of the plants
 White floury patches appear on both sides of leaves as well as on pods and
stems
 When the attack is advanced, large area on the aerial parts of the host may be
covered with these white floury patches

Causal organism:
 Erysiphe polygoni
 Mycelium is ectophytic, producing haustoria
 Conidia are formed on conidiophores
 Cleistothecium contains asci and ascospores

Disease cycle:
 The pathogen is seed borne.
 In addition, cleistothecia that develop on dead plant debris also serve
as source of primary inoculum.
Lecture notes25 Cluster bean diseases Page 1
 Compiled and Prepared by Dr. S. S. Kansara

 Ascospores formed in these fruiting bodies are released by decay of

the fruit and blown by wind to lower leaves.
 Secondary spread occurs through wind blown conidia

Management:
 Field sanitation
 Spray with Karathane (0.2%), Calixin(0.5 L a.i. /ha), thiovit (5
kg/ha)
 Grow resistant varieties

2. Bacterial blight
As per given in Diseases of Bean

3. Bean common mosaic

Symptoms:
 Crinkle, chlorosis and stiffness of the leaf lamina
 The leaves droop and petioles are much shortened.
 On the trifoliate leaves the mosaic pattern is present and leaves looks
rough.
 Abnormal growth of tissues causes the veins to bend downward and
leaves may look cupped.
 Diseased plants produce fewer pods which are small in size.

Lecture notes25 Cluster bean diseases Page 2

 Compiled and Prepared by Dr. S. S. Kansara

Causal virus:
 Bean common mosaic virus
 Potyviruses group
 It contains ssRNA

Transmission:
 Seed transmission is common and most important source of initial
infection
 Virus is present in the embryo and cotyledons but not in seed coat.
 Transmission in the field occurs through aphid vectors Myzus
persicae, Aphis fabae, Aphis gossypii

Management:
 Grow resistant varieties
 Control of insect vector through insecticides

Lecture notes25 Cluster bean diseases Page 3