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Practical Manual

The document outlines a practical course on the study of diseases affecting vegetable, ornamental, and spice crops, focusing on pathogens such as fungi, bacteria, and viruses. It includes objectives, requirements for studying, and detailed exercises on various diseases, symptoms, causal organisms, and control measures. Additionally, it provides a certification section for course completion and emphasizes the importance of understanding disease cycles and management strategies.

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0% found this document useful (0 votes)
3 views69 pages

Practical Manual

The document outlines a practical course on the study of diseases affecting vegetable, ornamental, and spice crops, focusing on pathogens such as fungi, bacteria, and viruses. It includes objectives, requirements for studying, and detailed exercises on various diseases, symptoms, causal organisms, and control measures. Additionally, it provides a certification section for course completion and emphasizes the importance of understanding disease cycles and management strategies.

Uploaded by

sahiltamhane01
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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INDEX

Expt. Title of the exercise Page Date Sign


No. No.
Objectives, requirements for studying 2
symptoms and cause of diseases of vegetable,
ornamental and spice crops and class
work/exercise
STUDY OF DISEASES CAUSED BY FUNGI
1&2 Diseases caused by Oomycetes fungi 3
3&4 Study of powdery mildews 10
5 Study of rust diseases 18
6&7 Study of anthracnose diseases 22
8&9 Study of blight and leaf spot diseases 27
10 & 11 Study of wilt, root and rhizome rot diseases 32
12 Study of scab of potato and club root of 42
crucifers
13 & 14 Study of diseases caused by bacteria 45
15 &16 Study of diseases caused by viruses and 50
phytoplasma
17 Study of Phanerogamic plant parasites and 58
deficiency diseases
CERTIFICATE

This is to certify that Shri/Ku . _______________________________________ Enrol.


No.____________ has completed the practical work of Course No. H/PATH-363(Diseases of
Vegetable, Ornamental and Spice Crops) as per the Syllabus of B.Sc. (Hort.) Second Year,
Third Semester in the laboratory of College as prescribed by M.C.A.E.R. Pune during the year
20 -20 .

Date :Course Teacher

STUDIES ON DISEASES CAUSED BY FUNGI, BACTERIA, VIRUSES,


PHYTOPLASMAS, PHANEROGAMIC PLANT PARASITES AND NUTRITIONAL
DEFICIENCY IN VEGETABLE, ORNAMENTAL AND SPICE CROPS

Objectives:
1. To get acquainted with the occurrence, diagnostic symptoms, cause, disease cycle,
favourable environment/predisposing factors and control measures of important diseases
of vegetable, ornamental and spice crops.
2. To collect and preserve the specimens of important diseases of vegetable, ornamental and
spice crops.
3. To examines the cultures of important pathogens of vegetable, ornamental and spice crop.
Requirements for studying symptoms and cause of diseases of vegetable, ornamental and
spice crops :
Samples of different diseases of diseases of vegetable, ornamental and spice crops,
binocular research and stereo zoom microscopes, slides, cover slips, cotton blue, distilled
sterilized water, sharp blade, desiccators, absorbent cotton, two pointed needles and wash bottles.
Class work/Exercise :
1. Collection and preservation of specimens of different diseases of vegetable, ornamental
and spice crops.
2. Study the diagnostic symptoms of different diseases in the field as well as in the
laboratory from the collected specimens and study their disease cycle and control
measures.
3. In order to observe the fungal structures and to identify the causal organisms of the
diseases carry out the following tests/studies.
a. Mount the specimen of different diseases directly under stereo zoom microscope,
observe the various structures of fungi, and try to identify the pathogen or
b. Take a fine section of typical samples of diseases on glass slide in cotton blue,
mount under the binocular research microscope, and observe the fungal structures.
c. For observing the bacterial ooze, take the section of diseased sample in glass
distilled sterilized water on glass slide and observe immediately under
microscope.
d. Keep the disease samples in the moist chamber for 4 to 5 days, observe the fungal
growth appearing on disease portion by slide culture technique under binocular
research microscope and identify the pathogen.
4. Draw neat diagrams of various structures of causal agents of different diseases of
vegetable, ornamental and spice crops.

DISEASES CAUSED BY FUNGI

EXERCISE NO. 1 & 2

DISEASES CAUSED BY OOMYCETES FUNGI

I) DAMPING OFF OF VEGETABLE SEEDLINGS

The seedlings of vegetable crops viz., tomato, brinjal, chili, onion, peas, cabbage.
cauliflower, broccoli, okra, leafy vegetables, etc. are infected by damping off disease.

Symptoms :

The disease occurs in two stages i) Pre-emergence phase and ii) Post-emergence phase. In the
pre-emergence phase of disease, the young seedlings are killed before they reach to the surface
of the soil. The radical and pllumule undergo complete rotting. In the post-emergence phase of
disease, infection usually occurs at or below the ground level and the infected tissues appears
soft and water soaked. As the disease advances, the stem becomes constricted at the base and
plant collapes. Such symptoms are very common in seedbeds.

Causal organism : Pythium debaryanum Hesse

Etiology :

The mycelium of the pathogen is hyaline, coenocytic, and highly branched. The Sporangia
produced terminally or intercalary are round or barrel shaped and germinate by zoospores by
forming vesicle or by germ tube. Sexual reproduction by oospores formed by the gametangial
contact. The fungus is homothallic, facultative parasite and aquatic.

Perpetuation :

The fungus survives in the form of oospores or mycelium in soil through which primary
infection takes place. Secondary infection takes place by zoospores carried by irrigation water.

Control measures :

1. Avoid waterlogged and low-lying land.


4. Use seed from disease free area.
5. Soil treatment with formaldehyde (Formalin 36 - 40%) diluted to 25 times with water (i.e.
40 ml/L water) or 1% Bordeaux mixture 15 to 20 days before sowing.

6. Seed treatment with suitable fungicide (metalaxyl 35 WS, i.e., Apron @ 6g or thiram 75
WP or captan @ 2 to 4 g/kg seed) before sowing.
7. Sowing on raised beds and avoid over-crowding. I
8. Soil drenching with B. M. (1.0%) 10 days after seed germination.

II) LATE BLIGHT OF POTATO AND TO MA TO

Symptoms :

The disease first appears as circular or irregular water-soaked light brown lesions,
usual1y at the tips or edges of the lower leaves. Under humid and cloudy weather, these lesions
spread fast over the entire leaflet and petiole. The lesions that are dirty brown in the beginning
soon turn black. If the infected leaves are examined closely, whitish growth of the fungus can be
seen on the lower surface. The growing shoots are blighted in the beginning and then the disease
spreads up to tuber, which show brown or purple discolouration of the tuber skin and under
moist conditions, tissues, become soft. Finally, the affected tubers turn brown and decay before
harvest. In dry soils, spread of the disease is slow and may result in the dry rot of tubers.

Causal organism : Phytophthora infestans (Hont.) de Bary.

Etiology :
Mycelium is hyaline, non-septate, branched and is both inter and intracellular. The
sporangiophores are aerial and arise from the internal mycelium through stomata and lenticels
on the tubers. They are slender, hyaline, branched and intermediate. The sporangia are
multinucleate, thin walled, hyaline, oval or pear shaped with a definite papilla at the apex,
germinating by zoospores of by genm tube. Oospores are thick-walled and yellowish.

Perpetuation :

The primary infection is through dormant mycelium in infected tubers or through


oospores present in the soil or in the debris. The secondary infection is through sporangia spread
by wind or irrigation water.

Control measures :

9. Use healthy tubers for planting. Select seed material from the disease free fields. Follow
clean cultivation.

10. Dip the seed tubers for 2 to 5 minutes in the solution of mercurial fungicide or metalaxyl
(25 g in 10 liters of water) before planting.
11. Give two or three sprays at an interval of 15 to 21 days starting from 25 days after
planting with Bordeaux mixture (1%) or metalaxyl MZ-72 or chlorothalonil or copper
oxychloride or mancozeb or ziram 80 WP (0.25%).
12. Grow resistant varieties. like Kufri Kishan, Kilfri Sindhuri, Kufri Kuber, Khufri Jivan,
Kufri Moti and Kufri Khashigaro.

III) DOWNY MILDEW DISEASES

i) Downy mildew of crucifers

Symptoms :

The purplish brown spots are observed on the underside of the leaves with thin downy
growth of the fungus. The upper surface of the leaf on the lesion is yellowish. Infected leaves dry
up, shrivel and fall off. Swelling of the stem becomes evident.

Causal organism: Peronospora brassicae Gaum

Etiology:

The mycelium is coenocytic and intercellular with large finger shaped branched
haustoria. Sporangiophores are dichotomously branched. The sterigmata are long, slender and
pointed at acute angle with each other. The sporangia borne singly at the tip of each branch those
are ovate hyaline, readily fall off and geminate by lateral germ tube. The fungus is an obligate
parasite.

Perpetuation:

The fungus perpetuates in the soil through oospores. The primary infection is through
contaminated seeds. Sporangia are responsible for secondary spread of the disease.

Control measures :

13. Maintain sanitation.


14. Follow crop rotation for 2-3 years,
15. Destroy weed hosts.
16. Hot water seed treatment at 50°C for 30 minutes or
17. Seed treatment with metalaxyl 35 WS @ 6 g/kg seed.
18. Spray the crop with 0.25 % mancozeb or chlorothalonil or copper oxychloride or B. M.
(0.5 to 0.6%) 2-3 times at 10 days interval. Metalaxyl MZ - 72 or fosetyl AL (0.25%) are
the best systemic - selective fungicides for the management of downy mildew of
crucifers.

iii) Downy mildew of cucurbits

Symptoms :

Yellow angular spots appear on the leaves. In humid atmosphere, purplish downy growth
appears on the underside of spots. Infected plllnts remain stnnteo fInd severely infected leaves
become necrotic, turn brown and shrivel. The entire leaf dries quickly.

Causal organism : Pseudoperonospora cubensis (B & C) Rostow.

Etiology :

The mycelium is coenocytic, intracellular with small and oval haustoria. Sporangiophores
arise in groups through stomata, which are branched either dichotomously on intermediately. The
sporangia are ovoid to ellipsoidal, papillate and

germinate by production of biflagellate zoospores. Oospores if formed, they are light

yellow or hyaline.

Perpetuation:

The fungus survives in the form of mycelium and sporangia on cultivated and wild hosts.
Secondary infection is caused by the sporangia.

Control measures:

1. Remove the badly affected plants.


2. Spray the crop with metalaxyl MZ-72 or fosetyl AL mancozeb or chlorothalonil or
copper oxychloride @0.25 per cent or B.M. (0.5 to 0.6%) 2-3 times at, 10 days interval.
are the best systemic - selective fungicides for the management of downy mildew of
crucifers.
iii) Downy mildew of onion
This is serious disease of onion in all the subtropical and temperate regions of the world.
In India, the disease was first reported by Mir (l977) from hilly tract of Jammu and Kashmir
State and later from the Northern plains by Gupta and his coworkers.

Symptoms:

The symptoms vary with the type of infection. The systemic infection occurs when the
plants are grown from diseased bulbs wherein, the plants remain - stunted, become distorted and
pale green. In humid atmosphere, the downy growth of the fungus develops over the entire leaf
surface. In dry weather, this growth is absent and only white spots are seen. In local infections
caused by wine-borne conidia, oval to cylindrical pale spots are formed on the leaves. Usually,
these spots contain green and chlorotic zones. In humid weather, the .fungus (develops as white
to purplish downy growth on these spots. Usually, the older leaves, are attacked first and the
infection spreads to the sheath. Inner leaves are then affected but new and young central leaves,
remain healthy. If the leaf is attacked in the middle part, it drops from the point of infection and
the tip dries. The entire plant is not killed but only undersized bulbs are produced. The bulb
produced on diseased plants can remain small with succulent necks. Succulent necks are subject
to attack by fungi and bacteria in storage. The fungus can invade floral parts and thus infect a
small proportion of the seed.

Causal organism : Peronospora destructor (Berk) Casp.

Etiology :

Conidiophores non-septate, dichotomous branching, sterigmata are sub acute or acute. Conidia
germinate by one or two germ tube.

Perpetuation :

The mycelium over winters in the infected bulbs of onion and some other wild Allium sp.
that is a primary source of inoculum. Secondary infection takes place through conidia. Fungus is
seed borne and it persists from year to year as mycelium in infected bulbs in storage.

Control measures :
1. Collection and burning of onion debris.
2. Eliminate the collateral and alternate hosts.
3. Long crop rotation.
4. 4. Use healthy seed/planting material. .
5. Spray the crop with ziram or mancozeb or chlorothalonil or metalaxyl MZ - 72 or fosetyl
AL (0.25%) along with spreaders for effective control.
6. Treat the bulbs with hot water at 43-450C for 8 hours followed by fungicidal treatment.

iv) Downy mildew of fenugreek

Symptoms:

Yellow patches appear on the upper surface of leaves. The corresponding lower surface shows
the presence of cottony grayish-violet fungal growth. The conidiophores emerge through the
stomata in small fascicles.

Causal organism: Peronospora trifoliorum de Bary (Syn. P. trogonella Gaum.).

Etiology :

The conidiophore is a stout and erect_trunk and five to eight times dichotomously
branched. Primary branches are straight and intermediate branches are bent but not spreading,
ultimate branches are sharply pointed, in pairs, arising at right to

obtuse angle. Single, ellipsoid conidia that are narrow at one end and broad at the other

end are borne on conidiophores.

Control measures : Same as onion downy mildew

IV) WHITE RUST OF CRUCIFERS


Symptoms :

All the parts of the plant, except root, are affected. White, cremy, yellow pustules of
various sizes and shapes are produced on leaves and affected parts. Leaves may become
thickened, and fles Young stem and inflorenscence may show hypertrophy. The infection may be
systemic. Affected flowers are malformed and discoloured.

Causal organism : Albugo cruciferarum (Lev.) Kunze.

Etiology :

The mycelium is hyaline, coenocytic, endophytic, intercellular and possesses knob-like


haustoria for absorption of food. It produces short, club shaped sporangiophores beneath the
epidermis of the host in thick masses. Sporangia are formed in chains in basipetal succession and
they are attached by disjuncture cells.

Germination of sporangia is by zoospores at lower temperature or by germ-tube at high

temperature. Sexual reproduction is by oospores by the method of gametangial contact. Oospores


germinate by germ-tube and produce mycelium.

Perpetuation :

The fungus persists in the soil in the-form of oospores in the diseased host tissue or
perennial weed host. Secondary spread of the disease is through sporangia and zoospores which
are disseminated by wind.

Control measures :

1. Follow clean cultivation, i.e., removal of diseased plant debris.

2. Follow crop rotation with non-host crop.

3. Seed treatment with metalaxyl 35 WS @ 6 g/kg seed.


4. Spraying : as per downy mildew disease.

5. Destruction and burning of collateral host.

EXERCISE NO. 3 & 4

STUDY OF POWDERY MILDEWS

I) ECTOPHYTIC POWDERY MILDEWS

i) Powdery mildew of cucurbits

Symptoms :

White powdery patches appear on leaves and stem. On the cucurbits. The appearance of the
disease is favoured by humid condition. If the attack is severe, there may be premature
defoliation of the plants. The fruits remain undersized. Black, pinpointed bodies, i.e.,
cleistothecia may be seen on these white spots later in the season.

Causal organism : Erysiphe cichoracearum DC. on cucurbits

Sphaerotheca fuliginea (Schelechti) Poll. on melon.

Etiology :

Mycelium is septate and ectophytic. Conidiophores, erect, bear hyaline barrel shape conidia in
long chain. In Erysiphe cichoracearum, cleistothecium contains gloose asci with myceloid
appendages and two ascospores each. In Sphaerotheca fuliginea, cleistothecia contain
singleascus and 8 ascospores in each ascus.
Perpetuation :

Cleistothecia survive on left over cucurbit crop as primary inoculum. Secondary

spread is through windborne conidia.

Control measures :

1. Spray dinocap (0.1 %) or tridemorph or triadimefon or penconazole, or carbendazim (0.1


%). sulphur fungicides may be phytotoxic to cucurbits under certain climatic conditions
hence are not recommended for use in these crops.
2. Clean cultivation.
3. Use resistant varieties if available.

ii) Powdery mildew of pea Symptoms:

The disease first appears on the leaves and then on other green parts of the plant. White
powdery patches appear on both the sides of the leaves as well as on tendrils, pods, etc. In severe
attack, whole plant is affected, and the leaves turn yellow and drop down. The immature pods are
also affected, get wrinkled and finally dry up.

Causal organism: Erysiphe polygoni DC.

Etiology :

The superficial powdery mass consists of mycelium and spores of the fungus. The
mycelium is ectophytic, septate and produces the tubular haustoria. The cleistothecia are black
with mycetoid appendages over the infected plant parts, Asci are ovate and nearly sessile.
Hyaline ascospores are elliptical and unicellular. The pathogen is an obligate parasite.

Perpetuation :
Primary infection is by means of dormant mycelium in the seed and cleistothecia present
in the soil and plant' debris. Secondary infection is by means of oidia disseminated by wind.

Control measures :

1. Field sanitation.
2. Grow early maturing varieties.
3. Dust 300 mesh sulphur @ 20 kg/ha or spray the crop with Wettable sulphur (0.25%) or
tridemorph 0.05% dinocap (0.1 %) or triadimefon or penconazole, or carbendazim (0.1
%)..
iii) Powdery mildew of coriander

Symptoms :

It appears as small, white circular patches on young parts of stem and leaves. These
increase in size, often coalesce to cover extensive area of leaf surface. Affected leaves reduce in
size. Appearance of whitish powdery mass on leaves and stem is the characteristic of disease. If
the disease is unchecked at early stage, the whole plant becomes almost white with powdery
coating. Early infection does not permit seed formation. However, if the infection occurs at late
stage, seed formation may take place but the seeds will be small and shriveled thus affecting the
yield and quality.

Causal organism : Erysiphe Polyoni

Etiology :

Fungus is ectoparasite, spreading over the surface of the host and sending haustoria into
the epidennal cells. Conidia are produced in chains on conidiophures, which are ovate to
rectangular, hyaline and thin walled. In advance stage of fungal growth on the host tissues, the
sexual stage is found. The cleistothecium contains two to eight asci and each ascus contains four
to eight ascospores.

Perpetuation :
Fungus survives on collateral host. The cleistothecium can also survive on the host tissue
during off-season, which serves as primary source of infection. Secondary spread is through air
borne conidia.

Disease appears late in the season and observed during February to March. Dry season
and high temperature favours the disease development. Early sown crop show less incidence as
compared to late sown crop.

Control measures :

1. Removal and destruction of left over plant debris after the crop is harvested.
2. Adjustment in sowing dates is advocated and early sowing in October is recommended.
3. Sulphur dusting (25 kg/ha) when the crop is about two months and again after fruit
setting is found effective.
4. Spray the crop with 0.25 per cent Wettable sulphur or dinocap or tridemorph or
triadimefon or penconazole. or carbendazim (0.1 %).
5. Use of resistant varieties.

iv) Powdery mildew of beans

Symptoms :

Whitish floury patches on the leaves characterize the disease. Under favourable
conditions, these spots enlarge and cover the whole leaf lamina. Ultimately, leaves turn yellow to
brown in colour and then dry up. The infection may spread on pods, get wrinkled and finally dry
up.

Causal organism : Erysiphe polygoni DC.

Etiology :

The superficial powdery mass consists of mycelium, conidiophores and spores of the
fungus. The mycelium is ectophytic, septate and produces the tubular haustoria. The cleistothecia
are black with myceloid appendages over the body. Asci are ovate and nearly sessile. Hyaline
ascospores are elliptical and unicellular. The pathogen is an obligate parasite.
Perpetuation :

Primary infection is by means of dormant mycelium in the seed and cleistothecia present
in the soil and plant debris. Secondary infection is by means of oidia disseminated by wind.

Control measures :

Dust the crop with 300 mesh sulphur at the rate of 20 kg/ha or spray the crop with
Wettable sulphur (0.25%) or dinocap or tridemorph or triadimefon or penconazole, or
carbendazim (0.1 %).

v) Powdery mildew of roses

Symptoms :

This disease affects all above ground parts of the plant. The leaves, flower buds

and young shoots are most seriously attacked.

The first symptom of the diseases is raised, blister-like areas on the young leaves, covered
with white-powdery fungus growth. Growing leaves are twisted and malformed. Young growing
tips are generally covered by the mildew resulting in curling of leaves. Infected buds do not
open. The petals may become discoloured, dwarfed and finally die.

Causal organism : Sphaerotheca pannosa var. rosae.

Etiology :

The mycelium is ectophytic, slender, hyaline and branched. Conidiophores are straight
bearing conidia in chain that are hyaline and egg-shaped. Cleistothecia contain only one ascus.
Each ascus contains eight ascospores. The fungus is an obligate parasite.

Perpetuation :

Dormant mycelium and cleistothecia act as primary source of infection while conidia
carried by wind act as secondary source of infection.
Control measures :

1. Diseased and fallen leaves should be collected and burnt


2. Dust 300 mesh sulphur @ 20 kg/ha or spray Wettable sulphur 0.2% or dinocap (0.05%).
3. Use of resistant varieties.

vi) Powdery mildew of cumin

At flowering stage if the disease appears yield losses were reported up to 50 per cent and
in infection occurs at seed formation stage, the yield losses up to 15 per cent were reported.

Symptoms :

Small, white or grayish specks appear on lower leaves. They gradually enlarge, mix, and
cover the entire surface with white mycelial growth and conidia of the fungus. Later on, the
young leaves are also affected. In severe cases, the leaves turn ashy white in appearance. The
infection rapidly spreads on stem, flowers and fruits under warm moist conditions. Mycelial
growth on flowers affects seed setting and development. The seeds of affected plants are small
and light weight.

Causal organism : Erysiphe polygoni DC.

Etiology :

Fungus is an obligate parasite. Mycelium is superficial and septate. Conidia are borne in
chains; conidiophores are unicellular, hyaline, elliptical, barrel shaped or cylindrical.

Perpetuation :
Fungus survives as the dormant mycelium on the seed and thus disease is carried over
from one season to another by infected seeds. Secondary spread is through wind borne conidia.

Disease is favoured by warm, moist conditions. Temperature range from 26.5 to 35 0C is


most suitable for disease development.

Control measures :

1. Avoid late sowing of the crop.


2. Collect seed from disease free area.
3. Spray dinocap (0.1%) or tridemorph or triadimefon or penconazole, or carbendazim (0.1
%) in. early stage of disease development or dusting sulphur @ 25 kg/ha or spraying
Wettable sulphur twice at an interval of 15 days commencing from 451h day after
germination.

vii) Powdery mildew of okra (bhendi)

Symptoms :

The leaves show the presence of white or grayish patches of powdery fungal growth on
the upper surface of the leaves. The fungal growth is diffused without any marked boundary
covering the entire leaf surface. The lower surface may also show infection. In severe infection,
the affected leaves dry up and fall off prematurely. Early infectin causes more effect on plant
growth and yield.

Causal organism : Erysiphe cichoracearum DC

Etiology:

Conidia are single celled, hyaline, barrel-shaped and in long chains and 30 to 64 x 13 to 32 μm.
Cleistothecia are globose and dark with hyaline to dark brown myceloid appendages. The asci
are pedicellate, ovate or ellipsoid and 30 to 90 x 22.5 to 50 μm. The number of ascospores is
usually 2 rarely 3 per ascus. The ascospores are single celled, hyaline, oval to sub cylindrical and
18 to 30 x 12 to 18 μm.

Dry weather conditions favour powdery mildew. The disease is observed commonly
during September to December. Favourable temperature for disease development is 15 to 300C.

Control measures:

1. Application of Wettable sulphur 0.2 per cent or sulphur dust at 25 kg/ha thrice at 120
days interval or four times at 15 days interval is effective. First spray should be given
immediately after the appearance of the disease. Spraying with carbendazim 0.1 per cent
or benomyi 0.1 per cent is also effective.

viii) Powdery mildew of fenugreek

The disease generally appears late in the season. It becomes serious during December
when relative humidity is 60 to 70 per cent and temperature is 15 to 25°C. Symptoms:

It usually appears late in the season. Powdery white growth can be seen on both the surfaces of
the leaves.

Causal organism: Erysiphe polygoni DC.

Etiology:

It produces superficial mycelium and sends haustoria into epidermal cells. Mycelium is
septate, branched and 4.6 to 5.0 μm in diameter. Conidiophores are 106.5 to 166.5 μm in length
and bear conidia in chain. Conidia are unicellular, hyaline, elliptical, barrel-shaped to cylindrical
and 20 to 45 x 13 to 16 μm.

Perpetuation :
The fungus is an obligate parasite. It perpetuates as cleistothecia in the plant debris.
Ascospores from the cleistothecia infect old leaves near the soil. The disease spreads through
wind-borne conidia.

Control measures :

The disease is controlled by spraying dinocap (0.1 %) or tridemorph or triadimefon or


penconazole, or carbendazim (0.1 %) at 15 days interval.

II) ENDOPHYTIC POWDERY MILDEW'S

Powdery mildew of cluster bean, chilli, tomato and fenugreek

Symptoms:

Powdery growth of the fungus is observed on the lower side of the leaves covering the
lower leaf surface. The upper leaf surface turns yellow. The leaves, petiole and young stems are
affected by the fungus. If the infection is severe the withering of leaves and defoliation takes
places.

Causal organism : Leveillula taurica (Lev.) Aruand.

Etiology:

The fungus is endophytic and intercellular. Conidiophores emerge through stomata


bearing single oidium at the tip. Conidia are pear shaped or rectangular and germinate by germe-
tube. The cleistothecium has definite mycetoid appendages. Perpetuation :

The fungus perpetuates as dormant mycelium or cleistothecia which serve as primary source of
infection. Secondary infection is through air borne conidia. Control Measures:

Spray dinocap, tridemorph, triadimefon, penconazole, or myclobutanil @ 0.10 per cent at


fortnightly interval.
EXERCISE NO. 5

STUDY OF RUST DISEASES

i) Rust of beans

Symptoms:

The disease mostly attacks leaves. It may occasionally infect pods, On leaves, the disease may
appear on both the surfaces depending upon the host species, but it is most common on under
surface. Minute, almost white, slightly raised spots appear on susceptible varieties. These spots
enlarge to form circular reddish brown sari, containing the rust spores. Often, the sori are
surrounded by a ring of secondary sari or yellow hallow. With the formation of teliospores, the
sori turn dark brown or black. When powdery pustules develop, they give a rusty appearance to
the leaf. Leaves may turn yellow and dry or they may fall off resulting in total loss of the crop.

Causal organism : Uromyces phaseoli typica Arth - on bean


Uromyces phaseoli vignae (Barol) Arth. on cowpea.

Etiology :

The urediniospores are globose or ellipsoid, continuous (aseptate) echinulate, uninucleate,


walls are golden brown with 2 equatorial or subequatorial germ pores. Teliospores are globose or
broadly ellipsoid, pedicellate, one-celled, smooth or with few verrucose marks. Wall of the
teliospores is chestnut brown and with a hyaline papilla over the pore. Orange coloured aecia are
formed on the under surface of the leaf around the pycnia on the opposite side. The aecia are
cupulate. Aeciospores are ellipsoid, one-celled, hyaline and minutely verrucose.

The fungus is not seed-borne. It survives from season to season through continuously
grown bean crops and other Phaseolus species. In cooler areas, it can survive through
teliospores. The urediniospores spread the disease during the season through wind dispersal
(secondary).

Control measures :

1. Removal and destruction of plant debris.


2. Long crop rotations.
3. Wide space planting and remove weeds so that humidity is reduced.
4. Spray mancozeb, chlorothalonil or copper oxychloride (0.25%) or propiconazole (0.05%)
at 10 days interval.
5. Sulphur dust (300 mesh) is also good for control.

ii) Rust of brinjal

Symptoms :

The infected portion of the leaf is light green, thickened and usually concave on

the upper surface with a corresponding convex bulge on the lower surface. The spots increase in
size to a maximum of 2 cm in diameter. Sometimes the petioles are also affected. Pycnia
(Spermogonia) develop on the upper surface and appear as orange yellow, minute dots with
glistening drops of nectar. Aecia are produced on the lower surface of the leaves and petioles.
The uredinial and telial stages appear and cause an important disease on pearl millet, i.e.,
Penisetum (_phoides.

Causal organism- Puccinia penniseti Zimm. (P. substriatum var. penicillariae)

Control measures :

Spraying the crop with 0.25 per cent mancozeb or copper oxychloride at 10-15

days interval.

iii) Rust of roses


Symptoms:

The disease first makes its appearance on the leaves and young stems in the spring or in
early summer. The under side of the leaves, stems and calyxes show orange to lemon yellow
pustules (1.0 mm in diameter), which increase in size as the season advances. This is the
aeciospores stage of the fungus. In the mid-summer, the orange yellow spots on the leaves are
replaced by brick red spots and it represents the urediniospores stage of the fungus. Later in the
season, the same leaves show minute black, hair-like tufts on the under surface, indicating the
presence of teliospores. The affected leaves turn yellow, deformed and fall prematurely to the
ground. Some times blossoms develop badly or not at all. The diseased bushes are greatly
weakened and may die.

Causal organism- Phragmidium mucronatum Fr.

Etiology :

Aeciospores are verrucose, orange yellow, 24 to 25 x 18 to 21 μm. They are surrounded


in the aecidium by club shaped paraphyses. Urediniospores are ellipsoid or ovate, echinulate,
orange yellow, measuring 2 i to 28 x 14 to 20 11m in size and are home on short pedicles and are
surrounded by paraphyses. Teliospores are dark coloured, cylindrical, 6 to 8 celled with a
pointed papilla and 65 to 120 x 30 to 40 11m. Pedicels are persistent and are as long as the spore.
They are hyaline and swollen at the base.

Perpetuation:

Teliospores which are produced in autumn help in over wintering and causing fresh
infection through basidiospores in the next spring. The fungus also over winters as perennial
mycelium in the stem. Secondary spread is through wind-borne urediniospores.

Epidemiology:

In Rajasthan, the rust has been observed throughout the year on the rose variety, Chaiti
Gulab. Uredial stage of the rust fungus is found throughout the year. Maximum rust infection
occurs at a temperature ranges from 18 to 21°c. Temperature between 20
and 25°C is favourable for urediniospore formation.

Control measures:

1. Diseased fallen leaves and stems harboring perennial mycelium should be collected and
burnt.

2. Three sprayings during March-April at 15 days interval with mancozeb (0.20%) or


propiconazole or difenoconazole (0.10%) are effective.

iy) Rust of jasmine

In India, the disease was first reported from Maharashtra in 1931 and now it is widely
distributed throughout the country. Symptoms:

The fungus attacks all aerial parts like leaves, stems and int1orescence and causes
numerous blisters or tumors and other abnonnalities on the plant. The disease appears as orange
coloured pustules on both the surfaces of leaves but predominantly on the lower surface. Infected
portions become hypertrophied. In severe cases, it causes yellowing and falling of leaves. Oval
and orange coloured cankers are seen on the stems and twigs. Infected flower buds are swollen
and defonned. Flower production in such plants is highly reduced. Buds do not open when
attacked. Symptoms like splitting of barks of affected branches and subsequent death of the
branches occur.

Causal organism : Uromyces hobsoni Vize.

Etiology :

It is autoecious rust. The fungus does not produce uredial stage. Teliospores are

dark brown, one celled, mostly ovate, thick walled.


The fungus infects Jasminium angustifolium, J auriculatum, J communis, J flexile and J sambac.
It is observed during rainy season (June-July) and persists until the flowering in March.

Control measures :

1. Pruning and burning of infected parts.


2. Dusting sulphur at 20-25 kg/ha or spraying mancozeb (0.2%) or tridemorph (0.05%) or
triadimefon or propiconazole (0.05%). Bordeaux mixture (1.0%) or copper oxychloride
(0.25%) spray is also effective.

EXERCISE NO. 6 & 7

STUDY OF ANTHRACNOSE DISEASES

i) Anthracnose of beans Symptoms:

The disease appears as angular spots on the lower side of the leaves. They ultimately
become visible on the opposite side. Similar lesions are also found on seed, petiole and' stem.
Black cankers may appear on the cotyledon. Deep cankers on the coleoptiles result in plant
collapse. On immature pods, small brown spots develop into lesions, which look light brown at
centre and borders are brown to black.

Causal organism : Colletotrichum lindemuthianum (Sacc. and Magn.) Soribner.

Etiology :

The mycelium is hyaline, septate, branched and intracellular. Conidiophores are short,
septate intermingled with dark brown to black setae in the acervuli. Conidia are hyaline,
cylindrical, oblong with rounded ends or pointed at one end, and single-celled.
Perpetuation :

The fungus survives in the form of dormant mycelium or haustoria on diseased plant
debris and seed and causes primary infection to the seedlings. Secondary infection is through
splashing rains and air borne conidia.

Control measures :

1. Follow field sanitation and crop rotation.


2. Use healthy seed from disease free plot.
3. Seed treatment with carbendazim @ 2g/kg of seed.
4. Spray the crop with Bordeaux mixture (1 %) or copper oxychloride (0.25%) or
carbendazim (0.1 %) or propiconazole (0.05%).
ii) Anthracnose of chillies

Symptoms:

The disease occurs in three forms, i.e., leaf spots, dieback and the ripe rot while, ripe fruit
rot is more destructive. Typical anthracnose type symptoms are produced on the leaves. Dieback
is severe only when conditions are very favourable for infection of the branches. In dieback, the
necrosis starts at the tip and proceeds downwards. Entire twig of a branch withers away.
Affected portion of the stern turns ashy-white in colour and large number of acervuli in the form
of minute black dots are produced on affected portion. Fruits are damaged partly or completely
in the field as well as during transit and storage. The spots are usually circular and sunken, with
black margins. Under high humid condition, the sunken spot is covered with a pinkish mass of
fungal spores. As the disease advances, the spots spread, forming concentric markings with dark
fructifications representing the fungal acervuli. The fruits with many spots drop off prematurely,
resulting in heavy loss in yield.

Causal organism- Colletotrichum capsici (Syd.) Butler and Bisby.

Perpetuation:

Primary infection takes place through infected seed and plant debris and secondary
spread through air borne conidia.

Control measures:
1. Collection and destruction of affected fruits.

2. Use disease free seed.

3. Seed treatment with thiram (0.2 -0.3%) or carbendazim (0.1 %).

4. Spray the crop with mancozeb (0.25%) or carbendazim or benomyl or propiconazole or


difenoconazole (0.1 %) staring first spray at flowering and second at fruiting.

iii) Anthracnose of turmeric

It is one of the most destructive diseases first reported from Coimbatore in 1917 by
McRae. This disease is prevalent throughout India. The losses are estimated to be about 50 per
cent.

Symptoms :

Small, elliptic or oblong spots of different sizes appear on both sides of the leaf

surface but, more in number on upper surface. Two or more spots may join and develop into
irregular patches often involving major portion of the leaf, which eventually dries

up. These spots may attain a length of 4 to 5 cm and breadth of 2 to 3 cm. The centre of

the spot is grayish-white with numerous black dot-like acervuli arranged in concentric rings.
There is brown margin all around the spots. This is surrounded by chlorotic halo. In case of
heavy disease incidence most of the leaves dry up and the field presents a patchy appearance.

Causal organism : Colletotrichum capsici

Etiology :

Hyphae are inter and intra-cellular, septate, hyaline, later turn pale brown. Acervuli are
with dark brown to black stout setae. Conidia are borne singly on conidiophores, which are
hyaline, unicelled and sickle or falcate in shape.

Perpetuation :
The pathogen persists through infected rhizomes and other plants debris left in the soil
that serves as primary source of infection. Numbers of alternate and collateral hosts also help in
survival of Pathogen, e.g., chilli. Secondary spread is through air borne conidia.

Infection is severe during July to August when high relative humidity continuously
prevails.

Control measures:

1. Collection and burning of plant debris.


2. Planting material/seed rhizomes be obtained from disease free area.
3. Three foliar sprays at fortnightly interval with carbendazim or benomyl or propiconazole
or difenoconazole (0.1 %) or Bordeaux mixture (0.6%) starting from one month after
sowing are effective
4. Seed rhizome treatment with copper oxychloride (0.25%) or carbendazim or henomyl
(0.1 %) is recommended.
5. Use resistant varieties like TS-2, TS-4, TS- 79 and TS-88.
iv) Anthracnose or smudge of onion

The disease was first described by Berkley (1851) from England. It is a common disease
of white onion. Most coloured varieties are resistant to the disease.

Symptoms :

The most common symptom of the disease is appearance of subcuticular, dark green to
almost black smudge (the minute stroma of the fungus) on the bulb, neck or green leaves that are
clinging to the bulb after digging. The black colour appears in the form of circular, concentric
rings of dark stroma and mycelium. The outer most ring is broadest. When examined with hand
lens the black portion shows prominent bristles that are setae of the acervulus of fungus. On the
inner scale of infected onion, the lesions are small, sunken and yellow those enlarge and
coalesce.

Causal organism: Collectotrichllm circinans.

Etiology :

Mycelium septate, branched, hyaline when young. Intercalary chlamydospores are also
formed. Thick walled hyphae form dark green to black stroma. Acervuli are formed on stromata
and filled with conidia on a short colourless conidiophore. Conidia are fusiform or falcate and
borne singly at the tips or conidiophores.

Perpetuation :

The fungus over winters on infested onions, on sets and in the soil as a saprophyte. Moist
atmosphere is essential for production of conidia. Raindrop splashes helps in their dispersal.
Warm temperature and high relative humidity or wet weather at the time of bulb maturity
favours spread of fungus infection.

Control measures:

I. Use coloured resistant varieties.

2. Drying of bulbs before storage at 37 to 48°C.

3. Spraying with fungicides as mentioned above.

4. Dipping of bulbs in the solution of captan (0.25%) or carbendazim or benomyl (0.1 %) for five
minutes.

5. Store the bulbs in cold storage.

v) Anthracnose of clove, cinnamon, black pepper, nutmeg and all spices

Symptoms :

The disease infects leaves, young twigs and flowers. Small circular to oval brown specks
scatter .all over the surface of the leaf lamina. These specks gradually enlarge and develop into
distinct spots with an ash grey centre surrounded by a dark margin. In later stage, the adjoining
spots coalesce and form irregular necrotic patches. Infection is also observed on petioles causing
defoliation.

Brownish spots appear on young twigs, which mix together to fom1 necrotic patches. In
severe cases, the affected twigs show die-back symptoms resulting in defoliation.

Causal organism: Colletotrichum gloeosporioides Penz.


Etiology :

Fungal mycelium is septate, hyaline and branching. Fungus produces acervuli, which
have dark, septate, pointed setae. Conidia produced on conidiophores are hyaline, single celled
and cylindrical.

Perpetuation :

The diseased fallen leaves, flower buds and twigs on the tree serve as the primary source
of infection. The organism has a very wide host range including mango, cashew, areca nut,
custard apple, etc. Secondary spread is through splashing rains and air borne conidia. Humid
conditions favour the disease development. Usually, during September and October the disease is
more severe.

Control measures:

1. Collect diseased leaves, fallen flower buds, prune the diseased twigs from time to time, and
paste the cut ends with Bordeaux paste.

2. Perennial weed, Clerodendron infortunatum is the alternate host for pathogen, which neeus
removal from the clove garden.

3. Spray carbendazim or benomyl or propiconazole or difenoconazole (0.1 %) or Bordeaux


mixture (1.0 per cent) twice at fortnightly interval for effective control of the disease.

EXERCISE NO. 8 &. 9


STUDY OF BLIGHT AND LEAF SPOT DISEASES

I) BLIGHT DISEASES

A) Alternaria blights

i) Early blight of potato and tomato

Symptoms:

The spots are irregular, brown to dark in colour and with concentric rings inside the spots.
Several spots often coalesce to form large patches, resulting in the leaf blight. In severe cases,
the entire foliage is blighted. The concentric rings on the leaves in necrotic tissues are the most
characteristic symptoms of the disease. In case or potato, sometimes it may affect the tubers near
the soil surface, causing brown discolouration and dry rot, and at times affecting the stem and
leaf petiole to cause slightly sunken, dark coloured, linear lesions.

In case of tomato, dark black or brown spots with velvety black mass of spores over the
surface of infected fruit are seen.

Causal organism: Alternaria solani (Ellis and Martin)

Etiology :

The mycelium is septate, branched and light brown in colour. The conidiophores are septate
and emerge out though the stomata. Conidia are borne singly or in chains of 2 to 4, light brown
possessing longitudinal and crossed septa (muriform), gradually tapering into a beak. The fungus
produces a toxin called “Alternaric acid”.

Perpetuation :

The mycelium of the fungus remains viable in dry infected leaves for a year or more,
which serves as primary source of infection. Secondary infection is by means of conidia
disseminated by wind or water.

Control measures :
1. Collection and destruction of infected plant debris.
2. Use disease free seed.
3. Foliar sprays with chlorothalonil or mancozeb (0.3%) or Bordeaux mixture (0.4 to 0.6%)

ii) Alternaria blight / purple blotch of onion

Symptoms:

Small, whitish, sunken lesions appear on the succulent leaves. These lesions first appear
towards the leaf tip and later at the lower portion of leaves. The spots enlarge, several of them
coalescing to cover large patches of the leaves and to girdle the succulent leaf. As the disease
advances, the leaves are blighted and the infection Spreads to the bulb resulting in its decay. The
affected plants fail to flower.

Causal organism: Alternaria cepulicola Rag.

Etiology:

The mycelium is septate, branched, /hyaline when young and turning brown when old.
Conidiophores bulged at the base, short, usually straight or slightly curved. dark olivaceous
brown and septate. Conidia are produced in chains of 2 to 3, obclavate, muriform and mostly
double-walled. The apical portion tapering to a simple beak. The spores have 2-6 longitudinal
and 3-9 transverse septa.

Perpetuation:

Primary source of infection is through the infected plant debris and secondary through
conidia carried by wind and water.

Control measures:

I. Clean cultivation.

2. Selection of seed from disease free area.

3. Spray the crop with mancozeb or chlorothalonil or iprodione or copper oxychloride (0.25%)
with sticker (0.1 %) immediately after appearance of the disease.
iii) Alternaria blight of jasmine

Causal organism: Alternaria jasmini

Symptoms:

On the affected leaves, dark brown spots are noticed. In each leaf, the number of leaflets
affected may vary depending upon the variety and the prevailing environmental conditions. Both
young and older leaves in a vine are equally prone to infection. During humid conditions, the
spots in each leaflet enlarge very quickly and coalesce. In the lesion concentric rings
characteristic of Alternaria blight can be seen. From a distance, blighted vines appear as if they
are burnt by fire. Later, blighted leat1ets dry and easily fall off. They are a so brittle. In a
severely affected garden, large number of fallen leaves can be easily seen on the ground near the
base of the diseased vine. Oval to elongated light brown spots develop on petioles, stem, calyx
and even on tubular corollas. In severe cases of infection, vegetative buds and young branches
dry up.

Perpetuation:

The disease perpetuates in the diseased leaves and vines and further spreads through wind
borne conidia.

Control measures:

1. Diseased and fallen leaves should be collected and burnt. It helps in checking the secondary
spread of the disease.

2. The disease can be controlled by spraying with chlorothalonil or mancozeb or copper


oxychloride (0.25%). Spraying should be started immediately after the appearance of disease.
Number of sprayings depends upon the prevailing weather conditions. Spraying can be repeated
at 7 to 10 days interval covering all the foliage in the vine.

B) Phomopsis blight of brinjal :


The disease is widespread in its occurrence that causes about 20 to 50 per cent loss in yield. It
also adversely affects the seed quality, which reduces the rate of seed germination and viability.

Symptoms :

The disease appears as damping off or leaf blight or fruit rot however, the most
destructive phase of the disease is fruit rot.

Damping off:

The damping off of seedlings results from the infection of the stem just above the soil
level. The young seedlings fall down and dry up.

Leaf spot:

The disease on the leaves is more prominent during the early stage of the plant growth. It
appears as small spots more or less circular, buffy alive and later turn to cinnamon buff with
irregular blackish margins. The old leaf spots are irregular in shape and vary in size. The lesions
at the petiole or at a lower part of the midrib cause the death of the entire leaf. The blight
symptoms are usually prominent under humid conditions. The affected leaves drop prematurely
and the infection spot is covered with numerous pycnidia. The disease spreads to the stem also as
elongated blackish-brown lesions and when there is girdling of the stem due to infection, the
shoot above wilts and dries up.

Fruit rot:

The fruit is attacked while on the plant. The disease appears as pale sunken spots which
progress to cover the entire fruit surface. The spots are marked by the presence of numerous
black pycnidia arranged in concentric rings. If the pathogen enters the fruit through calyx, the
whole fruit becomes mummified due to dry rot.

Causal Agent - Phomopsis vexans (Sacc. And Syd.) Hartar

Etiology:
Pycnidia with or without beak are found in the affected tissue. They become erumpent,
brown to black, measures 60 to 200 μm in diameter on the leaves and 120 to 350 μm in diameter
on fruits and are globose or irregular.

Conidiophores in the pycnidium are hyaline, simple or branched, sometimes

septate, 10-16 μm in long.

Pycnidiospores (conidia) are hyaline, one celled, sub cylindrical, 5-9 x 2-2.8 μm in size.
Another form of conidia, the stylospores are filiform, curved, hyaline, septate and 20-30 x 0.5-
1.0 μm.

Perpetuation:

The fungus is seed borne. It survives in the infected plant debris in the soil. The spores
(pycnidiospores) are spread by rain splashes. They can also be disseminated by implements and
insects. The optimum temperature for fungal growth is 29° C. Disease develops fast in wet
weather with temperature around 26° C. The fungus requires wet weather and high temperature
(30-32° C) for disease development.

Control measures :

a) Cultural :

1. l. Use of disease free seeds.


2. Since the pathogen attacks only brinjal, three-year crop rotation is effective for its
control.
3. The diseased crop debris should be collected and burnt in the field.
4. Soil should be given deep summer ploughing.
5. Hot water seed treatment (at 50° C for 30 minutes)

b) Chemical :

1. Seed treatment with carbendazim or benomyl (2 g/kg of seed). Spraying with captan or
mancozeb or copper oxychloride (0.25%) or difenoconazole or carbendazim or benomyl
(0.1 %) in the nursery as well as in the field at 7-10 days interval controls the disease.
C) Leaf spot diseases
Taphrina leaf spot of turmeric

Symptoms :

The spots appear in great numbers, thickly covering both the sides of the leaves.
Individual spots are minute and are arranged in rows along the leaf veins, often they run together
to fonn linear iITegular lesions. Infected leaves appear reddish-brown, in contrast to lhc golden
yellow or yellowish-green of heaithy ieaves. The ieaves later become chlorotic and pale yellow.
As the disease advances, the affected tissues wither and dry while. The diseased plants are not
killed the leaves are severely blotched and blight.

Causal organism: Taphrina maculans Butler.

Etiology :

The mycelium is septate, endophytic and intercellular between cuticle layer and epidennis
producing haustoria. Asexual reproduction is by means of budding i.e. budlike structures are
formed (conidia), which are called blastospores. Sexual reproduction is by ascospores that are
produced in asci. Asci are naked and contain unicellular, oval ascospores.

Perpetuation:

Primary infection takes place through dormant mycelium in rhizomes. It is also possible
that the dried leaves having spots and laying in the field with the asci function as the chief source
of primary inoculum for the next crop.

Secondary infection by asci and ascospores carried by wind and raindrops from spots.
The fungus is homothallic and favoured by cool and moist weather.

Control measures :

1. Clean cultivation.
2. Spray with Bordeaux mixture (0.6%), copper oxychloride (0.25%), mancozeb, or ziram
(0.25%).
EXERCISE NO. 10 & 11

STUDY OF WILT, ROOT AND RHIZOME ROT DISEASES

I) FUSARIUM WILTS

i) Fusarium wilt of cumin

Symptoms :

The plants are attacked at all the stages of growth but the disease usually appears in
patches in the field, when the crop is about a month old. The affected plants turn brown and later
show wilt symptoms and dry up. The roots of diseased plants show dark brown margins. In the
affected roots, vascular bundles show presence of chlamydospores and fungal mycelium.

Causal organism : Fusarium oxysporum f. sp. cumini

Etiology :

Fungus produces micro and macro conidia and chlamydospores. Microconidia are one-
celled, hyaline, ovoid to ellipsoid, straight or curved. Macroconidia are 2 to 3 septate, straight or
slightly curved at the apex. Chlamydospores are terminal or intercalary, spherical, thick walled
and smooth.

Perpetuation :

Fungus is seed and soil borne. It is present between the seed coat and endosperm. Seed
infection occurs in field or in the storage. Infected seeds act as the primary source of infection.

The disease is favoured by temperatures ranging from 12.5 to 19.30C.

Resistant varieties:

Cumin varieties viz., MC 43, UC 33, UC 62 and UC 90 are resistant to the wilt disease.
ii) Fusarium wilt of tomato

This is the most important disease of tomato occurring in many parts of the world
including India where it is found in every state.

Symptoms :

The affected plants show yellowing of lower leaves in the initial stages followed soon by
discolouration of younger leaves. The leaves droop, wilt and die. The disease may affect a few
branches in a plant or the entire plant may wilt irreversibly. The affected plants are usually
stunted in growth and fruits ripen prematurely. The vascular bundles become brown and
branches dry up.

Causal organism: Fusarium oxysporum f. sp. lycopersici (Sacc.) Snyder and Hansen

Etiology:

Mycelium is septate, hyaline at first becoming cream coloured with age, finally showing
ochraceous strands throughout colony in culture. Macroconidia measure 25 to

33 x 3.5 to 5.5 μm. Microconidia are one-celled, hyaline, ovoid to ellipsoid and 2.5 to

4.0 x 6 to 15 μm. Two races of the pathogen have been identified.

Perpetuation:

The fungus is soil as well as seed-borne. It survives in the soil as chlamydospores or as


saprophytically growing mycelium in infected crop debris for more than 10 years. One of the
chief methods of its distribution is by seedlings raised in infected soil. Wind-borne soil
containing spores, surface drainage water and agricultural implements also help in distribution of
the pathogen from field to field.

Disease development is favoured by alternating high and low soil temperatures and high
humidity levels. The optimum temperature for disease development is 28°C. Other favourable
factors include light sandy soils, low soil moisture, pH and relative humidity and short day
length. The presence of root knot nematodes cause infection in even resistant tomato varieties
and greatly increase infection in susceptible ones.

iii) Fusarium wilt of brinjal

Symptoms:

The disease makes its appearance at different stage of the crop growth. Young plants of
one month old as well as mature plants of 3 to 4 months are equally susceptible. The leave
become flaccid, hang down and in the course of a week the plant dries up. The roots exhibit
varying degrees of rotting. The collar region and base of the stern are found to be shrunk.
Sometimes whitish growth of the fungus is visible on the surface-of the stem base.

Causal organism: Fusarium solani (Mart.) Sacco

Etiology :

Mycelium of the fungus is white to grayish. Microconidia are hyaline, cylindrical, wedge
or allantoid in shaped, one septate and are formed in chains. Microconidia have few septa and
cylindrical to falcate or straight. They are slightly wider towards apex with short and blunt
apical cell. Chlamydospores are globose to oval, smooth to rough walled, intercalary or terminal.

iv) Fusarium wilt of bhendi

Symptoms:

The symptoms appear as yellowing and stunting of plants followed by wilting and rolling
of leaves. Finally, the whole plant dies. Brown vascular discolouration is observed in the affected
plants. In severe cases of attack the stem becomes black.

Causal organism: Fusarium oxysporum f.sp. vasinfectum

Etiology:
Macroconidia are fusifonn, curved inward at both ends, 3 to 5 septate and formed on
sporodochia and pionnotes. In mass, conidia appear buff or salmon orange in colour.
Microconidia are one septate and hyaline. Terminal and intercalary chlamydopores are broadly
ovate.

Perpetuation:

The fungus is soil borne. Young plants are most susceptible compared to mature ones.
The fungus grows well at temperature between 12.5 to 37.5°C but the optimum temperature is
25°c. The optimum temperature for disease development is 22 to 28°C.

Resistant varieties: Varieties viz. Phule Utkarsha, CS 3232, CS 8899, IS 6653, IS 7194,
IS 9273, IS 9857, Pusa Makhamali and Pusa Sawani are resistant.

Specific control measure: Sowing of okra in February to March.

v) Fusarium wilt of pea

It is an important disease in India reported from Punjab, Delhi, West Bengal. From
Northern India, losses due to this disease are reported to the tune of 13-95 %.

Symptoms:

The earliest symptoms are seen at or after blossoming time. The characteristic symptoms
are dwarfing and yellowing of stipules and leaflets. At first, lower leaves and then upper leaves
show loss of turgidity. The entire plant wilts and then the stem shrivels. The vascular tissues
show a brown to orange or deep red discolouration that extends throughout the invaded root
system. The plant may die quickly or remain partly alive during the entire season. Plant fails to
develop pods.

Causal organism: Fusarium. oxysporum f.sp. pisi (Lin) Shn and Han.
Etiology:

Fungus produces delicate mycelium having purple tinge. Generally, abundant


macroconidia are produced that are septate, sickle shaped or cylindrical and straight. The
macroconidia are borne on elaborately branched conidiophores or on the surface of tubercular
sporodochia.

Perpetuation:

Pathogen is seed and soil borne. Initial infection of disease is through seed while,
secondary spread is through conidia. The fungus is more uestructive in wet soiL Resistant
varieties:

Cultivation of resistant varieties like Sylvia, Selection 1, T-17, Grey Giant, Alaska, Monark,
Kala nagini, Asauji.

vi) Fusarium wilt or yellows of cabbage

Symptoms:

Affected plants show unifonn yellowing however, more often yellowing is intense on one
side of the leaf. Stem and leaves curl laterally and lower leaves become yellow. Later, upper
leaves also show such symptoms. Leaves become brown, die and become brittle. When the
affected stem is split open yellowing or browning of vascular system can be seen.

Causal organism: Fusarium. oxysporom f. sp. conglutinans (Wollenw.) Synder and Hansen

Etiology:

Mycelium is septate. Chlamydospores, microconidia and macroconidia are produced.


Microconidia are hyaline, ovoid to ellipsoid and 6 to 15 x 2.5 to 4.0m. Sporodochia, pionnotes
and sclerotia are absent.

Perpetuation:
The fungus is seed and soil borne that persists in soil for many years and can be carried
to long distances in seeds. It is disseminated through diseased seedlings, implements, rain and
irrigation water to neighboring on-infested soil.

Epidemiology:

Disease development is favoured by warm weather conditions. The fungus attacks


broccoli, cabbage, caulit1ower, Chinese cabbage, mustard, radish and turnip. Resistant varieties
: Badger Ball head, Badger market, Banner, Blue crown, Empire Danish, Enterprise, Gladiator,
Red Hollander, Resistant Flat Dutch, Wisconsin Hollander, etc. are resistant to yellows in
cabbage.

Control measures for all wilt diseases:

1. Use disease free seeds for sowing. Similarly, diseased seedlings from sick plots should
not be used for planting.
2. Long crop rotation with non-host plants helps to reduce the disease incidence.
3. Sowing / planting in nematode free soil.
4. Application of Trichoderma bioagent @ 5-6 kg/ha (talk based) or 12-13 kg/ha (grain
based) by mixing in to sufficient quantity of well decomposed FYM or compost.
5. Early sowing also reduces the disease incidence.
6. Hot water treatment of seed at 54°C for 15 minutes controls the fungus in some heat
tolerant crops.
7. Seed treatment with thiram or captan 3-4 g/kg or benomyl or carbendazi 2g/kg of seed.
8. Incidence of wilt is significantly reduced with the application of carbendazim (0.1 %) or
benomyl (0.2%) or Bordeaux mixture (1.0%) as soil drench in space planted crops like
tomato, cabbage, etc.
9. Summer fallow decreases the wilt incidence.
10. The infected plants should be removed and destroyed.
11. Grow resistant varieties wherever available.

II) VERTICILLIUM WILT DISEASES

1) Verticillium wilt of tomato

Symptoms:
Affected plants are stunted in growth and leaves develop dark green patches followed by
interveinal and marginal yellowing. Leaves wilt, dry and eventually fall. A brown discolouration
can be seen in the xylem vessels on cutting through the stem and roots. Many adventitious roots
develop 'at the base of the stem of diseased plants. In Verticillium dahliae infected plants, tiny,
black microsclerotia begin to form as the plant dries and become numerous on plant residues.
Apart from the rapid development of symptoms, Verticillium infected plants can be distinguished
from Fusarium infected plants by the lighter brown colour of the infected vascular tissue.
Fusarium wilt usually has a more localized distribution within an area and requires higher
optimum temperature for its development and it develops a more intense yellowing of the leaves.
Tomato plants can be infected by both the pathogens at the same time.

Causal organism : Verticillium dahliae Kleb., V. albo-atrum Reinke & Berthold V. tricorpus
Issac

ii) Verticillium wilt of brinjal

It is common in Western countries and India. It was recorded for the first time in India from
Pune in 1938. The disease is prevalent in Karnataka, Maharashtra, Tamil Nadu and other states.

Symptoms :

The initial stages of infection is marked by the presence of temporary drooping of old
leaves and irregularly scattered pale yellow patches in the interveinal areas of the leaf lamina. In
some cases the initial stages of infection is detected by the appearance of marginal yellowing and
drying which proceeded from one margin to the other. In advanced stage, marginal flagging and
curling of leaf lamina characterize symptoms. Affected area become necrotic, coalesces and
cause complete drying. The lower leaves are the first to show symptoms. The newly formed
leaves at the top remain healthy until they become old. The disease progresses and causes
complete drying. The leaves droop down and give a sleepy look during daytime and the plants
are recovered during night. However, this type of sleepy look is observed at the beginning of
symptom development. At later stages, the leaves gradually drop off leaving the plant with
barren branches. Occasionally some diseased plants revive and give new flushes. The most
characteristic symptom of the disease is conspicuous browning of the vascular tissue of the root
and stem, which is observed by splitting the root and stem.

Causal organism : Verticillillm dahliae Kleb.

Etiology :

Verticillium dahliae: Freshly growing mycelium is white to grayish whole; resting mycelium is
dark brown to black, septate and swollen between septa. Hyphae are 3 to 7 μm. Microsclerotia
arise from a single hypha by budding. They are elongate to irregularly spherical and 18 to 50 μm
in diameter. Conidiophores are erect, hyaline, vertically branched, 3 to 4 phialides arising at each
node. Phialides are sometimes secondarily branched and 16 to 35 x 1 to 2.5 μm. Conidia arise
singly at apices of phialides. They are elliptical to irregularly sub-cylindrical and hyaline. They
may be unicellular or bicellular and 2.5 to 8.0 x 1.4 to 3.2 μm. Chlamydospores are not formed.
Verticillium albo-atrum: Produces microsclerotia that are dark brown to black and torulose to
botryoidal having swollen globular cells. Each microsclerotium arises from single hyphae by
repeated budding. They are 18 to 100 μm in diameter.

Verticillium tricarpus : It produces chlamydospores, which are dark brown.

In all the three species, the conidiophores, phialides and conidia are same as described
under V. dahliae. Conidia are held in a glistening droplet of liquid. Perpetuation:

In India, cotton, Dahlia, Datura, Brinjal, Bhendi, Physalis sp., potato, soybean,

sunflower, tobacco and tomato have been reported to be the hosts of V. dahliae. The fungi
survive in the soil on diseased plant debris and infect healthy plants by contact with roots. It is
more likely to survive and transported over long

distances through seeds or other plant parts. Secondary infection of aerial parts of brinjal is by
air-borne conidia. Similarly, furrow irrigation, organic manure and tillage spread the pathogens.

Alkaline soil and initial low soil and air temperatures favour disease infection and
development. Saturation of soil for at least a day is essential for infection. Low nitrogen nutrition
reduces disease severity. The optimum temperature for the disease development is from 22 to
24°c.
Control measures :

1. Cultivation of solanaceous and other susceptible crops should be avoided in the affected
fields to reduce the inoculum.
2. Soil fumigation with 1:1 mixture of methyl bromide and chloropicrin 12 to 15 days
before planting.
3. Avoid the use of seeds obtained from localities where the disease is prevalent.
4. To eliminate the spores sticking on the surface, treat the seed with benomyl or
carbendazim (0.20%) prior to sowing.
5. Isolation of infected field and raising the crops like paddy, pearl millet, ragi and sorghum
instead of solanaceous crops.
6. Incorporation of increased doses of organic manures and potash.
7. Avoided application of nigher doses of nitrogenous fertilizers.
8. Infected materials should not be left in the field and should be destroyed by burning at the
end of every season.
9. Polyethylene mulching reduces wilt effectively.
10. Deep ploughing and exposing the soil during summer.
11. Drenching the soil around the plants or spraying the plants with benomyl (0.10%).

III) ROOT OR STEM ROT DISEASES

i) Root or stem rots of vegetables

The disease is also known as charcoal rot or Macrophomina rot

Symptoms:

Damping off and death of young plants result in poor plant stand. In case of seed
infection, a conspicuous black sunken, cankerous lesion appears near the base of the cotyledon
and spreads downwards into the stem and first pair of unfolded leaves. Later, infection progress
more slowly. Sunken and reddish brown lesions begin at or below the soil level and extend
downward into the roots and upward. As lesions enlarge, turn grey at the center with numerous
minute, black2Ycni_ia. Root infection causes blackening called as charcoal rot. When leaves are
infected, spots usually occur first at the leaf tip as irregular brown dead areas marked by black
fruiting bodies. The spot expands after which the entire leaf may die.

Causal organism : Macrophomina phaseolina (Tassi) Goid.

Etiology :

The mycelium is both inter and intracellular. It produces numerous sacerdotal bodies on
the host tissue. Often the conidial or pycnidial stage is produced on the host. The pycnidia are
dark brown, and ostiolate. The pycnidiospores are elliptical, thin walled, single celled and
hyaline.

Perpetuation:

The fungus is a facultative parasite that survives in infected seed, many leguminous and
other hosts and in diseased plant debris left in the soil. The sclerotia and pycnidiospores are
disseminated by wind and cause further spread of the pathogen.

Control measures:

1. All debris from previous crop should be destroyed.

2. Use of disease free seeds.

3. Seed treatment with thiram or captan @ 4 g/kg of seed.

ii) Rhizome rots of ginger and turmeric

In India, average yield reduction in ginger due to rhizome rot ranged from 5 to 15 per cent. In
severe incidence, losses reported are as high as 50 to 80%.

Symptoms :

The tips of the leaves turn yellow that proceeds downwards resulting in drying and
withering of leaves. Further, the infection proceeds to the shoots. The affected rhizomes turn
pale. The portion just above the ground level becomes watery and soft. The rhizomes gradually
rot and decompose. The roots arising from these affected rhizomes also undergo rotting. The
disease is carried through rhizomes. The disease is aggravated by the infection of rhizome fly.
Causal organism - Pythium myriotylum P. aphanidermatum and other Pythiwn spp. Etiology :

The mycelium is hyaline, coenocytic and freely branching. Sporangia are terminal or
intercalary. Zoospores are formed in vesicle developed from sporangium. Zoospores are
reniform, laterally biflagellate. Sexual reproduction is by gametangial contact resulting in
formation of oospores, which are slightly yellowish and thick walled.

Perpetuation :

The pathogen is soil borne and survives in soil in the form of oospores or diseased
rhizomes also carry inoculum (dormant mycelium) to the field. In the field, disease spreads to
adjacent clumps mostly through irrigation water.

High soil moisture, temperature (25 to 28°C) and poor drainage are conducive for disease
development.

Control measures :

1. Crop rotation
2. Use of disease free planting material (rhizomes).
3. Growing turmeric and ginger crops in light soils with good drainage.
4. Use of disease free rhizomes for planting.
5. Apply Trichoderma bioagent @ 5-6 kg/ha (talk based) by mixing in to sufficient quantity
of well decomposed FYM or compost.
6. Dip rhizomes in fungicidal solution of metalaxyl MZ - 72 or thiram 75 WP or captan @
25 g/10 L water or in Bordeaux mixture (1.0%) for 30 – 40 minutes before planting.
7. Drench the soil once on seeing the initial symptoms of the disease with captan or copper
oxychloride or metalaxyl (0.25%) or Bordeaux mixture (1.0%) at the root zone @ 4-5
litre/ sq.m.
8. Spray the crop with metalaxyl MZ - 72 or fosetyl AL (0.25%) Bordeaux mixture (1.0%)
at 2-3 weeks interval soon after emergence.
9. Early planting in Mayor June results in to less disease incidence.
10. Use of resistant varieties, i.e., turmeric varieties PCT - 13 and PCT -14 are resistant to
this disease.
EXERCISE NO. 12
STUDY OF SCAB OF POTATO AND CLUB ROOT OF CRUCIFERS

I) SCAB OF POTATO

Symptoms :

Two types of lesions viz.. a) shallow and b) deep lesions are formed.

In shallow scab, tubers show superficial rough area, which is sunken and rarely raised as
compared to the normal surface. Lesions consist of corky tissues, which arise from the abnormal
proliferation of cells of tuber peridium.

In deep-seated scab, lesions are 1-3 mm in depth and are darker. Entire tuber surface
becomes corky and rough, which seriously reduces the market of the tubers,

Causal organism: Streptomyces scabies

Etiology :

The pathogen is actinomycetes possessing characters of both, fungus and bacteria, It is


filamentous that is often assuming fungal appearance and about 0.2 μm in diameter. Spores are
formed in chain on the filament, which are chief source of reproduction. Bacterium is Gram
positive and aerobic.

Perpetuation :
Bacterium is basically soil inhabitant that gets displaced through movement of soil by wind,
water and cultural operations. Infected tubers play main role for spread of the disease on large
area.

Entry of the bacterium is through lenticels, stomata, wounds and directly through

the cuticle.

Optimum temperature for disease development is 20 to 22° C and the pH range is 5-8. The
pathogen is more active in dry soils. In sandy soil, the disease incidence is more.

Control measures :

1. Use disease free tubers. Tubers with deep lesions should not be used for seed
2. Tuber disinfection by dipping for ten minutes in 0.10 per cent suspension of an
organomercurial fungicide such as Emisan-6, Agallol-6 or Aretan.
3. Application of elemental sulphur to soil to reduce pH
4. Keeping the field well irrigated from the fifth week after planting up to the ninth week
reduces infection successfully
5. Green manuring with soybean before potato season.
6. A rotation of four years avoiding beet, fleshy rooted crucifers and carrot, whichare
susceptible to this pathogen. Take cultivation of soyabean in crop rotation.
7. Use of resistance varieties - red skin varieties like Kufri Sindhuri and some hybrids
So1anum andigena X S. tuberosum
8. Application of antagonistic bacteria, such as Bacillus subtilis

II) CLUB ROOT OF CRUCIFERS

Symptoms :

The above ground plant parts show stunting, reduction in the size of the head, or chlorosis and
other general non-specific unhealthy symptoms. When such plants are pulled out and the roots
are examined, the characteristic club-root symptoms may be seen. The roots are malformed into
club-like structure, due to thick fleshy growth of the roots. In general, the root tips are
malformed, leaving the basal portion of the root mostly normal. Malformed tissues may rot and
turn black due to secondary- organism like bacteria.

Causal organism : Plasmodiophora brassicae Woronin.


Etiology :

The vegetative structure of the fungus is a plasmodium. It is a multinucleate naked


protoplast. The plasmodia are always formed within the host cell. The fungus produces
numerous resting spores inside the host cells by division of the plasmodium into uninucleate
portions. When resting spores germinate, they produce anteriorly biflagellate zoospores those are
naked, devoid of cell wall with uninucleate protoplasm, irregular or amoeboid in shape. The
resting spores are capable of germinating immediately after formation and may be viable for two
to three years. It is an obligate endoparasite. Temperature, moisture, soil reaction (pH rang 5.0 to
7.0) and aeration play an important role in the development of the disease.

Perpetuation :

The disease is soil-borne. The spores can live in the soil for 2 to 3 years.

Secondary infection by zoospores.

Control measures :

1. Eradication of Cruciferous weeds from around the field.


2. Usse of well drained disease free plots.
3. Use of seedlings raised in disease free soil.
4. Very long rotations avoiding any type of cruciferous crop.
5. Soil fumigation with Vapam (2-2.5 litre/ten sq.m) or methyl bromide 0.5 to 1 kg/l0 sq. m
or formalin 3-4% @ 10L/m2, two week before planting).
6. Raising the soil pH to 7.2 by adding lime (hydrated lime) six weeks before planting, a
soil with pH 5 may require about 2.5 tons of lime/ha.
7. Soil drenching with a systemic fungicide, benomyl (Benlate).
8. Seedlings dip treatment in solution of benomyl or carbendazim or thiophanate methyl
(0.5 %) for 15 to 20 minutes before transplanting.
EXERCISE NO. 13 & 14

STUDY OF DISEASES CAUSED BY BACTERIAL

I) BLACK ROT OF CRUCIFERS

Symptoms :

In the seedling development from infected seed, the first lesions appear mostly on the
cotyledons. The lesions enlarge and coalesce. Cotyledons turn yellow to black, wilt and drop
prematurely. Severely affected plants become stunted and the leaves defoliate prematurely. The
most common symptom in the field is the 'V-shaped' yellowish necrosis on the leaflet, which
turns black showing discolouration of the vascular bundles. The infection is systemic.

Causal organism : Xanthomonas axonopodis pv. campestris (Pammel) Dowson. Etiology :

The bacterium is short rod, monotrichous, producing yellow pigment, Gram negative,
capsulated, non-spore former and is a facultative saprophyte.

Perpetuation :

Primary source of infection is through the plant residues and the seed. Secondary spread
is through irrigation water, wind, implements and tools.

Control measures :

1. Field sanitation and crop rotation.


2. Use disease free seed.
3. Seed treatment with 0.1 per cent Mercuric chloride solution for 30 minutes is effective in
eradicating the surface borne bacteria.
4. Hot water treatment of the seed at 50° C for 30 minutes is effective in killing both
internally and externally seed borne pathogen.
5. Spray the crop with streptomycin sulphate (150-200ppm) + copper oxychloride (0.25%).
First spray should be given when the crop is 5-6 weeks old. Subsequent sprays at an
interval of 15 days.
6. Use of resistant varieties if available.

II) RING ROT OR BROWN ROT OF POTATO

Symptoms :

The characteristic symptoms of the disease are yellowing and wilting of the foliage.
Plants show stunting. They may later collapse. In the brown rot phase, xylem tissues become
brown. In the tuber, a brown ring due to discolouration of vascular bundles is seen. Skin of the
tuber may be discolouredand in case of severe infestation, the eye buds become dark.

Causal organism : Pseudomonas solanacearum E.F. Smith

Etiology :

The bacterium is rod shaped with mono or lophotrichous flagella, Gram negative, non-
acid fast.

Perpetuation :

The primary infection takes place through diseased tubers and soil or infected plant
debris. Secondary infection is through water. The bacterium enters through stomata and wounds.

Control measures :

1. Use healthy potato tubers for planting.


2. Follow crop rotation to avoid potato, tomato and eggplants in the field for not less than
two and preferably three years. E.g., a) Wheat-Green manure crops, b) Corn-Soybean,
etc.
3. Dip the seed potato in Streptocycline 200 ppm for 30 min before planting.
4. Sterilize the cutting knife frequently.
5. Chemical and non-chemical control of root knot nematodes,
6. Proper drainage should be maintained,
7. Infected crop debris should be destroyed,
8. Highly susceptible varieties (Kufri Jyoti) should not be grown in endemic areas,
9. Use resistant varieties - Culture BRB/ A-24 of S. tuberosum x S. microdontum resistant
to bacterial wilt and brown rot.

III) SOFT ROT OF VEGETABLES

Soft rot bacteria attack vegetables such as carrots, potatoes, onions, beans, spinach, celery, etc.
The disease is more common in transit, storage and market than in field.

Symptoms :

Soft, water-soaked, irregular lesions appear on the tubers. First, these lesions are more or
less superficial but soon they spread covering the inner tissues. The foliage may remain green
until the disease in the tuber advances considerably. Wilting occurs only when the tuber is more
or less completely rotted. The pathogen may be carried on the tuber from the field to the storage
place, where it spreads rapidly, entering the tubers through incidental wounds and bruises caused
in transit. Once inside the tuber, bacteria multiply rapidly, causing damage to the entire harvest.
The damage caused by the bacterium is relatively more in soils with pH above 6 than in acid
soils. On leafy vegetables, similar kind of spots, i.e., soft, water-soaked, irregular patches appear
that result in to rotting of leaves.

Causal organism : Erwinia caratovora (Jones) Holland.

Etiology :

The bacterium is Gram-negative rod with peritrichous flagella and produces no spores or
capsule. It enters the host through wounds.
Perpetuation :

The bacterium lives saprophytically on dead and succulent plant tissues in soil.

Control measures :

1. Avoid injury to tubers and other produce during harvesting, transit and storage.

2. The diseased tubers should not be stored with healthy ones.

3. Use only healthy tubers as seed material.

4. Keep the stores dry, well ventilated and cool.

5. Remove the plant debris and tubers from the field after harvest and destroy them.

6. Avoid wetting of leafy vegetables after harvesting.

IV) BACTERIAL BLIGHT OF BEANS

Symptoms :

The disease is characterized by irregular sunken, red to brown leaf spots surrounded by
yellow halo. Several spots coalesce to form irregular patches causing the distortion of leaf,
shriveling and cause premature defoliation. Cankerous spots are observed on pods.

Causal organism : Xanthomonas axonopodis pv. phaseo!i (E. F. Smith) Dowson.

Etiology :
The bacterium is rod shaped with single polar flagellum, Gram-negative, aerobic, non-
spore former.

Perpetuation :

Primary source of infection is through seed and infecieu pianl paris. SeconualY spread of
infection is through wind, water.

Control measures :

1. Use healthy seed.

2. Field sanitation.

3. Crop rotation.

4. Spray the crop with Streptomycin sulphate (150 - 200 ppm) + copper oxychloride (0.25%) at
an interval of 15 days.

V) BACTERIAL WILT OF SOLANACEOUS CROPS

Symptoms :

The first symptom of the disease in the field is dwarfing of plants and bronze
discolouration of the leaflets. The characteristic symptom of the disease is sudden wilting of the
plants. If the diseased plant is cut across in the stem, white bacterial ooze may come out and the
xylem vessels are seen discoloured dark brown. The bacterium is mainly confined to the vascular
region but in advanced cases. it may invade the cortex and pith regions and cause discolouration
of the tissues.
Causal organism : Ralstonia solanacearum

Etiology :

The bacterium is rod shaped with mono or lophotrichous flagella, Gram-negative, non-
spore former.

Perpetuation :

Primary infection is through infected plant materials, seeds and soil. Secondary infection
by means of bacterium present in soil.

Control measures :

1. Selection of disease free seed material.

2. Follow crop rotation with non-solanaceous crops for at least 2 to 3 years in the field.

3. Spray the crop with Streptocycline 200 ppm + copper oxychloride (0.25%) at an interval of 15
days.

4. Use of resistant varieties:

a) Tomato - Arka Alok, BWR-1, SUN- 7610 etc.

b) Brinjal - Sawarna Prabha, Arka Nilkanth, Arka Keshav, SM-6-6, etc.

EXERCISE NO. 15 & 16

STUDY OF DISEASES CAUSED BY VIRUSES AND PHYTOPLASMA

VIRAL DISEASES
I) Mosaic of potato, tomato and beans

i) Mosaic of potato

In India, latent or mild mosaic, rugose mosaic and crinkle are important.

Mild mosaic

It is caused by Potato virus viz., potato mottle virus or potato mosaic virus or PYX
(Solanum virus-I).

Symptoms :

lnterveinal mottling or mosaic symptoms appear on leaves. Under favourable growth


conditions of the host, the symptoms are masked thus, making the recognition of the disease
difficult. There is little dwarfing of the plant or deformation of the foliage, Button flower plants
or wild chilli are the local lesion hosts of potato viruses.

The virus also infects tomato, Datura, tobacco, Solanum nigrum, etc.

It is transmitted by sap inoculation, contact between healthy and diseased plants, diseased
seed stock and cutting knives.

b. Vein banding severe mosaic :

Varietal reactions vary from mild mosaic to severe mosaic and necrosis of veins followed
by leaf drop. The affected plants are stunted and the size and number of tubers are reduced.
Solanum demissum is a local lesion host.

It is transmitted by sap and aphids Myzus persicae, Aphis gossypii

c. Rugose mosaic of potato :


It causes very serious damage to individual plant. The foliage is not only mottled

but it is severely wrinkled, puckered and markedly reduced in size, The leaflet margins are rolled
downwards and the entire plant is severely dwarfed. The lower leaves generally have black
necrotic veins. It is caused by potato virus X and potato virus Y (vein-banding virus). In severe
cases, the plant may die before producing any tuber.

Germination of diseased tubers is reduced by 20 per cent.

The rugose mosaic is transmitted by small tubers from diseased plants and vector Myzus
persicae

d. Crinkle of potato: \
It is caused by combination of potato virus X and potato virus A. The yellowish patches on the
foliage are bigger and more prominent. As death approaches, this colour becomes more
pronounced and accompanied by rusty brown spots, beginning near the tip of the leaves. The
foliage is brittle and easily injured.

The crinkle is transmitted by diseased tubers, sap-inoculation (transmits Potato virus -X)
and Myzus persicae transmits Potato virus-A

Control measures :

1. Use disease free seed tubers.

2. Control of vectors by application of granular insecticides viz. Phorate 10 G @ 10-15kg/ha or


spray with any insecticide.

3. Rouge out sick looking plants as and when located.

4. De-top plants in the third or fourth week of December.

5. Use large sized potatoes for planting.

ii) Mosaic of tomato

Several viruses incite mosaic diseases in tomato. They are

1. Tobacco mosaic virus (TMV)


2. Cucumber mosaic virus (CMV)

3. Potato mild or latent virus. Also potato vein banding virus.

4. Tobacco acuba mosaic virus

a) Tobacco mosaic virus (TMV) :

Mottling with dark green areas and some distortion and stunting of leaves are common
symptoms. The mottling of leaves is very severe under conditions of high temperature and
intense light. At low temperature and low intensity, mottling is masked but stunting and
distortion of leaves (leaf blade reduced to fern like) as well as production or anthocyanin the
stem is prominent. Yellow chlorosis, necrosis and distortion of fruits, necrosis of stem and leaf
are also common symptoms. It has longest longevity among all plant viruses known so far. It
remains active in plant juice up to 25 days at room temperature.

b) Primary source of infection:

Plant debris of infected pi ants and certain manufactured tobacco products.

Tobacco mosaic virus is seed transmitted in tomato.

c) Tobacco acuba mosaic virus:

It is caused by a strain of tobacco mosaic virus (TMV).

Downward curling of the whole leaf with slight turning down at the margins can be easily
noticed. Surface of the leaf is rough, wrinkled or corrugated. Chlorosis starts as small pinpoints
of yellow areas and gradually spreads. Leaves become pale yellow or white. The plant is not
killed but the growth is checked and there is stunting.

The virus can withstand 98° C for 10 minutes and dilution upto 1:1000,000. The virus in
extracted sap remains active after storage of 77 days.

d) Cucumber mosaic virus:


Sometimes affects the tomato crop. Shoestring like foliage dwarfing of plant, necrotic
streaks and fruit distortion are the major symptoms. It is aphid borne but short lived and persists
in perennial weed hosts.

Transmission :

Mechanical means such as contaminated hands of workers during transplanting, staking,


training, and contact through man, animal and machinery during interculturing operations.
Vector Mvzus persicae transmits the disease from tomato to tomato and to tobacco.

Control measures :

1. Avoid soil, which is likely to contain infected debris.

2. Use seed from disease free plant.

3. Seed treatment: The tomato seeds are to be soaked ion the solution of trisodium phosphate (90
g/L water) for 15 minutes followed by 3-4 washings in clean water, drying in shed and treatment
with fungicides.

4. Take care to eliminate chances or spread through man, animal and machinery.

5. Avoid chewing of tobacco and thorough washing of hands of workers with soap while
working.

iii) Mosaic of bean

Virus : Bean mosaic virus, Yellow bean mosaic virus or Bean virus-1, Bean virus-2

RNA-a) Bean common mosaic-cowpea, cluster bean, soybean, etc.

DNA-b) Golden mosaic (Gemini virus)- field bean, horse gram, etc.
Symptoms :

Infected leaves show yellow and green patches of irregular size on the leaf lamina in
mosaic fashion. Pods generally show no signs but under certain conditions, chlorosis of
immature pods is noticed. The plant growth is reduced, blossom tends to drop and pods are
shorter than normal.

Transmission :

a) Common mosaic: by Aphis sp.

b) Golden mosaic and Yellow bean mosaic: by white flies (Bemisia tabaci).

Bean common mosaic is also transmitted by infected seed.

Control measures :

1. Use seed from disease free plant.


2. Remove and destroy the infected plants.
3. Grow resistant varieties.
4. Control of insect vectors by spraying proper insecticides, e.g., diamethoate or endosulfan
(0.03 - 0.05%) + Neem oil 0.5% 3 times at interval of 10-15 days.
II) Enation mosaic of pea

This virus disease of pea is easily identified by small outgrowth i.e. enation on

lower surface of some leaves.

Symptoms :

The initial symptoms appear on younger leaves and stipules as indistinct light green and
dark green mottling, which becomes more evident as the disease progress. There is only slight
vein clearing. In < some varieties, necrotic lesions are also found. Terminal growth of plant is
checked, puckered, twisted or curled with shortening of the internodes below. Finally, tip of the
plant looks like rosette. Leaves on the branches are deformed. Diseased plants do not usually
bear pods but if they are formed, they contain only small yellow seed.

Causal organism : Pea Enation Mosaic Virus (PEMV) also known as Pea virus. Transmission :
Sap transmissible with difficulty. Also transmitted by aphid vectors such as
Macrosiphllm pisi and M solanifolii.

Control measures :

1. Collection and destruction of affected plants.

2. Control of vector i.e. aphid by spraying the crop with insecticides.

III) Yellow vein mosaic of Bhendi/okra

Symptoms :

Infected plants are stunted. The leaves are reduced in size and often curled. All veins and
vein lets turn yellow while, entire leaf lamina remains green. Most of the affected leaves show
thickening of veins on the lower side of the leaves. The fruits produced on diseased plants are
small, pale in colour and often defonned.

Causal organism : Yellow vein mosaic virus.

Transmission :

Under artificial conditions it can be transmitted by grafting,

Vector - whitefly, Bemisia tabaci and the okra leaf hopper Empoasca devastans.

Wild plant hosts - Cruton sparsiflora, Malvasirum tricuspidatum and Ageraium sp. Control
measures :

i. Rouging diseased plants during early stage of plant growth.


ii. Destruction of weed and wild host plants and other malvaceous plants viz., Hibiscus
abelmosches, H. tetraphyllus, Althaea rosea.
iii. Use of resistant varieties like Phule Utkarsha, Varsha Upahar, Janardhan, Haritha, Arka
Anamika, and Arka Abhay.
iv. Protection of the crop from white fly and leaf hoppers by spraying/soil application of
insecticides.
v. Soil application of Thimet granules (10 kg/ha.), once at the time of planting
vi. Sprays with phosphomidon and dichlorovos (3.5 ml each in 10 lit. water) or spray the
crop at every 10 days interval with dimethoate 0.05% or endosulfan 0.06% (3 sprays).
vii. First spray - Within 7 days after emergence of the plants, and subsequent sprays at 10 to
15 days interval.
IV) Pea top necrosis

Symptoms :

The infected plants exhibit withering of the top wherein, necrosis and grayish brown
discolouration of leaves, petioles and stems occur. Internally, the host tissues are highly
necrotized. Severely infected pea plants die prematurely whereas; plants with mild infection
develop malformed pods with wrinkles or even abortive seeds.

Causal organism : Virus

Perpetuation :

The virus is transmitted by mechanical sap inoculation and by wedge or cleft grafting.
Transmission through seed is up to 13 per cent. The nematode, Trichodorus spp. also transmit
the virus.

Control measures :

1. Use virus free seed.

2. Soil application of nematicides.

V) Leaf curl diseases

Leaf curl of chilli

Symptoms :

The diseased plants show curling of leaves, intensive reduction in leaf size, short
internodes and dwarfing. These symptoms produce witches-broom effect causing failure in fruit
settings. If fruits set, they are usually small and deformed.

Causal organism - Chilli leaf curl vims.


Transmission : White flies and thrips

Severe reduction in leaf size and curling of leaves is usually brought about by toxic
effects of thrips, Scirtothrips dorsalis. The disease is also transmitted by white fly Bemisia
tabaci.

Control measures :

i. Eradication of affected plants at an early stage of crop growth.


ii. Three sprayings with 0.1 % monocrotophos, dimethoate, endosulphan, or
metasystox.
iii. Application of thimate / phorate @ 10 kg/ha at seed sowing in nursery and
10-15 days after transplanting to control the vectors.

PHYTOPLASMA DISEASES

i) Little leaf of brinjal

Symptoms :

The diseased plants show reduction in leaf size that becomes thin, soft and pale green in
colour. Auxiliary and latent buds are stimulated to grow and internodes are shortened. The
affected plants become bushy and can be easily recognized. In heavily infected plants, flower
and fruit setting is negligible wherein, phyllody of flowers are very common.

Transmission :

The phytoplasma is not transmitted through sap or by the mechanical methods of


inoculation. It spreads in nature by leaf hoppers, Eutettix phycitis and Empoasca devastans. The
disease is graft transmissible and can be transmitted to tomato and tobacco.

Perenllation through weed hosts occurs in nature on Daturafastuosa and Vinca rosea.

Resistant varieties : Use of resistant/moderately resistant/tolerant cultivars - Varieties such as


Pusa Purple Cluster, Arka Sheel, Aushy, Manjari Gota and Banaras Giant found moderate
resistant to resistant. Tolerant cultivars are Black Beauty, Brinjal Round and Surati.
ii) Aster yellow

It is an important phytoplasma disease of onion.

Symptoms :

The characteristic symptoms of the disease are yellowing (chlorosis) and stunting
(dwarfing), abnormal production of shoots, sterility of flowers, malformation of organs and
general reduction in quality and quantity of yield.

Trausmission :

Vector - leaf hopper (Macrosteles fascilerous). Virus is also transmitted by budding, grafting and
by dodder (Cuscuta campestris).

Phytoplasma survives in perennial ornamental, vegetable and weed plants.

Control measures :

1. Uprooting and destruction of infected plants in early stage of growth.


2. Planting of new crop only when diseased plants in the field and its neighbourhood have
been removed,
3. Phorate application @ 20 gibed of 2 x I m size.
4. Dipping of the seedlings in metasystox (0.05%) + tetracycline (200 ppm).
5. Destruction of the weed Datura spp.
6. Use of antibiotics like tetracyclines to suppress the disease symptoms.
7. Vector control by sprays with insecticides viz., metasystox or malathion or
monocrotophos @ 0.05 per cent
EXERCISE NO. 17

STUDY OF PHANEROGAMIC PLANT PARASITES AND

DEFICIENCY DISEASES

A) PHANEROGAMIC PLANT PARASITES

Although fungi, bacteria, viruses and nematodes cause most of the plant diseases, there
are few seed plants also called as flowering plants (Phanerogams) which are parasitic on crops or
plants. The flowering plants attack valuable crops and trees causing considerable loss as some of
these parasites attack roots of the host, while some are parasitic on the stem. Some are devoid of
chlorophyll and depend entirely upon their hosts for food supply while, some have chlorophyll
and obtain only the mineral constituents of food from the host.

The common flowering parasites may be grouped as follows:

1. Stem parasites:

a) Entirely dependent (Complete parasite), e.g., Cuscuta (dodder).

2. Root parasites:

a) Entirely dependent (Complete parasite), e.g., Orobanchae.

1) Dodder (Love vine, Amarvel, Cuscuta spp.)

These are non-chlorophyllus, leafless parasitic seed plants. The vines are yellow, orange or pink
in colour. They entwine stem of the host. The leaves are represented by minute functionless
scales, which are evident on close examination. When the stem of the parasite meets the host,
minute root like organs called haustoria, penetrate into the host cortex and serve as an organ of
food absorption. When the relationship with the host is firmly established, the dodder plant
looses the contact from the soil. The flowers are found in clusters. They are tiny, white, pink or
yellowish in colour. The seeds are formed in the capsules.
The seeds germinate just like the seeds of other plants. Usually, their germination occurs
few days after the germination of the seed of host plant in the field. A young seedling of the
parasite is a slender, yellowish, unbranched thread like. The open end is raised into a vertical
position and growing tip moves in a circle in search of suitable host. When a support comes in
contact, the young stem begins to entwine around it. .

The common dodder (Cuscuta gronovii) attacks clover, alfalfa, berseem, flax and many
other crops. It also attacks ornamental and hedge plants. It is a fast developing parasite and
within 2-3 seasons may destroy the complete plant.

The dodder perpetuates through seeds, which remain dormant in the soil until favourable
season returns. Stem portion of the parasite is also means for perpetuation.

Control measures :

1. Selection of dodder free seeds for sowing.


2. Preventing the movement of grazing animal from infected to clean fields.
3. Restricting the flow of irrigation water through infected area.
4. Destruction of the parasite by burning before seed fonl1ation.
5. Fallowing or rotation should be taken with anon-host crop like sweet maize.
6. Use of weedicides like butachlor or fluchlorazole at proper concentration.

2) Broomrape (Orobanchae)

Orobanchae spp. are complete root parasite affecting tobacco, brinjal, tomato, cabbage,
cauliflower, cotton, turnip and many other solanaceous and cruciferous plants. It is especially
destructive to tobacco and brinjal. In India, Orobanchae aegyptiaca is commonly observed.

The parasite consists of a stout, fleshy stem, 20 to 40 cm long. This stem is pale yellow or
brownish red in colour and is covered by small, thin and brown scaly leaves. The flowers
appearing in the axils of leaves are white to blue violet and tubular. The seeds are very small,
black in colour and may remain viable in the soil for several years.

The haustoria of the parasite penetrate into the roots of the host and draw its nourishment.
A large number of parasites may arise around the stem of the host plant. When the host is
carefully uprooted, the parasitic roots are seen entangled with the host root system. Because of
the drain of the food supply, the growth of the host is retarded and they later remain stunted and
sometimes may die.

Control measures :

1. Destroy the parasite before flowering by physical removal and burning. I f the seeds have
been formed and shed in soil, it becomes difficult to eradicate the parasite.
2. Long dry period during summer may heir in reducing the soil population of the seed.
3. Long crop rotation may be followed.
4. Spraying of the soil with 0.25% copper sulphate solution.
5. Sun hemp is potential trap crop of orobanchae.
6. Biological control: An insect viz.. Phytomyzia orobanchia that feed only on orobanchae
and in absence of host can remain in diapauses for a period of three years. Laboratory
multiplication of this pest can be effective. This fly can senseorobanchae in the vicinity
of 3 km. release of this pest can be effective in controlling parasite.
7. Fungi like Fusarium orobonchae and Clerocinia spp. also cause diseases of orobanchae
and can be used as biological control agents.

DEFICIENCY DISEASES

Black heart of potato

Black heart is an important storage, transit and market disease of potatoes. It is due to
unfavourable oxygen relations. The disease usually occurs in tubers stored in poorly ventilated
rooms and closely packed conditions. A set of three different environmental conditions can cause
this disease viz.,

1) Poor ventilation in storage,


2) High temperature (> 37°C) during transit and

3) High temperature (> 37°C) of the soil during growth and maturity in the field.

Dark grey to purplish or black discolouration occurs in-the central tissues of the tubers.
In advanced stages, the affected tissues may dry out and separate thus forming cavities. The
discolouration may be extended to the surface. Large size tubers are more susceptible to black
heart.

Control measures :

1. To avoid the disease, the tubers should not be stored or transported at temperature above
37°C.
2. Storage of tubers should be made in well-ventilated room and the bags of tubers should
not be piled very high upon each other.
3. Heap covering with grass in pit can check black heart of potato.
4. Storage of potatoes in cold storage.

2) Blossom end rot

It is a physiological disorder. Blossom end rot begins with light tan, water soaked lesions
which then enlarge, turn black and leathery and often become over run with secondary black
mold. The disease generally occurs at-the blossom end of the fruit. However, it can occasionally
occur at the side, and sometimes it produces an internal black lesion not visible from the exterior
of the fruit. Fruit affected by blossomed rot ripens more rapidly than normal.

A localized calcium deficiency at the distal end of the fruit results in blossom-end rot.

Control measure :

1. Liming with dolomites or high calcium limestone 2-4 months before planting can reduce
blossom-end rot.
2. During the growing season, foliar sprays of anhydrous calcium chloride may be helpful.

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