PAT 303 e Notes 2022
PAT 303 e Notes 2022
COURSE TEACHERS
Dr. P.V.Patil, AC, Dharwad
Dr. M.S.L.Rao, AC, Dharwad
Dr. R.L.Ravikumar, AC, Hanumanamatti
Dr. S.M.Vastrad, AC, Vijayapur
Dr. Prema G.U., AC, Vijayapur
Diseases of Wheat
Symptoms
The first symptom of rust infection is flecking of leaves, leaf sheaths, culms and floral structures.
These flecks soon develop as oblong, reddish brown uredo-pustules, frequently merging into one
another, finally bursting to expose a mass of brown uredospores. When large number of uredosori
burst and release their spores, the entire leaf blade and other affected parts will have a brownish
appearance even from a distance. Later in the season, teleutosori are produced. They are
conspicuous, linear or oblong, dark brown to black, and often merging with one another, to cause
linear patches of black lesions, which account for the name black rust. On maturity the teleutosori
burst open, exposing masses of dark brown teleutospores. In the transitional stage, there is a
mosaic of brown and black masses of spores on the affected tissues, which dry up prematurely.
Moreover, in the case of severe infections the diseased plants are stunted and produce small
spikes and shrivelled grains, or no grain at all.
Pathogen
Black stem rust is heteroecious full cycle rust. It requires more than one host species to complete
its life cycle. The uredial and telial stages occur on wheat, barley and some grasses and the
pycnial and aecial stages on the species of Berberis (Barbery) and Mahonia, the alternate hosts.
The uredospores are brown, oval shaped, thick walled and marked with thin short spines and
borne singly on stalks. The teleutospores are dark or chestnut brown, two celled, germinating by
producing thin walled, hyaline four celled promycelium (basidium). The fungus is highly
specialized and has number of physiological races (over 250). Races 11, 15c, 34-A and 122 are
most predominant appearing in virulent form in wheat growing tracts of India.
Disease cycle
Primary infection is mainly through barberry, i.e., Berberis vulgaris. These barbery plants play a
role in USA, Europe and Australia, where as in India they are not known to play any role in the
perpetuation of the fungus. The source of inoculum for black rust comes from south, i.e., Nilgiri
and Pulney hills. In plains of North India during summer months the uredospores cannot survive
because of the high temperatures. The possibilities of the fungus surviving on ratoon tillers or self
sown wheat plants, late and off season wheat crops and certain grasses growing in cool areas
particularly in the foot hills of Himalayas in the North, the Nilgiris and Pulney hills in the South
appear to be great.
The grasses, viz., Briza minor, Bromus patula, Brachipodium sylvaticum and Avena fatua, harbor
the fungus in the off-season. It is believed that the fungus over summers on the wheat plants and
grasses in the hilly areas and spreads to the plains in the main wheat crop season. In the central
Nepal, the wheat crop sown in August and harvested in December, January becomes infected by
P. graminis tritici from October. This may be a source of inoculum for the main crop sown in the
plains, which becomes infected from February each year.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management
Eradication of self sown wheat plants and weed hosts
Adjust time of sowing
Grow resistant varieties like Kalyanasona, Sonalika, Choti Lerma, Lerma Rojo, Safed
lerma, NP 700 & 800.
Avoid late sowing
Balanced application of nitrogenous fertilizers
Seed dressing with [email protected]% followed by two sprays with the same chemical.
Spray twice or thrice with [email protected]% or [email protected]% or [email protected]% , at
15 days interval.
As the disease advances, the telial stage may be found in the same pustule. The telia are small,
oval to linear, black and covered by the epidermis. The telia are also found on the leaf sheath.
Severe rusting of leaves causes reduction in yield.
Pradesh, Haryana, U.P, and parts of Rajasthan and Bihar. It is totally absent from South India
except in Nilgiris and Pulney hills. It appears every year, but the damage is seen only in
occasional years. Sonara-64 is susceptible to yellow rust.
Symptoms
The uredosori appear as bright yellow pustules chiefly on the leaves. But in severe infections they
may be seen on leaf sheaths also. The sori are elongated and are arranged in linear rows between
the veins of the leaf and hence it is referred as stripe rust. The sori are mostly sub-epidermal and
are remained covered by the epidermal layer and break only at the time of crop maturity. The
teleutosori appear late in the season and are also arranged in linear rows. They are compact,
elongated, and black which remain sub- epidermal. They do not break through epidermis for a
long time remaining as black crust.
The symptoms are evident only at the time of emergence of the panicle from boot leaf. All the
spikelets in a panicle transform into a mass of black powdery spores. The infected panicle
emerges two days earlier than healthy and the spores are covered with the silvery membrane. This
thin membrane gets ruptured exposing the mass of black spores. The spores are easily blown by
wind leaving the bare rachis.
Pathogen
Chlamydospores of the fungus are pale, olive brown, spherical to oval in shape. These smut
spores germinate and produce promycelium or sporidium. The promycelial cells fuse and give rise
to germ tubes that enter the ovary through the stigma and become established in the embryo
remaining dormant until seed germination.
Disease cycle
It is internally and externally seed borne and is systemic. The fungus is carried over in the seed as
dormant mycelium. When the planted seed germinates the mycelium becomes active. It grows
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
along with the plant and when the panicle is produced the mycelium reaches the ovaries and
transforms the ovaries into a mass of black smut spores. Secondary spread occurs through wind
borne smut spores. The sporidia infect the healthy flowers. The mycelium enters the ovary and
remains in the seed as dormant mycelium.
Management
Grow resistant varieties kalyanasona, PV 18, WG 307 and HD 450.
Hot water treatment (Jensen, 1908): Soak the seed in cold water for 4 hours and then
immerse the seed in hot water at a temperature of 132 0F or 520C for about 10 minutes. Dry the
seed in shade before sowing.
Solar seed treatment (Luthra and Sattar, 1934): Soak the seed in water for 4 hours (8 AM
to 12 Noon) and expose the seed to the hot sun for 4 to 5 hours (from 12 Noon to 5 PM) on
cement or rocky surface. This can be practiced in the areas where the summer temperatures are
high (42-440C)
Anaerobic seed treatment (USA): Soak the seeds for 2-4 hours in water between 60- 700F
and keep the moist seeds in air tight containers for 65-70 hours and there after dry the seed.
Seed treatment with systemic chemicals like [email protected]% or [email protected]%
Karnal bunt Neovossia indica (formerly Tilletia indica)
Economic importance
The disease was first reported in India from Karnal (Haryana) by Mitra in 1931. The disease was
less severe till 1970’s, however it assumed greater importance in early seventies with the adoption
of high yielding, semi dwarf nutrient responsive varieties. The disease appeared in epidemic form
in different parts of India in 1976, 1979, 1981-83 and 1986.
Symptoms
The infection is usually confined to a few grains in the spike with irregular arrangement. In some
cases the infection may spread to only a part of the grains. In severe cases, the grain is reduced to
black shiny sac of teliospores. As the grains mature the outer glumes spread and the inner glumes
expand, exposing the bunted grains. The bunt balls are first enclosed by the pericarp but when it
bursts the masses of bunt spores are exposed. The bunt affected plants emits a foul smell which is
mainly due to the presence of Trimethyl amine.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Pathogen
Teliospores are smooth walled measuring 22-49µ in diameter and require a long resting period.
Teliospores germinate and produce a large number (60-120) of needle shaped primary sporidia on
a short stout basidium. Later, sickle shaped (allantoid) secondary sporidia are produced which
help in the dispersal of karnal bunt.
Disease cycle
The teliospores in soil germinate producing primary sporidia. The sporidia become air borne and
deposit on leaves of host plants. Under high humid conditions they produce a secondary crop of
secondary sporidia (allantoids). If boot emergence stage coincides with drizzle, the secondary
sporidia get washed down to sheath. The sporidia germinate on glumes to enter epidermal cells to
penetrate ovary. The sporidial germ tubes penetrate stomata in rachis, glumes, lemma and palea.
The disease progresses systemically to other florets within an infected spikelet. The infection
mostly starts from the embryonal end and spreads along the grain suture. The hyphae grow
through the base of the glumes into sub-ovarian tissue and enter pericarp through funiculus.
Hyphae of the pathogen proliferate, remain restricted to pericarp and produce teliospores
terminally. In severe cases grain is reduced to black shiny sack of teliospores. The embryo and
endosperm are not colonized. The pericarp ruptures during threshing and teliospores deposit in
soil and adhere to the surface of the seed.
Favourable conditions
Moderate temperatures (19-230C), high humidity (>70%) and cloudiness or rainfall during
anthesis favours disease development in susceptible host varieties.
Management
Grow tolerant varieties, viz., WL 1562, HD 2281, etc. Use resistant sources like wild
species of Aegilops and Triticum, HD 2329, HD 29 and HD 20 for breeding programme.
Follow strict quarantine measures
Use disease free seed for sowing
Judicious application of nitrogenous fertilizers
Adjust date of sowing
Intercropping with Gram or Lentil
Seed treatment with copper carbonate or Thiram@3g/kg seed
Spray with [email protected]% or [email protected]% or [email protected]% or bitertanol
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Leaf blight Alternaria triticina/ Spot blotch or Black point disease Bipolaris sorokiniana
Economic importance
Reported by Prasad and Prabhu in 1962 from India. It is prevalent in parts of Maharashtra, Bihar,
West Bengal and UP. Seedlings are not prone to infection.
Symptoms
Reddish brown oval spots appear on young seedlings with bright yellow margin. In severe cases,
several spots coalesce to cause drying of leaves. The young leaves are not usually infected.
Heavily infected fields display a burnt appearance even from a distance. In some varieties
reduction in grain yield is as high as 90% if the infection takes place at or before the boot leaf
stage.
Pathogen
Fungus produces light brown coloured multicellular conidia, with 1-10 transverse septa and 1-5
longitudinal septa, singly or in chains (2-4).
Disease cycle
Pathogen over summers in plant debris and soil. Primary spread is by externally and
internally seed-borne conidia. Secondary infection is mainly through wind-borne conidia.
Favourable Conditions
Temperature of 25 0C and high relative humidity favours the disease.
Management
Soak the seeds in water for 4 hrs followed by 10 min. dip in hot water at 520C.
Grow resistant varieties like Co.25, Sonalika, Arnautka, E6160 and K7340.
Spray the crop with [email protected]% or [email protected]%
Pathogen
Fungus produces septate, superficial, hyaline mycelium on leaf surface with short
conidiophores. The conidia are elliptical, hyaline, single celled, thin walled and produced in
chains. Dark globose cleistothecia containing 9-30 asci develop with oblong, hyaline and
thinwalled ascospores.
Disease cycle
Fungus remains in infected plant debris as dormant mycelium and asci. Primary spread is
by the ascospores and secondary spread through airborne conidia.
Favourable Conditions
Temperature of 20-21˚C.
Management
Spray Wettable Sulphur 0.2% or Carbendazim @ 500 g/ha
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Ear cockle
Causal Organism: Anguina tritici
Ear-cockle is caused by the nematode. Its occurrence has been reported from all major
wheat growing regions of the country. Heavy infestation exceeding 50 per cent in individual
fields has been reported from Punjab, Haryana, Rajasthan, Uttar Pradesh and Bihar. The losses
caused are dependent on the extent of infestation.
Symptoms
Leaf blades generally twisted; infected ears are shorter and remain green longer; awns are more
spreading; affected grains transformed into one or more small galls.
Control Measures
To get rid of the ear-cockle disease, pure seed free from nematode galls should be used for
sowings.
The galls can be removed mechanically by sieving, as they are smaller in size than the
seeds.
These can also be removed by the floatation in 2 per cent common salt solution as they
float on the solution because of their lighter weight. Precaution must be taken to wash the wet
seeds in plain water and then to dry before sowing.
When the bacterium is associated with the nematode, the disease symptoms are intensified at the
flowering stage and yellow ear rot sets in due to combined action of the nematode and bacterium.
The earhead becomes chaffy and the kernels are replaced by dark nematode galls which also
contain the bacterium. The infected plants produce more tillers than the healthy ones. Another
interesting feature is the early emergence of ears in the nematode infected plants which is about
30 to 40 days earlier than the healthy ones.
Pathogen
Corynebacterium is rod shaped, Gram positive and is motile by single polar flagellum.
Disease cycle
The disease starts from the seeds contaminated with the nematode galls. When such contaminated
seeds are sown in the field, they absorb moisture from the soil and the larvae (juveniles) escape
from the galls and climb upon the young wheat plants. At the time of flowering, the nematodes
enter the floral parts and form galls in the ovaries. When once the nematode is inside the tissues of
the ovary, the bacterium becomes active and causes rotting. The yellow ooze coming out of the
rotting earhead provides the inoculum for the secondary spread of the disease which is favoured
by wind and rain. The nematode probably functions as a vector transporting the bacterium to
otherwise inaccessible meristematic regions of the host. The nematodes secrete some substances
in the presence of the host bacterium which can remain viable for atleast 5 years in the galls of A.
tritici. The nematode galls are reported to remain in the soil for 20 years or more and the
bacterium can also survive for the same period inside the nematode gall.
Management
Sow gall free seeds. Separate the galls from the seed by floating in brine at 160 g of
sodium chloride in liter of water.
Wheat, barley or oat should not be sown in the infested soil.
Spray the crop with streptocycline, 1g in 10 liters of water.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
RUST DISEASES
• Plant rusts, belong to Phylum Basidiomycota
• (Order-Uredinales) are among the most destructive plant diseases.
• There are about 5000 species belonging to about 140-150 genera of rust fungi and the
most important genera are;
Puccinia
Uromyces
Hemileia
Phragmidium
Gymnosporangium
Melampsora
Phakopsora
Microcyclic or short cycled rusts: Rusts caused by fungi that produce only teliospores.
Macrocyclic or long cycled rusts: Those rusts which typically produce all the five spore
states.
Demicyclic rusts: Those rust genera which lack the uredinal stage.
Puccinia graminis tritici – Macrocyclic, pleomorphic and heterocious
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
• Rust fungi are morphologically identical but attack different host genera and thus they
are regarded as formae specialis
• e.g., Puccinia graminis f. sp. tritici on wheat and
• Puccinia graminis f. sp. hordei on barley
• Within each special form of rust there are many so called physiological races. These can
attack only certain varieties within species and can be detected and identified only by the set
of differential varieties they can infect.
• Although these subspecies or varieties may differ in uredospore size and colour but more
clearcut differences in host range and specificity are useful. Puccinia graminis var. tritici
does not infect rye and Puccinia graminis var. secalis does not infect wheat whereas both
can infect barley plants.
• Stakman et al (1915) from University of Minnesota, USA, showed specialization of
some of the subspecies is further carried to enable differentiation into races and biotypes
within subspecies. They divided Puccinia graminis var. tritici into many pathologically
distinct strains or races based on the symptoms and pathogenic patterns produced on
standard different varieties of wheat in different species of Triticum. Those are called as host
differentials used for this differentiation are as follows
1) Little club, 2) Marquis, 3) Reliance, 4) Kota, 5) Arnautka, 6) Mindum,
7) Spelmar, 8) Kubanka, 9) Acme, 10) Einkorn, 11) Vernal, 12) Khapli
• The fungus being obligate pathogen is cultured on living host under controlled conditions
in a glasshouse. The rust collections are inoculated on these 12 differentials, pathogenic
patterns, symptoms, and pustule type they are graded.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Puccinia Path in India
Management Strategies
• Use of resistant varieties
• Gene deployment
• Gene pyramiding
• Gene recycling
• Chemical management
• Multilines
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
II. Sexual spores and spore bearing structure / organs / fruiting bodies
1. Spores
• Pycniospore – a uninucleate spore like gamete produced in a flask shaped structure called
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
pycnium.
• Teliospore – a thick walled, resting spore of rusts and smuts.
• Basidiospore – haploid spore borne on a club shaped basidium or a promycelium.
2. Spore bearing organs and fruiting bodies
• Pycnium/ Spermagonium: a flask shaped fruiting body with Pycniospore/ spermatia and
receptive hypha.
• Telium – a fruiting body of rust fungi in which teliospores are produced.
• Basidium – a club shaped structure bearing basidiospore at the tip.
History
• 1865: Anton de bary demonstarted heteroceous nature of stem rust of wheat
• 1894: Erikson showed physiological specialization in stem rust of wheat
• 1905: Biffen demonstarted inheritance of rust resistance in wheat in Mendelian fashion
• 1914: Stakman distinguished biological forms in cereal rusts
• 1927-31: Craigie discovered the function of pycnia
• 1940: K.C. Mehta cereal rust studies in India
• 1951: Cutter and Hotson -the first artificial culture of cedar rust of apple
• 1966-67: Williams et al., the first artificial/auxenic culture of black stem rust of wheat
• Norman Ernest Borlaug (March 25, 1914 – September 12, 2009) was an
American agronomist and humanitarian who led initiatives worldwide that contributed to the
extensive increases in agricultural production termed the Green Revolution. Borlaug was
awarded multiple honors for his work, including the Nobel Peace Prize, the Presidential
Medal of Freedom and the Congressional Gold Medal.
• Borlaug was often called "the father of the Green Revolution"
• Borlaug received his B.S. in forestry in 1937 and Ph.D. in plant
pathology and genetics from the University of Minnesota in 1942.
• He took up an agricultural research position in Mexico, where he developed semi-dwarf,
high-yield, disease-resistant wheat varieties.
• In 1953, he acquired a Japanese dwarf variety of wheat called Norin 10developed by the
agronomist Gonjiro Inazuka in Iwate Prefecture, including ones which had been crossed with
a high-yielding American cultivar called Brevor 14 by Orville Vogel.Norin 10/Brevor 14 is
semi-dwarf (one-half to two-thirds the height of standard varieties) and produces more stalks
and thus more heads of grain per plant.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Cotton
Symptoms
The bacterium attacks all stages from seed to harvest. Usually five common phases of
symptoms are noticed.
i) Seedling blight: Small, water-soaked, circular or irregular lesions develop on the
cotyledons. Later, the infection spreads to stem through petiole and cause withering and
death of seedlings.
ii) Angular leaf spot: Small, dark green, water soaked areas develop on lower surface of
leaves, enlarge gradually and become angular when restricted by veins and veinlets and spots
are visible on both the surface of leaves. As the lesions become older, they turn to reddish
brown colour and infection spreads to veins and veinlets.
iii) Vein blight or vein necrosis or black vein: The infection of veins causes blackening
of the veins and veinlets, gives a typical ‘blighting’ appearance. On the lower surface of the
leaf, bacterial oozes are formed as crusts or scales. The affected leaves become crinkled and
twisted inward and show withering. The infection also spreads from veins to petiole and
cause blighting leading to defoliation.
iv) Black arm: On the stem and fruiting branches, dark brown to black lesions are formed,
which may girdle the stem and branches to cause premature drooping off of the leaves,
cracking of stem and gummosis, resulting in breaking of the stem which hang typically as
dry black twig to give a characteristic “black arm” symptom.
v) Square rot / Boll rot: On the bolls, water soaked lesions appear and turn into dark black
and sunken irregular spots. The infection slowly spreads to entire boll and shedding occurs.
The infections on mature bolls lead to premature bursting of bolls. The bacterium spreads
inside the boll and lint gets stained yellow because of bacterial ooze and looses its
appearance and market value. The pathogen also infects the seed and causes reduction in size
and viability of the seeds.
Pathogen
The bacterium is a short rod with a single polar flagellum. It is gram negative, non-spore
forming and measures 1.0-1.2 X 0.7-0.9 µm. The bacterium is aerobic, capsule forming and
produces yellow colonies in culture medium.
Disease cycle
The bacterium survives on infected dried plant debris in soil for several years. The bacterium
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
is also seed-borne and remains in the form of slimy mass on the fuzz of seed coat. It
multiplies soon after the seed is sown and infects the seedling through the micropyle.
Volunteer plants that arise from the bolls falling off prematurely also provide a source of
primary infection. The bacterium also attacks other hosts like Thurbaria thespesioides,
Eriodendron anfructuosum and Jatropha curcas. The primary infection starts mainly from
the seed-borne bacterium. The secondary spread of the bacteria may be through wind, wind
blown rain splash, irrigation water, insects and other implements. The bacterium enters
through natural openings or insect caused wounds.
Favourable Conditions
Optimum soil temperature of 280C, high atmospheric temperature of 30-400C, relative
humidity of 85 per cent, early sowing, delayed thinning, poor tillage, late irrigation and
potassium deficiency in soil. Rain followed by bright sunshine during the months of October
and November are highly favourable.
Management
Remove and destroy the infected plant debris.
Rogue out the volunteer cotton plants and weed hosts.
Follow crop rotation with non-host crops.
Early thinning, good tillage, early irrigation, early earthing up and addition of potash to
the soil reduces disease incidence.
Grow resistant varieties like HG-9, BJA 592, G-27, Sujatha, 1412 and CRH 71. Suvin is
tolerant.
Gossypium herbaceum and G. arboreum are almost immune. G. barbadense, G.
hirsutum, G. herbaceum var typicum and G. herbaceum var acerifolium have considerable
resistance.
Delint the cotton seeds with concentrated sulphuric acid at 125ml/kg of seed.
Treat the delinted seeds with Carboxin at 2 g/kg seed or soak the seeds in 1000 ppm
Streptomycin sulphate overnight or treat the seed with hot water at 52-560C for 10-15
minutes.
Spray with Streptomycin sulphate (Agrimycin 100), 500 ppm along with Copper
oxychloride at 0.3%.
Pathogen
The fungus produces three types of spores. Macroconidia are 1 to 5 septate, hyaline, thin
walled, falcate with tapering ends. The microconidia are hyaline, thin walled, spherical or
elliptical, single or two celled. Chlamydospores are dark coloured and thick walled. The
fungus also produces a vivotoxin, Fusaric acid which is partially responsible for wilting of
the plants.
Disease cycle
The fungus can survive in soil as saprophyte for many years and chlamydospores act as
resting spores. The pathogen is both externally and internally seed-borne. The primary
infection is mainly from dormant hyphae and chlamydospores in the soil. The secondary
spread is through conidia and chlamydospores which are disseminated by irrigation water.
Favourable Conditions
Soil temperature of 20-300C, hot and dry periods followed by rains, heavy black soils with
an alkaline reaction, increased doses of nitrogen and phosphatic fertilizers, soil amendment
with manganese and wounds caused by nematode (Meloidogyne incognita) and grubs of
Ashweevil (Myllocerus pustulatus).
Management
Treat the acid-delinted seeds with Carboxin or Chlorothalonil at 4 g/kg or
Carbendazim@2g/kg seed
Remove and burn the infected plant debris in the soil after deep summer ploughing.
Apply increased doses of potash with a balanced dose of nitrogenous and phosphatic
fertilizers.
Multiply Trichoderma viride (2kg) in 50 kg of Farm yard manure for 15 days and then
apply to the soil.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Apply heavy doses of farm yard manure or other organic manures at 10 t/ha. Follow
mixed cropping with non-host plants to lower the soil temperature below 200C by providing
shade.
Soil amendment with zinc.
Grow disease resistant varieties of G. hirsutum and G. barbadense like Varalakshmi,
Vijaya, Pratap, Jayadhar, Jarila, Jyothi, G 22 and Verum.
Economic importance
The disease is a major disease in cotton in USA and USSR and was first reported in India
during 1968 on hirsutum cottons in Coimbatore, Tamil Nadu. The disease usually appears
in November and December when the crop is in squares and bolls, about three months
after sowing.
Symptoms
The symptoms are seen when the crop is in squares and bolls. Plants infected at early
stages are severely stunted. The first symptoms can be seen as distinct mottling of leaves
with pale yellowish irregular areas at the margins and between the principal veins. The
yellowish areas become pale, more whitish and extensively necrotic. The necrosis of the
leaves spreads from lower to upper leaves and there is heavy defoliation. The affected
leaves fall off leaving the branches barren. Infected stem and roots, when split open,
show a pinkish to pinkish brown discolouration of the woody tissue which may be
continuous or interrupted. Pinkish streaks alternating with healthy tissue (Tiger stripe)
are seen on removing the bark of the roots, stem and petiole. The affected plants may
bear a few smaller bolls with immature lint.
Pinkish discolourations Conidiophore & conidia
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Pathogen
The fungus produces hyaline, septate mycelium and two types of spores. The conidia are
single celled, hyaline, spherical to oval, borne singly on verticillate conidiophores. The
micro sclerotia are globose to oblong, measuring 48-120 X 26-45um.
Disease cycle
The fungus also infects the other hosts like brinjal, chilli, tobacco and bhendi. The
fungus can survive in the infected plant debris and in soils as microsclerotia upto 14
years. The seeds also carry the microsclerotia and conidia in the fuzz. The primary spread
is through the micro sclerotia or conidia in the soil. The secondary spread is through the
contact of diseased roots to healthy ones and through dissemination of infected plant
parts through irrigation water and other implements.
Favourable Conditions
Low temperature of 15-200C, low lying and ill-drained soils, heavy soils with alkaline
reaction and heavy doses of nitrogenous fertilizers favours the disease.
Management
Treat the delinted seeds with Carboxin@4g/kg or Carbendazim at 2 g/kg.
Remove and destroy the infected plant debris after deep ploughing in summer
months.
Apply heavy doses of farm yard manure or compost at 10t/ha.
Follow crop rotation by growing paddy or Lucerne or chrysanthemum for 2-3
years.
Spot drench with 0.05 per cent Benomyl or Carbendazim.
Grow disease resistant varieties like Sujatha, Suvin and CBS 156.
Symptoms
The fungus causes three types of symptoms, viz., seedling disease, sore-shin and root rot.
Germinating seedlings of one to two weeks old are attacked by the fungus at the
hypocotyl and cause black lesions, girdling of stem and death of the seedling, causing
large gaps in the field. In sore-shin stage (4 to 6 weeks old plants), dark reddish-brown
cankers are formed on the stems near the soil surface which later turns dark brown or
black and plant breaks at the collar region leading to drying of the leaves and
subsequently the entire plant. Typical root rot symptom appears normally at the time of
maturity of the plants. The most prominent symptom is sudden and complete wilting of
plants in patches in concentric circles. Initially, all the leaves droop suddenly and die
within a day or two. The affected plants when pulled reveal the rotting of entire root
system except tap root and few laterals. The bark of the affected plant shreds and even
extends above ground level. In badly affected plants the woody portions may become
black and brittle. A large number of dark brown sclerotia are seen on the wood or on the
shredded bark.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Pathogen
The fungal hyphae are septate and fairly thick and produce black, irregular sclerotia
which measure 100 µm in diameter.
Disease cycle
The disease is mainly soil-borne and the pathogen can survive in the soil as sclerotia for
several years. The spread is through sclerotia which are disseminated by irrigation
water, implements, heavy winds and other cultural operations.
Favourable Conditions
Dry weather following heavy rains, high soil temperature (35-39OC), low soil moisture
(15-20 per cent), cultivation of favourable hosts like vegetables, oil seeds and legumes
preceding cotton and wounds caused by ash-weevil grubs and nematodes.
Management
Treat the seeds with Trichoderma viride @ 4g/kg or Pseudomonas fluorescens @
10g/kg of seed.
Treat the seeds with Carboxin or Thiram at 4 g or Carbendazim at 2g/kg.
Spot drench with 0.1% Carbendazim or 0.05% Benomyl.
Apply farm yard manure at 100 t/ha or neem cake at 2.5t/ha.
Adjust the sowing time, early sowing (First Week of April) or late sowing (Last
week of June) so that crop escapes the high soil temperature conditions.
Adopt intercropping with sorghum or moth bean (Phaseolus aconitifolius) to lower
the soil temperature.
Grow resistant varieties like KH 33/1146, 15/KW-2 (MB)
Symptoms
The disease usually appears on the under surface of the lower leaves when the crop is
nearing maturity. Irregular to angular pale translucent lesions which measure 1-10
mm (usually 3-4 mm) develop on the lower surface, usually bound by veinlets. On the
upper surface, the lesions appear as light green or yellow green specks. Whitish grey or
frosty powdery growth, consisting of conidiophores of the fungus, appears on the lower
surface. When several spots coalesce, the entire leaf surface is covered by white to grey
powdery growth. The infection spreads to upper leaves and entire plant may be affected.
The affected leaves dry up from margin, turn yellowish brown and fall off prematurely.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Pathogen
The fungus produces endophytic, septate mycelium. Conidiophores are short, hyaline and
branched at the base. Conidia are borne singly or in chains at the tips of conidiophores.
The conidia are hyaline, irregularly oblong with pointed ends, sometimes rounded to
flattened ends, unicellular or 1-3 septate. The perfect stage of the fungus produces
perithecia containing many asci. The ascospores are hyaline and usually two celled.
Disease cycle
The fungus survives during the summer in the infected crop residues. The perennial
cotton plants and self-sown cotton plants also harbor the pathogen during summer
months. The primary infection is through conidia from infected plant debris and
secondary spread is through wind, rain splash, irrigation water and implements.
Favourable Conditions
Wet humid conditions during winter cotton season, intermittent rains during North-East
monsoon season, low temperature (20-300C) during October-January, close planting,
excessive application of nitrogenous fertilizers, very early sowing or very late sowing of
cotton and growing highly susceptible varieties/hybrids like Suvin, DCH 32, MCU 5, and
MCU 9.
Management
Remove and burn the infected crop residues.
Rogue out the self-sown cotton plants during summer months.
Avoid excessive application of nitrogenous fertilizers/manures.
Adopt the correct spacing based on soil conditions and varieties.
Spray the crop with [email protected]% or BM@1% or Wettable sulphur at 1.25-
2.0 kg/ha, repeat after a week.
Grow the resistant varieties like Sujatha and Varalakshmi.
Pathogen
The pathogen forms large number of acervuli on the infected parts. The conidiophores
are slightly curved, short, and club shaped. The conidia are hyaline and falcate, borne
single on the conidiophores. Numerous black coloured and thick walled setae are also
produced in acervulus.
Disease cycle
The pathogen survives as dormant mycelium in the seed or as conidia on the surface of
seed for about a year. The pathogen also perpetuate on the rotten bolls and other plant
debris in the soil. The secondary spread is by air-borne conidia. The pathogen also
survives in the weed hosts, viz., Aristolachia bractiata and Hibiscus diversifolius.
Favourable Conditions
Prolonged rainfall at the time of boll formation and close planting predispose the disease.
Management
Treat the delinted seeds with Carbendazim or Carboxin@2g/kg or Thiram or Captan
at 4g/kg.
Remove and burn the infected plant debris and bolls in the soil.
Rogue out the reservoir weed hosts.
Spray the crop at boll formation stage with [email protected]% or Copper
[email protected]% or [email protected]% or [email protected]%.
Disease cycle
The pathogen survives in the infected crop debris as dormant mycelium. The secondary
spread is mainly by air-borne conidia.
Pathogen
The fungus produces dark brown, short, 1-8 septate, irregularly bent conidiophores with a
single conidium at the apex. The conidia are obclavate, light to dark brown in colour with
3-9 transverse septa and 4 longitudinal septa, with a prominent beak.
Favourable Conditions
High humidity, intermittent rains and moderate temperature of 25-280C favours the
disease incidence.
Management
Remove and destroy the infected plant residues.
Deep summer ploughing
Avoid seeds from infected crop
Spray [email protected]% or Copper [email protected]% at the initiation of the
disease. Four to five sprays may be given at 15 days interval.
Disease cycle
The pathogen survives in the infected plant debris as conidia. The secondary spread is
mainly by air-borne conidia.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management
Remove and destroy the infected plant residues.
Spray [email protected]% or Copper [email protected]% or [email protected]% or
[email protected]% at the initiation of the disease.
Rust Phakopsora gossypii (Tropical rust), Puccinia cacabata (South western rust),
Puccinia schedonnardi (Cotton rust-USA)
Economic importance
The disease usually occurs after September, i.e., at the end of the season. It is difficult to
assess the loss due to bacterial blight.
Symptoms
Most common symptom is the appearance of bright yellow orange spots usually on under
surface of the lower leaves. These pustules are surrounded by purple borders. Spots
become brown with age. Spots may appear on any of the above ground parts including
bracts and bolls. Severe infections may cause defoliation and reduction in the size of the
bolls. On stems and petioles these pustules are usually elongated and are not much raised.
Pathogen
Phakopsora uredia are yellowish brown, varying from 0.5 to 3.0 mm in diameter and are
surrounded by purplish borders. Uredia first appear as oval, corky pustules and then
become round. The pycnial and aecial stages of Puccinia occur on cotton, whereas
uredial and telial stages occur on grasses, most of which are species of Bouteloua
(Gramma grass).
Disease cycle
Pycnial pustules occur mostly on upper leaf surfaces of cotton and are bright yellow to
orange in colour. Aecia of similar colour occur on lower leaves. The spores from cotton
infect gramma grass (Bouteloua) producing elongate brownish spots (Uredial stage). The
black telial stage appears on gramma grass later. The spores produced from telial stage
during summer rains infect cotton to complete the cycle.
Favourable Conditions
High humidity and moderate temperatures are conducive for the disease.
Management
Remove and destroy the infected gramma grass.
Spray [email protected]% prior to first spore showers.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Leaf Curl Disease- Cotton leaf curl virus
Symptoms
Downward and upward curling of leaves and thickening of veins and enation on
underside of leaves are the characteristic symptoms of the disease. In severe infection all
the leaves are curled and growth retarded. Boll bearing capacity is reduced.
Pathogen
It is caused by Cotton leaf curl virus - a begomovirus of family geminiviridae.
The virions are typical geminate particles, ss circular DNA, bipartite genome with DNA-A
and DNA- B components.
Disease Cycle
The primary source is the viruliferous whitefly vector Bemisia tabaci. The
alternate hosts and cultivated hosts serve as virus reservoirs throughout the year. Not
transmitted by seed or contact.
Management
Management of planting date to avoid peak vector population.
Elimination of volunteer perennial cotton and alternate hosts including malvaceous hosts
like wild okra
Use of fungus Paecilomyces farinosus which parasitizes B.tabaci. It brings down vector
population.
Foliar application of neem leaf extract and 1% neem oil resulted in 80% reduction of
virus transmission.
Vector management by application of granular systemic insecticides.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Sugarcane
Symptoms
The first external symptoms appear as discolouration of the young leaves. The margins
and tips of the leaves wither and the leaves droop. The discolouration and withering
continues from the tip to the leaf base until the whole crown withers away in four to eight
days. In a single stool, most of the stalks may wither almost simultaneously. Typical
symptoms of red rot are observed in the internodes of a stalk by splitting it longitudinally.
These include the reddening of the internal tissues, especially the vascular bundles,
which are usually elongated at right angles to the long axis of the stalk. The presence of
cross-wise white patches interrupting the reddened tissues are the important diagnostic
character of the disease. Split open stems emit a characteristic acidic-sour odour. As the
disease advances the entire stem rots and the stalk becomes hollow and covered with
white mycelial growth. Later the rind shrinks longitudinally with minute black, velvetty
fruiting bodies protruding out of it.
The pathogen also produces tiny reddish lesions on the upper surface of leaves with dark
dots in the centre. Minute red spots also appear on the centre of the mid-rib and develop
in both directions forming small or long lesions. The lesions are initially blood red with
dark margins and later on with straw coloured centres. Often the infected leaves may
break at the lesions and hang down, with large number of minute black dots.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Pathogen
The fungus produces thin, hyaline, septate, profusely branched hyphae containing oil
droplets. The fungus produces black, minute velvetty acervuli with long, rigid bristle-
like, septate pointed setae on the surface of rind, leaf midrib and sometimes in the pith
region. Conidiophores are closely packed inside the acervulus, which are short, hyaline
and single celled. The conidia are single celled, hyaline, falcate, granular and guttulate.
Five pathotypes of the fungus have been reported. In general, light coloured physiological
races sporulate readily and are more virulent than the dark coloured strains that sporulate
sparsely. The perfect stage of the fungus produces large number of globose and dark
brown to black perithecia with a papillate ostiole. Asci are clavate, unitunicate and
eight-spored. Large number of hyaline, septate, filiform paraphyses is also present among
asci. Ascospores are ellipsoid or fusoid, hyaline, straight or slightly curved and
unicellular.
Disease cycle
The fungus is sett-borne. The fungus also persists in the soil on the diseased clumps and
stubbles as chlamydospores and dormant mycelium. The primary infection is mainly
from infected setts. Secondary spread in the field may be through irrigation water and
cultivation tools. The rain splash, air currents and dew drops also help in the spread of
conidia from the diseased to healthy plants in the field. The fungus also survives on
collateral hosts like Sorghum vulgare, S. halepense and Saccharum spontaneum.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Favourable Conditions
Mono-culturing of sugarcane, successive ratoon cropping, water logged conditions and
injuries caused by insects.
Management
Removal and destruction of infected plant debris, stubbles and trash.
Deep tillage to incorporate the left over debris.
Adopt crop rotation by including rice and green manure crops.
Select the setts from the disease free fields or disease free area.
Avoid ratooning of the diseased crop.
Avoid flow of irrigation water from diseased to healthy plants.
Soak the setts in 0.1% Carbendazim solution for 20 minutes before planting.
Hot water treatment of setts at 520C for 30 min or 500C for 2 hours followed by steeping
in 0.1% carbendazim solution.
Setts can be treated with aerated steam at 520C for 4 to 5 hours and by moist hot air at
540C for 2 hours.
Grow resistant varieties like CO 6907, CO 7219, CO 8013, CO 8021, CO 7706, CO A
7602, CO A 89082, CO A 89085, 87 A 397, CO T 8201, etc.
Symptoms
The affected plants are stunted and the central shoot is converted into a long whip-like,
dusty black structure. The length of the whip varies from few inches to several feet. In
early stages, this structure is covered by a thin, white papery membrane. The whip may
be straight or slightly curved. On maturity it ruptures and millions of tiny black smut
spores (teliospores) are liberated and disseminated by wind. All the shoots arising from
the diseased clump produce whip like structures. The smutted clumps also produce
mummified arrows in which lower portion consists of normal inflorescence with typical
flowers and the upper portion of the rachis is converted into a typical smutted whip.
Occasionally smut sori may develop on the leaves and stem. The ratoon crops are
severely affected.
Pathogen
The fungal hyphae are primarily intercellular and produce tiny black teliospores. The
thin membrane which covers the smut whip represents the host epidermis. The smut
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
spores are light brown in colour, spherical and echinulate. Smut spores germinate to
produce 3-4 celled, hyaline promycelium and produce 3-4 sporidia which are hyaline and
oval shaped with pointed ends.
Disease cycle
Teliospores may survive in the soil for long periods, upto 10 years. The spores and
sporidia are also present in the infected plant debris in the soil. The smut spores and
dormant mycelium also present in or on the infected setts. The primary spread of the
disease is through diseased seed-pieces (setts). In addition, sporidia and spores present
in the soil also spread through rain and irrigation water and cause soil-borne infection.
The secondary spread in the field is mainly through the smut spores developed in the
whips, aided by air currents. The fungus also survives on collateral hosts like Saccharum
spontaneum, S. robustum, Sorghum vulgare, Imperata arundinacea and Cyperus
dilatatus.
Favourable Conditions
Mono-culturing of sugarcane, continuous ratooning and dry weather during tillering stage
favours the disease.
Management
Plant healthy setts taken from disease free area.
Remove and destroy the smutted clump (Collect the whips in a thick cloth bag/polythene
bag and immerse in boiling water for 1 hr to kill the spores).
Discourage ratooning of the diseased crops having more than 10 per cent infection.
Follow crop rotation with green manure crops or dry fallowing.
Grow redgram as a companion crop between 2 rows of sugarcane.
Treat the setts in hot water at 500C for 2 hours.
Grow resistant varieties like Co 6806 and Co 62175
Symptoms
The first symptom of the disease is visible in the canes of 4-5 months age. The canes
may wither in groups. The affected plants are stunted with yellowing and withering of
crown leaves. The midribs of all leaves in a crown generally turn yellow, while the leaf
lamina may remain green. The leaves dry up and stem develop hollowness in the core or
pith. The pith shows reddish discolouration with longitudinal red streaks passing from
one internode to another. In severe cases, spindle shaped cavities tapering towards the
nodes develop in each internode. The canes emit a disagreeable odour, with lot of white
mycelial threads of the fungus covering the cavity. Weight gets reduced due to hollow
canes.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Pathogen
The fungal mycelium is hyaline, septate and thin walled. The conidiophores are simple,
slender or swollen on which hyaline, single celled, hyaline, oval to elliptical
microconidia collecting in a slime drop. Macroconidia are not produced.
Disease cycle
The fungus is primarily sett borne and also survives in the soil as saprophyte for 2-3
years. The disease is primarily transmitted through infected seed setts. The secondary
spread is aided by wind, rain and irrigation water.
Favourable Conditions
High day temperature (30-350C), low humidity (50-60 per cent), low soil moisture,
alkaline soils and excess doses of nitrogenous fertilizers.
Management
Select the seed material from the disease-free plots.
Avoid the practice of ratooning in diseased fields.
Burn the trash and stubbles in the field.
Grow coriander or mustard as a companion crop in the early stages of crop.
Avoid alkaline soils for growing the crop
Treat the setts in hot water at 500C for 2 hours followed by dipping in 0.05%
Carbendazim for 15 minutes.
Dip the setts in 40ppm Boron or Manganese for 10 minutes
Grow resistant varieties like CO 617 and BP 17.
Pathogen
The fungus produces both macroconidia and microconidia. Conidiophores are
linear, thin walled with short cells at the base and a long terminal cell. The microconidia
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
are hyaline when young but become almost black at maturity. They are thinwalled,
cylindrical and produced endogenously in chains in the long cells of conidiophores and
pushed out in succession. Macroconidia are produced singly or in chains on a short,
lateral conidiophores. Macroconidia are spherical or elliptical or truncate or pyriform and
are hyaline to olive green or black measuring 16-19x10-12 um.
The fungus also produces chlamydospores on short lateral hyphae in chains,
which are oval, thick walled and brown in colour. The perithecia are flask shaped with a
very long neck. The bulbous base of the perithecium is hyaline or pale yellow, 200-
300µm in diameter and ornamented with irregularly shaped, knobbed appendages. The
ostiole is covered by numerous pale-brown, erect tapering hyphae. Asci are clavate and
measures 25x10µm and ascospores are single celled, hyaline, ellipsoid, more convex on
one side, measures 7-10 x 2.5-4µm.
Favourable Conditions
Poorly drained fields.
Heavy clay soils
Temperature of 25-30o C
Prolonged rainfall after planting.
Disease Cycle
The fungus survives as conidia and chlamydospores in the soil and in the infected,
burried cane tissues. The inoculum moves from field to field through wind-borne conidia
or irrigation or rain water. Inside the sett it spreads rapidly through the parenchymatous
tissues and causes sett rot.
The insects like cane borer (Diatraea dyari) also helps in the spread of the disease. The
pathogen also survives on coconut, cocoa, mango, papaya, coffee, maize and arecanut.
Insects also play a part in the dissemination of the pathogen.
Management
Soak the setts in 0.05% Carbendazim 15 minutes.
Use long setts having 3 or 4 buds.
Provide adequate drainage during rainy seasons.
Symptoms
The disease symptoms are usually seen two months after planting. The disease is
characterized by the production of numerous lanky tillers from the base of the affected
shoots. Leaves become pale yellow to completely chlorotic, thin and narrow. The plants
appear bushy and ‘grass like’ due to reduction in the length of internodes, premature and
continuous tillering. The affected clumps are stunted and in many instances exhibit
premature proliferation of auxillary buds. In a diseased clump one or two thin, weak
and small canes are produced. In plant crop, young leaves of diseased plants are white
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
(Albino) and the buds on such canes are usually white, papery and abnormally
elongated.
Pathogen
Phytoplasma is found in the sieve cells of infected plants. Two types of bodies are
noticed, spherical bodies of 300-400 nm diameter and filamentous bodies of 30-53 mm
diameter.
Disease cycle
The pathogen is transmitted through planting material and within the crop by aphids,
viz., Aphis maidis, Rhopalosiphum maidis, Longiunguis sacchari, Melanaphis sacchari
and M. indosacchari. In addition, leaf hopper, Proutista moesta also involves in the
transmission. Sorghum serves as a natural collateral host.
Management
Plant disease free setts.
Remove and burn the infected clumps periodically.
Avoid ratooning in problem areas
Hot Water Treatment (HWT) of setts at 520C for 30min or Aerated Steam Therapy (AST)
at 500C for 1 hr followed by steeping in fungicidal solution of [email protected]% for
15 minutes.
Control vector by spraying Malathion or Dimethoate@2ml/lt
Ratoon stunting Clavibacter xyli pv. xyli (Xylem limited fastidious bacteria)
Economic importance
The disease is present throughout the sugarcane growing areas of our country. CO 419
variety was worst affected in parts of Karnataka where it was withdrawn from cultivation.
The disease appears in both plant and ratoon crop, but more pronounced in ratoon crop.
Symptoms
Diseased clumps usually display stunted growth, reduced tillering, thin stalks with
shortened internodes and yellowish foliage (mild chlorosis). When mature canes are split
open, vascular bundles appear discoloured. In young canes, pink colour is seen in the
form of minute pin head like areas near the nodes. The disease reduces the length, girth
and the number of canes per clump.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Pathogen
The pathogen is known to present in the xylem cells of infected plants. They are small,
thin, rod shaped or coryneform.
Disease cycle
The disease spreads through use of diseased setts. The disease also spreads through cane
harvesting implements contaminated with the juice of the diseased canes. Maize,
sorghum, Sudan grass and Cynodon are some of the collateral hosts of the pathogen.
Management
Select the setts from disease free field.
Remove and burn the clumps showing the disease.
Sterilization of cutting knives with lysol or any other antiseptic solution.
Hot air treatment of setts at 540C for 8 hours or hot water treatment at 500C for 2 hrs or
aerated steam treatment at 500C for 1 hour.
Pathogen
The mycelium is hyaline, branched and septate. P.kuehnii produces ovoid or pear shaped,
single celled uredospores with apical thickening and golden yellow in colour. Teliospores
are produced in abundance, which are pale to brick colour, two celled, smooth walled and
slightly constricted at septum. Occurrence of pycnial and aecial stages and the role of
alternate host are unknown.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Disease cycle
The fungus survives on collateral hosts like Erianthus fulvus and Saccharum
spontaneum. The uredospores also survive in the infected stubbles in the soil. The
disease is mainly spread through air-borne uredospores.
Favourable Conditions
Temperature of 300C, relative humidity between 70 and 90 per cent during winter
months, high wind velocity and continuous cloudiness favours disease development.
Management
Remove the collateral hosts.
Spray [email protected]% or [email protected]%, twice or thrice.
Amongst the foliar diseases, the pokkah boeng disease is becoming major disease of
sugarcane. Pokkah boeng, a Javanese term, which describe a disease as affecting to
sugarcane tops, was first recorded in Java by Walker and Went in 1886 and later reported by
Edgerton (1955) and Martin et.al(1961). Pokkah boeng, a major sugarcane disease in Java,
with the spread of the commercial variety POJ 2878 and was extensively investigated in that
country by Bolle during 1927 to 1937. It was observed for the first time in Maharashtra on
Co7219 and Coc671 varieties.
Susceptible varieties in Maharashtra: Co419, Co7219, Co7527, CoC 671, Co7527, Co86032,
Co8014.
Distribution
The occurrence of the disease has been recorded in almost all the cane growing countries in
the world. In India, it is in Punjab, Haryana, Uttar Pradesh, Gujarat, Madhya Pradesh,
Andhra Pradesh, Karnataka and TamilNadu States on most of the commercial varieties.
Economic Importance
The notable losses from pokkah boeng have occurred in Java, where susceptible varieties
have been grown in a climate, in which hot and dry season is followed by a wet season like
in India. Three to seven month old crop growing vigorously is more susceptible to infection
than the older cane.
Symptomatology
1. Chlorotic Phase,
2. Acute Phase or Top-Rot Phase and
3. Knife-cut Phase (associate with top rot phase).
1. Cholorotic Phase
The earliest symptom of pokkah boeng is a chlorotic condition towards the base of the young
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
leaves and occasionally on the other parts of the leaf blades. Frequently, a pronounced
wrinkling, twisting and shortening of the leaves accompanied the malformation or distortion
of the young leaves. The base of the affected leaves is seen often narrower than that of the
normal leaves.
In affected mature leaves, the irregular reddish stripes and specks are observed within a
chlorotic part. The reddish area sometimes develops into the lesions of a rhomboid shaped,
which showed no definite arrangement or formed ladder like lesions, with dark edges in
longitudinal rows, which turned the dark reddish to brown color, producing a burned
appearance. Leaf sheaths are also observed with chlorotic conditions in some cases. Later,
irregular necrotic areas of reddish color, similar on the leaf blades are also noticed on leaf
sheath and midribs.
3. Knife-cut Phase
The symptoms of knife-cut stage are observed in association with the acute phase of the
disease characterized by one or two or even more transverse cuts in the rind of the stalk
/stem in such a uniform manner as if, the tissues are removed with a sharp knife, This is an
exaggerated stage of a typical ladder lesion of a pokkah boeng disease. On stripping off the
leaves, large horizontal conspicuous cuts are develops on stalks.
Previously, the acute phase was considered as the most advanced and serious stage of a
pokkah boeng. However, critical observations on symptomatology reveled that the acute
phase (top rot) of pokkah boeng is always associated with the Knife-cut infection. In general,
the infection occurs uniformly on the cane tops, which are apparently responsible for the
spread of the disease.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Transmission
This is an air-borne disease and primarily transmitted through the air-currents and secondary
transmission is through the infected setts, irrigation water, splashed rains and soil.
Management
Spraying of 0.1% Bavistin (1 gm/ lit. of water) or 0.2% Blitox-50 (2gm/ lit. of water) or
Copper oxychloride or 0.3% Dithane M-45 (3 gm/ lit. of water) are the most effective
fungicides for reducing the pokkah boeng disease. Two to three sprayings with an interval of
15 days interval reduces the multiplication of a pathogen and losses in yield and quality of
cane and therefore, paired row or wider spacing planting of sugarcane is necessary to
facilitate the plant protection operations. Canes showing ‘top rot’ or ‘knife cut’ should be
rogued out.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Sunflower
Leaf blight Alternaria helianthi
Economic Importance
It is the most destructive disease and is widely distributed wherever sunflower is grown. It
occurs on all the varieties in the winter season and it spreads rapidly during the rainy
season. This disease has been reported to reduce the seed yield by 27 to 80% and oil yield
by 17 to 35%. The disease also affects the quality of seeds which adversely affects seed
germination and vigour of seedlings.
Symptoms
The fungus produces brown spots on the leaves, but the spots can also be seen on the stem,
sepals and petals. The lesions on the leaves are dark brown to black, circular to oval spots,
ranging from 0.2 to 0.5mm in diameter. The spots are often surrounded by a chlorotic
zone with necrotic center. The spots later enlarge in size with concentric rings and become
irregular in shape. Under high atmospheric humidity, several spots coalesce to show
bigger irregular lesions leading to drying and defoliation. The disease sometimes cause
rotting of flower heads and affects the quality of seeds by reducing the germination
percentage.
Pathogen
The fungus produces cylindrical conidiophores, which are pale grey-yellow coloured,
straight or curved, geniculate, simple or branched, septate and bear single conidium.
Conidia are cylindrical to long ellipsoid, straight or slightly curved, pale grey-yellow to
pale brown, 1 to 2 septate with longitudinal septa.
Disease cycle
The fungus survives on seed, host debris and weed hosts. The secondary spread is mainly
through windblown conidia.
Favourable Conditions
Rainy weather, cool winter climate and late sown crops are highly susceptible.
Management
Grow tolerant variety like BSH-1.
Remove and destroy infected plant debris.
Rogue out weeds at periodical intervals.
Sow the crop early in the season (June sowing).
Spacing of 60x30cm or 45x30cm reduces disease build up.
Treat the seeds with Thiram or Carbendazim at 2 g/kg.
Spray twice or thrice with zineb or Mancozeb at 0.2% or [email protected]% at 10 days
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms
Small, reddish brown pustules (uredia) covered with rusty dust appear on the lower
surface of bottom leaves. Infection later spreads to other leaves and even to the green
parts of the head. In severe infection, when numerous pustules appear on leaves, they
become yellow and dry. The black coloured telia are also seen among uredia on the lower
surface.
Pathogen
The disease is autoecious rust. The pycnial and aecial stages occur on volunteer crops
grown during off-season. The uredospores are round or elliptical, dark cinnamon-brown
in colour and minutely echinulate. Teliospores are elliptical or oblong, two celled, smooth
walled and chestnut brown in colour with a long, colourless pedicel.
Disease cycle
The pathogen survives in the volunteer sunflower plants and in infected plant debris in the
soil as teliospores. The disease spreads by wind-borne uredospores.
Favourable conditions
Weather parameters like temperatures of 25.5 to 30.50C with RH of 86-92% favours rust
disease severity. The incidence of rust increases with age, the maximum being on 75 days
old plants.
Management
Remove and burn the infected plant debris in the field.
Remove the volunteer sunflower plants.
Crop rotation for 3 years
Grow tolerant variety like BSH-1.
Spray Mancozeb or [email protected]%, 2-3 times at 10 days interval. The first spray should be
given as soon as the disease is noticed or 35 DAS.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms
White to grey powdery growth appears on upper surface of older but still green foliage.
Occasionally powdery growth is also seen on stem and bracts. As the plant matures black
pin head sized cleistothecia are visible in white mildew areas. The affected leaves curl,
chlorotic, dry and defoliate.
Pathogen
The fungus produces hyaline, septate mycelium which is ectophytic and sends haustoria
into the host epidermis. Conidiophores arise from the primary mycelium and are short and
non septate bearing conidia in long chains. The conidia are ellipsoid or barrel-shaped,
single celled and hyaline. The cleistothecia are dark, globose with the hyaline or pale
brown myceloid appendages. The asci are ovate and each ascus produces 2-3 ascospores,
which are thin walled, elliptical and pale brown in colour.
Favourable Conditions
Dry humid weather and low relative humidity favours the disease.
Disease cycle
The fungus is an obligate parasite and disease perenneates through cleistothecia in the
infected plant debris in soil. The ascospores from the cleistothecia cause primary
infection. The secondary spread is through wind-borne conidia.
Management
Remove and destroy infected crop debris.
Spray wettable [email protected]% or [email protected]%
Symptoms
The affected heads show water soaked lesions on the lower surface, which later turn
brown. The discoloration may extend to stalk from head. The affected portions of the head
become soft and pulpy and insects are also seen associated with the putrified tissues. The
larvae (Helicoverpa armigera) and insects which attack the head pave way for the entry of
the fungus which attacks the inner part of the head and the developing seeds. The seeds
are converted into a black powdery mass. The head finally withers and droops down
with heavy fungal mycelial growth.
Pathogen
Fungus produces dark brown or black coloured, non-septate hyphae. It produces many
aerial stolons and rhizoids. Sporangia are globose and black in colour with a central
columella. The sporangiospores are aplanate, dark coloured and ovoid.
Disease cycle
The fungus survives as a saprophyte in host debris and other crop residues. The disease is
spread by windblown spores.
Favourable Conditions
Prolonged rainy weather at flowering and damage caused by insects and caterpillars.
Management
Treat the seeds with Thiram or Carbendazim at 2g/kg.
Control the caterpillars feeding on the heads.
Spray fenthion 1ml plus wettable sulphur 2g per liter of water at the time of head
initiation.
Spray the head with Mancozeb at 1kg/ha during intermittent rainy season and repeat after
10 days, if the humid weather persists.
Symptoms
Initial symptoms of the disease appear 40 days after sowing. Infected plants can be spotted
from a distance by their sickly appearance, later the entire plant withers and dies. White
cottony mycelium and mustard seed sized sclerotial bodies are formed on the affected
stem near soil level.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Pathogen
The pathogen produces dark brown to black sclerotia.
Disease cycle
The fungus survives as sclerotia in soil and plant debris. The secondary spread of the
disease occurs through sclerotia by implements and irrigation water.
Favourable Conditions
Alternate periods of high soil moisture and water stress conditions predispose the disease.
Management
Collection and destruction of plant debris
Seed treatment with captan or [email protected]%
Drench the base of the plant with cheshunt [email protected]%
Addition of soil amendments like oat straw and finely grounded castor and neem cakes
reduces disease incidence.
Use of antagonistic fungi such as T. harzianum.
Symptoms
Various kinds of symptoms are being produced by the pathogen like damping off,
systemic infection, local lesions and basal rot or stem gall, etc. In systemic infections
plants are severely stunted. Chlorosis starts through midribs causing ultimately abnormally
thick, down ward curled leaves that show prominent yellow and green epiphyllous
mottling. A hypophyllous downy growth of the fungus develops.
Flower heads of affected plants remain sterile. Local foliar lesion symptoms are
characterized by small angular greenish yellow spots on leaves. Development of basal gall
symptoms occur independently of the infection that results in systemic infection. In
infected plants flower heads are erect.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Disease cycle
Primary infection of the crop occurs through soil borne oospores. Secondary spread of the
disease is through wind borne sporangia and zoospores.
Management
Regulatory measures to prevent races (other than race 1) of pathogen into India.
Follow spacing of 60x30cm or 45x30cm
Rogue out infected plants and destroy
Cropping sequence of sunflower followed by groundnut reduces the disease.
Seed treatment with [email protected]% (Apron 35SD) followed by foliar spray with
[email protected]% (Ridomyl MZ) is effective.
Hybrids like LSH-1, LSH-3, KBSH-1, Jwalamukhi, etc had high degree of resistance.
Symptom
The stems develop water-soaked spots which later may be covered with a cottony
white growth.
As the disease progresses, affected portions of the stem develop a bleached
appearance, and eventually the tissues shred.
Girdling of the stem results in premature ripening and in lodging of plants.
Hard black bodies, the sclerotia, are formed inside the stem and occasionally on
the stem surface. Basal stalk infections rarely occur.
Disease Cycle: Sclerotia are hard small black bodies produced by the disease in a host of
broad leaf crops. Sclerotia over winter in the soil and exist in the soil for many years.
Wet soil conditions over a period of 10 to 14 days can stimulate the sclerotia to germinate
creating tiny mushrooms. These mushrooms produce apothecia or tiny spores which can
be wind-blown to nearby fields. The spores need dew or rain and dead or senescing plant
tissue such as dead florets to germinate and infect. Wet and cloudy conditions are
necessary for the disease advancement.
Management
Use crop rotation; do not plant highly susceptible crops more than once in four years,
including dry edible beans, mustard and canola. Use at least a five year rotation for
severely infested fields.
Avoid planting next to a field that had severe Sclerotinia in the past four or five years.
Control broad-leaved weeds.
Plant thoroughly cleaned seed. Avoid dense stands of canola.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Sunflower necrosis virus (SND) Tobacco streak virus
Economic importance
The appearance of SND was observed for the first time during 1997 at Bangalore which
later spread to other parts of Karnataka, TN, A.P and Maharashtra. The disease was
observed on all stages of crop growth in Kharif as well as in Rabi and the incidence
ranged from 5-70%.
Symptoms
Initially small, irregular, necrotic patches appear on leaf lamina more near to the midrib.
As the necrosis advances it results into twisting of the leaf, later it extends through one
side of the leaf lamina to the petiole and stem and finally terminates at shoot of the plant
leading to paralytic symptom. Necrosis at bud formation stage makes the capitulum to
bend and twist. The necrosis symptoms appear on bracts and capitulum also. The early
infected plants become stunted, weak and die before flowering,. Necrosis affected flower
heads fail to open and no seed filling takes place.
Disease cycle
Tobacco streak virus of Ilar group causes the disease. The virus can be transmitted through
mechanical, sap inoculation from sunflower to other 22 hosts and vice versa. The virus is
transmitted by thrips through infected pollen as carrier. Weed hosts particularly,
Parthenium, Ageratum, Commelina and Achyranthus harbour the virus.
Management
Removal of weeds plants from the field and adjoining areas of crop.
Rouging of infected plants before flowering helps to destroy the virus source and spread
of the disease.
Avoid growing of chrysanthemum and marigold close to sunflower.
Growing 5-7 rows of border crop all around sunflower with sorghum or Bajra
Seed treatment with Imidachlorpid (Gaucho 70WS) @5g/kg followed by 2-3 sprays at 15
days interval starting from 25 days old seedlings to pre-seed setting stage with
Imidachlorpid (Confidor 200SL)@0.05% control the insect vector.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Sesamum
Pathogen
The mycelium of the fungus is dull brown and septate and produce large number of pale
grey-yellow conidiophores which are straight or curved. The conidia are light olive
coloured with transverse and longitudinal septa. There are around 3-5 septate and conidia
are borne in chain over short conidiophore.
Disease cycle
The fungus is seed-borne and also soil-borne as it remains dormant in the infected plant
debris.
Favourable Conditions
Low temperature (20-250C), high relative humidity, excessive rainfall and cloudy weather
favour the disease.
Management
Treat the seeds with Captan or [email protected]% or [email protected]% .
Hot water treatment at 530C for 30 minutes gives good control of the disease.
Spray twice with [email protected]% or Thiophanate [email protected]% or
[email protected]%
Pathogen
The fungus produces hyaline, septate mycelium which is ectophytic and sends haustoria
into the host epidermis. Conidiophores arise from the primary mycelium and are short and
non septate bearing conidia in long chains. The conidia are ellipsoid or barrel-shaped,
single celled and hyaline. The cleistothecia are dark, globose with the hyaline or pale
brown myceloid appendages. The asci are ovate and each ascus produces 2-3 ascospores,
which are thin walled, elliptical and pale brown in colour.
Disease cycle
The fungus is an obligate parasite and disease perenneates through cleistothecia in the
infected plant debris in soil. The ascospores from the cleistothecia cause primary
infection. The secondary spread is through wind-borne conidia.
Favourable Conditions
Dry humid weather and low relative humidity favours the disease.
Management
Remove the infected plant debris and destroy.
Spray Wettable [email protected]% or dust Sulphur at 25 kg/ha and repeat after 15 days.
Grow resistant varieties like Rajeshwari, SI-1926, KRR-2, etc.
Phyllody Phytoplasma
Economic importance
It is a serious disease capable of causing heavy losses. One per cent increase in disease
incidence reduces yield by 8 kg/ha. Its incidence in India ranges upto 20%.
Symptoms
The disease manifests itself mostly during flowering stage, where the floral parts are
transformed into green leafy structures, which grow profusely. The plants bear cluster of
leaves and malformed flowers at the tip. The flower is rendered sterile.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
The vein clearing can be seen in different floral parts. Stamens also become leaf like to
certain extent. Anthers become green and do not dehisce. Ovary is transformed into an
elongated out growth resembling a shoot. The plant is stunted with reduced internodes and
abnormal branching gives a bushy appearance. The infected plants generally do not bear
capsules, but if capsules are formed they do not yield quality seeds.
Disease cycle
The pathogen has a wide host range and survives on hosts like Brassica campestris var.
toria, B. rapa, Cicer arietinum, Crotalaria sp., Trifolium sp., Arachis hypogea and some
weed hosts. The disease is transmitted by jassid, Orosius albicinctus in a persistant
manner. Optimum acquisition period of vector is 3-4 days and inoculation feeding period
is 30 minutes. The incubation period of the pathogen in leaf hoppers may be 15-63 days
and 13-61 days in sesamum. Nymphs are incapable of transmitting the phytoplasma.
Vector population is more during summer and less during winter months.
Favourable conditions
Dry weather, moderate temperature (250C), low humidity (65%), minimum rainfall
(0.6mm) and dry season during February-March are congenial for the disease.
Management
Remove all the reservoir and weed hosts.
Delay sowing in the endemic areas to reduce the vector population and thereby the
disease.
Avoid growing sesamum near cotton, groundnut and grain legumes.
Rogue out the infected plants periodically.
Sesamum mulayanum is the resistant source to the pathogen.
Spray 2-3 times with Monocrotophos (0.03%) or [email protected]% at flowering stage
reduces the vector population.
Spray 500ppm tetracycline at flowering.
Pathogen
The bacterium is gram negative and rod shaped. It is an aerobic bacterium with one or
more polar flagella.
Disease cycle
The bacterium remains viable in the infected plant tissues. It is internally seed-borne and
secondary spread through rain splash.
Management
Keep the field free of infected plant debris.
Seed treatment with hot water at 520C for 10 minutes.
Steep the seed in Agrimycin 100 (250 ppm) or streptocycline suspension (0.055) for 30
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
minutes.
Spray twice with Streptomycin sulphate or Oxy-tetracycline hydrochloride at 100g/ha at
15 days interval.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Safflower
Symptoms
Dark brown lesions measuring 2-5mm in diameter are first found on hypocotyls and
cotyledons. The disease is severe on leaves and occasionally attacks stem and flowers.
Minute brown to dark brown spots with concentric rings of 1-2mm appear on leaves. The
centre of the spot is light brown with a dark brown margin. Elongated black lesions can be
seen on the petiole and stem. The fungal infection on flower buds leads to drying and
shedding. Seeds also may be affected. Dark sunken lesions are produced on the testa.
Pathogen
The mycelium of the fungus is sub-hyaline initially and become brown coloured on
maturity. The conidiophores are stout, erect, rigid, unbranched, septate and arise singly or
in clusters. The conidia are 3-11 celled with irregular shape, light brown in colour with a
long beak.
Disease cycle
The fungus is externally seed-borne and also survives in plant debris. The disease spread
is through windblown conidia.
Management
Collect and destroy infected plant debris
Treat the seeds with Thiram or Captan at 3g/kg or [email protected]%
Hot water treatment of seed at 500C for 30 minutes
Spray Mancozeb or [email protected]% or [email protected]%.
In seedling stage cotyledonary leaves show small brown spots either scattered or arranged
in a ring on the inner surface and they may be shrivelled or rolled or curved. Symptoms
become apparent when plants are in 6-10 leaf stage as yellowing of leaves followed by
wilting, Epinasty and vascular browning. Symptoms develop in acropetal succession. In
older plants the lateral branches on one side may be killed while the remainder of the
plant remains free from the disease. Infected plants produce small sized flower heads
which are partially blossomed. Most of the ovaries fail to develop seeds or they may form
blackish, small, distorted chaffy seeds.
Pathogen
The fungus produces hyaline, septate mycelium. Microconidia are hyaline, small, elliptical
or curved, single celled or two celled. Macroconidia are also hyaline, thin walled, linear,
curved or fusoid, pointed at both ends with 3-4 septa. The fungus also produces thick
walled, spherical or oval, terminal or intercalary.
Disease cycle
The fungus survives in seed, soil and infected plant debris. The primary spread is by soil-
borne chlamydospores and also by seed contaminant. The secondary spread in the field is
through irrigation water and implements.
Favourable conditions
The disease is severe in acidic soils with high nitrogen and warm moist weather with a
temperature of 15-200C is conducive for disease development.
Management
Avoid growing safflower in low lying areas
Collection and destruction of plant debris.
Follow crop rotation with sorghum
Grow wilt resistant / tolerant hybrids DSH 129, NARI-NH-1 and varieties A1, PBNS- 40
and NARI-6 in endemic areas.
Treat the seeds with Thiram or Captan at 3g/kg or [email protected]% or T. viride
@10g/kg seed
Symptoms
The fungus attacks cotyledons, young leaves, tender stems and underground parts.
Infection of the cotyledons is seen as yellow discoloration accompanied by drooping and
wilting. The pustules (uredosori) are chestnut brown in colour, erumpent and scattered
throughout the leaves. Later in the season, black teliosori are formed on the same spots.
Seedlings sometimes die suddenly without exhibiting symptoms in the aerial parts.
Infection on the hypocotyl causes hypertrophy of the tissues due to accumulation of
mycelium between cells. Stem girdling occurs in older plants. The rust pustules also
appear on tap root and lateral roots.
Pathogen
The fungus is an obligate parasite with autoecious life cycle in safflower. Uredia and telia
are produced and pycnial and aerial stages are unknown. Uredospores are single celled,
light brown coloured and echinulate. Teliospores are globose to broadly ellipsoid, two
celled, chestnut brown in colour, thick walled with hyaline pedicels.
Disease cycle
The fungus remains on the seeds and infected crop debris in the soil as teliospores for
more than a year. The fungus also produces uredial and telial stages in the collateral host
Carthamus oxyacantha and this also serves as primary source of infection in addition to
dormant teliospores in soil. The secondary spread occurs through wind-borne uredospores.
Management
Grow resistant varieties like Sagaramuthyalu, Manjeera and APRR-3.
Treat the seeds with Thiram or Captan@3g/kg or Carbendazim@2g/kg.
Remove and destroy the plant debris in the soil.
Rogue out the collateral host.
Spray wettable sulphur or [email protected]%
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Mustard
Economic importance
The disease makes its first appearance in the beginning of January shortly after the attack of
Alternaria leaf blight on the under surface of lower leaves.
Symptoms
Both local and systemic infection is observed. In case of local infection isolated white/
creamy yellow raised pustules appear on under surface of leaves which later coalesce to form
patches. Systemic infection causes hypertrophy and hyperplasia resulting in malformation
and distortion of floral parts. Entire inflorescence is replaced by swollen sterile structure
(Stag head). Maximum damage occurs when systemic infection of the stem is noticed.
Pathogen
The fungus is an obligate parasite. The mycelium of the fungus is non-septate, intercellular
which produces knob-like haustoria. Numerous short sporangiophores arise from the
mycelium on which sporangia are produced in a basipetal succession. In systemic infection,
Oogonia and antheridia join by means of a fertilization tube, resulting in oospore. The
oospores germinate to form zoospores in a vesicle. The zoospores are elliptical to kidney
shaped and are biflagellate.
Disease cycle
The fungus survives through oospores formed in affected host tissues. The secondary spread
is through zoospores disseminated by rain or irrigation water.
Management
Collect and destroy infected plant debris
Rotation with non-cruciferous crops
Early sowing of the crop (in first week of October)
Seed dressing with Metalaxyl (Apron 35SD)@6g/kg seed followed by a single spray with
Metalaxyl (Ridomyl MZ)@0.2%
Grow resistant varieties like RC 781, PYSR 8 and PR 10 (or) tolerant varieties like
Kranthi and Krishna
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms
Symptoms appear on all aerial parts but usually on leaves and inflorescence. Greyish white
irregular necrotic patches develop on the lower surface of the leaves. The most conspicuous
and pronounced symptom is the infection of inflorescence causing hypertrophy of the
peduncle or inflorescence (Stag head). The affected inflorescence does not produce any
siliqua or seed.
Pathogen: The fungus is an obligate parasite. The mycelium of the fungus is non-septate,
intercellular which produces haustoria. Sporangiophores are dichotomously branched with
sterigmata which are pointed with acute angles usually of equal length. Oval and non- papillate
sporangia are produced over the pointed sterigmata. Sporangia always germinate by germ tube
and behave as conidia.
Disease cycle
The fungus survives through oospores formed in affected host tissues and on weed hosts.
The secondary spread is through wind borne sporangia.
Management
Collect and destroy infected plant debris
Rotation with non-cruciferous crops
Early sowing of the crop (in first week of October)
Seed dressing with Metalaxyl (Apron 35SD)@6g/kg seed followed by a single spray with
Metalaxyl (Ridomyl MZ)@0.2%
Grow resistant varieties like RC 781, PYSR 8 and PR 10
Pathogen
The fungus is ectophytic, spreading on the surface of the leaf, sending haustoria into the
epidermal cells. Conidiophores arise vertically from the leaf surface, bearing conidia in short
chains. Conidia are of Oidium type. Later in the season, cleistothecia appear as minute,
black, globose structures with myceloid appendages. Each cleistothecium contains 4-8 asci
and each ascus contains 3-8 ascospores which are elliptical, hyaline and single celled.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Disease cycle
The fungus over-summers through cleistothecia as ascospores or as mycelium on
volunteer host plants. The disease spreads through wind borne conidia.
Favourable conditions
The disease is favoured by dry weather and becomes severe under irrigated conditions.
Management
Collect and destroy infected plant debris
Spray the crop with wettable [email protected]% or [email protected]% or [email protected]%
Symptoms
Symptoms of the disease start with formation of spots on leaves, stem and siliquae. The
spots produced by A. brassicae are usually gray compared to black sooty velvety spots
produced by A. brassicola.
Pathogen
The fungus produces dark brown, short, septate, irregularly bent conidiophores with a
single conidium at the apex. The conidia are obclavate, light to dark brown in colour with
both transverse and longitudinal septa, with a prominent beak.
Disease cycle
The pathogen survives in the infected crop debris as dormant mycelium. The secondary
spread is mainly by air-borne conidia.
Management
Removal and destruction of infected plant debris
Use disease free or treated seed (Mancozeb @2.5g/kg seed)
Spray with mancozeb (@0.25%) or Iprodione (0.2%) at 10 days interval.
Diseases of Linseed
•Rust - Melampsora lini
•Wilt -Fusarium oxysporum f.sp. lini
•Powdery mildew – Oidium lini
Rust - Melampsora lini
Symptoms:
•Bright orange and powdery pustules develop on leaves, stems and bolls but mostly on
the underside of the leaves.
•As the season progresses, the orange pustules turn black and produce overwintering
teliospores.
•Early infections may completely defoliate flax plants and reduce the seed yield.
Favourable conditions:
•High humidity during cool nights and warmer day temperatures
Management
•Destruction of plant debris from the diseased field.
•Seed treatment with Oxycarboxin.
•Spray of fungicides like oxathin derivatives, Dithane M-45, Cuman L.
Management :
Crop rotation of at least 3 years.
Seed treatment with Thiram or carbendazim@ 2.5g/kg seed.
Soil drenching with Carbendaazim @ 0.1 % or COC@ 0.25%
Pathogen
The fungus produces hyaline to light brown, septate and profusely branched hyphae.
Microconidia are oval to cylindrical, hyaline, single celled, normally arise on short
conidiophores. Macroconidia which borne on branched conidiophores, are thin walled, 3
to 5 septate, fusoid and pointed at both ends. Chlamydospores are rough walled or
smooth, terminal or intercalary, may be formed singly or in pairs in chains.
Disease cycle
The fungus may be seed-borne and survives in infected plant debris in soil. The primary
infection is through chlamydospores in soil, which remain viable upto next crop season.
The weed hosts also serve as a source of inoculum. The secondary spread is through
irrigation water, cultural operations and implements.
Favourable Conditions
High soil temperature (Above 250C), high soil moisture, monocropping and presence of
weed hosts like Cyperus rotundus, Tribulus terrestris and Convolvulus arvensis.
Management
Treat the seeds with Carbendazim or Thiram at 2 g/kg or treat the seeds with
Trichoderma viride at 4 g/kg or Pseudonomas fluorescens @ 10g/kg of seed.
Apply heavy doses of organic manure or green manure.
Follow 6-year crop rotation with non-host crops.
Grow resistant cultures like Kranthi (ICCC 37), Swetha (ICCV-2), ICCV 10, Avrodhi,
G 24, C 214, BG 244, Pusa 212 and JG 315.
surface. Sometimes a ring of small pustules can be seen around larger pustules which
occur on both leaf surfaces. Late in the season dark teliosori appear on the leaves. The
rust pustules may appear on petioles, stems and pods. It is heteroecious rust, but the
pycnial and aecial stages are unknown.
Pathogen
The uredospores are spherical, brownish yellow in colour, loosely echinulated with 4-8
germ pores. Teliospores are round to oval, brown, single celled with thickened apex and
the walls are rough, brown and warty.
Disease cycle
The fungus survives as uredospores in the legume weed Trigonella polycerata during
summer months and serve as primary source of infection. The spread is through wind-
borne uredospores.
Management
Destroy weed host.
Dust Sulphur at 20 kg/h or spray [email protected]%
Pathogen
The fungus produces hyaline to brown and septate mycelium. Pycnidia are spherical to
sub-globose with a prominent ostiole. Conidia are borne on short conidiophores inside
the pycnidia. They are hyaline, oval to oblong, straight or slightly curved and single
celled, occasionally bicelled. The perfect or perithecial stage is also seen on infected host
tissues, usually after the plant is dead. The perithecia are globose, dark coloured and
contain asci which are typically 8 spored. The ascospores are hyaline, thin walled and
two celled.
Favourable Conditions
Night temperatures of 100C and day temperature of 200C, rains accompanied by cloudy
weather and excessive canopy favour the disease spread.
Disease cycle
The fungus survives in the infected plant debris as pycnidia. The pathogen is also
externally and internally seed-borne. The primary spread is from seed-borne pycnidia
and plant debris in the soil. The secondary spreads is mainly through air-borne conidia.
Rain splash also helps in the spread of the disease.
Management
Grow resistant/tolerant varieties like Gaurav, C 235, G 543, GG 588, GG 688, BG
261 and GNJ 214.
Remove and destroy the infected plant debris in the field.
Follow crop rotation with cereals.
Deep sowing of seeds, i.e., 15cm or deeper.
Intercropping with wheat, barley and mustard.
Treat the seeds with Thiram 2g or Carbendazim 2 g /kg.
Exposure of seed at 40-500C reduced the survival of A. rabiei by about 40-70 per
cent. Spray with [email protected]% or [email protected]%.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Stem and Root rot or dry root rot Rhizoctonia bataticola (Pycnidial stage:
Macrophomina phaseolina) (Sexual stage: Thanatephorus cucumeris)
Symptoms
The disease generally appears around flowering and podding time in the form of scattered
dried plants. The seedlings can also get infected. The first symptom of the disease is
yellowing of the leaves. The affected leaves, petioles and leaflets droop within a day or
two. The leaves and stems of the affected plants turn straw coloured and plants wilt
within a week. The lower portion of the tap root usually remains in the soil when plants
are uprooted. The tap root is dark showing signs of rotting and is devoid of most of the
lateral and finer roots. Dark minute sclerotial bodies can be seen on the roots exposed or
inside the wood.
Pathogen
The hyphae of the fungus are dark brown, filamentous and septate with constrictions in
hyphal branches at the junction with main hypha. The sclerotia are brown and irregular in
shape. The fungus has its sexual stage, T. cucumeris, which produces 2-4 basidiospores in
terminal clusters on a celled hypha.
Disease cycle
The pathogen survives in the soil in infected host debris as sclerotia for several years. The
secondary spread is through farm implements, irrigation water and rain splash.
Favourable conditions
Maximum ambient temperatures above 300C, minimum above 200C, and moisture stress
favour disease development.
Management
Treat the seeds with Carbendazim or Thiram at 2 g/kg or seed pelleting with
Trichoderma viride at 4 g/kg or Pseudomonas fluorescens @ 10g/kg of seed.
Apply farmyard manure at 10 t/ha.
Grow tolerant genotypes like ICCV 10
Gray mold
Caused by Botrystis Cincerea.
Seed borne disease.
Excessive vegetative growth, close, spacing, and spreading varieties favor disease
development.
Symptoms:
Symptoms are usually seen at flowering time when the crop canopy is fully
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
developed.
Lack of pod setting is the first indication of the disease.
Lesions girdle the stem completely.
Rotting of affected leaves and flowers.
Water-soaked and irregular lesions on the pod.
The pods contain either small, shrivelled seeds or no seeds at all.
Management
Sowing late.
Adopting wider spacing.
Intercropping with linseed.
Avoiding excessive irrigation, and vegetative growth.
Adopting compact varieties.
Seed treatment with thiram 3 g kg-1 or vinclozolin or Dithane M-45 (maneb).
Foliar application of vinclozolin or carbendazim or carbendazim plus thiram.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Lentil
Wilt: Fusarium oxysporum f.sp. lentis
Symptoms
In India lentil wilt was first reported from undivided Bengal in 1934. The pathogen
causes serious disease and is widespread in India. It is a soil borne, root pathogen
colonizing the xylem vessels and blocking them completely to cause wilting.
The disease appears in the field in patches at both seedling and adult stages.
Seedling wilt is characterized by sudden drooping, followed by drying of leaves and
seedling death.
The roots appear healthy, with reduced proliferation and nodulation and usually no
internal discoloration of the vascular system.
Adult wilt symptoms appear from flowering to late pod-filling stage and are characterized
by sudden drooping of top leaflets of the affected plant, leaflet closure without premature
shedding, dull green foliage followed by wilting of the whole plant or individual
branches.
Seeds from plants affected in mid-pod-fill to late pod-fill are often shriveled.
Epidemiology
The fungus is soil borne, which can survive in the soil and plant debris in the absence
of its host for a period of 3-4 years.
The disease is favoured by low soil temperature, 30 per cent soil water holding
capacity and increasing plant maturity.
Yield losses depend on the stage at which the plant wilts; it can be 100 per cent when
wilt occurs at pre pod stage, about 67 per cent when it occurs at the pre harvest stage.
Management
The best method of controlling lentil wilt is to use resistant varieties, a number of
which are now available as Pant L-4, Pant L-6, Pant L-8 and Noori.
Seed treatment with benornyl (0.3%) or thiram + benomyl (1:1, 0.3%) reduces
wilt incidence and increases grain yield.
Soil amendment with organic matter enhances antagonism with other soil
microflora. – Ploughing of the field during summer.
Following crop rotation with cereal crops which are not affected by wilt pathogen.
Using antagonistic microflora like Bacillus subtilis, Trichoderma harzianum, T.
viride @ 4 g/kg seed.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Epidemiology
The disease generally starts from low-lying patches in the paddock and radiates
towards the border.
Rust is an autoecious fungus, completing its life cycle on lentil.
High humidity, cloudy or drizzly weather with temperatures 20 to 22°C favour
disease development.
The disease generally occurs during the flowering /early podding stage.
Management
Use of foliar fungicides as Hexaferb and Dithane M-45 give best control.
Fungicides as Mancozeb (0.2% a.i.), Bayleton (0.05% a.i) and Calixin (0.2% a.i.) are
found effective against the pathogen.
Foliar spray of benomyl, carboxin, metalaxyl, oxycarboxin thiram,triademafon either
alone or in combination of Dithane M-45 are also effective.
Lentil varieties Pant L-639, Pant L-406, Pant L-6, pant L-7 and Pant L-8 are resistant.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Pea
1. POWDERY MILDEW Erysiphe pisi
Powdery mildew is one of the most common and serious diseases of pea which is
prevalent throughout the world. In India this disease was first time reported by Butler
(1918) from Dehradun.
Symptoms:
Initial symptoms appear as minute discoloured patches with thin fine meshwork of
white mycelium arising at many places on the upper surface of lower leaves and these
white patches soon join together to form larger whitish floury areas.
In severe cases of disease development, both upper and lower surfaces of the leaf are
infected.
The conidia and condidiophores are produced in such profusion that the foliage looks
as if dusted with flour and the whole crop in the field appeared white from a distance.
With the progress of the disease, similar symptoms are also noticed on tendrils, petioles
and stems.
Pods are infected in all the developmental stages, but immature pods are more prone to
rapid infection.
The affected pods show white floury patches consisting of white powdery mass and
these patches then turn light brown and finally dark brown in colour and later become
necrotic.
Such infected pods are either unmarketable or fetch minimum price in the open market.
Pathogen:
Management:
Symptoms: Symptoms of the diseases appear as true wilt and near wilt which are
described below:
True wilt:
Initially, the lower leaves look pale yellow and droop downwards.
With the progress of the disease, similar symptoms appear on the upper leaves also and
the affected plants give a stunted look.
Slowly the upper plant parts loose their turgidity and the whole plants topple down.
Stems are shriveled and some of the root lets are also injured.
In diseased plants, yellow to orange brown discolouration of vascular system of upper
tap root extending up to the stem is evident.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Near wilt:
Symptoms are also similar to those described above except for their slow development.
In this case, the vascular discolouration of the roots is typically brick red and usually
extends up to the growing tip.
Cortical decay is also observed in lower parts of the stem and upper tap root.
Pathogen:
The disease is caused by Fusarium oxysporum Schlech. ex. Fr. f.sp. pisi (Hall) Snyd. &
Hansen (race 1= wilt; race 2= near wilt).
The hypha of the fungus is septate, delicate white to peach coloured, usually with a
purple tinge.
Micro-conidia are borne on simple phialides arising laterally on hyphae or from short
less branched conidiophores and these are oval ellipsoid to cylindrical or curved.
Macroconidia are borne on branched conidiophores or on the surface of sporodochia
and these are thin walled, 3-5 septate, fusoid-subulate and pointed at both ends.
Chlamydospores are both terminal and intercalary.
The pathogen is soil borne and can survive in the soil for several years.
The fungus causes infection of the fibrous roots or epicotyl region, grows both inter and
intracellularly in the cortex and ultimately concentrates in the xylem vessels.
After death of the plant, the fungus continues to grow and sporulate on the stem cortex,
resulting in the production of soil borne inoculum.
o o
The disease progresses fast at 21 C while near wilt requires 24-28 C.
True wilt is not serious in very wet soils while wet soils favour near wilt.
Neutral to alkaline soils favour true wilt while the acidic soils retard it.
Management:
Symptoms:
Late in the season, teleuto pustules also develop on the leaves but most commonly on
stems and petioles. They are dark brown or almost black in colour.
Pathogen:
It is an autoecious rust with all its spore stages on the same host.
The rust is seed borne in broad beans but in peas and lentil, it is mainly survive as
teliospores in crop debris.
In India, the rust appears to survive on weed hosts belonging to Lathyrus, Vicia etc. and
the spores are wind blown to the main crop.
The teliospores on germination produce a promycelium on which sporidia are borne.
The sporidia germinate and germ tube infects the host, produce pycnia and finally
aecial cups are produced.
Uredia occur late in the season and are not of much importance in secondary spread.
Later in the season, teliospores are produced which help in overwintering of the
pathogen.
o
Prevalence of low temperature (17-22 C) coupled with high humidity, dew or frequent
light rain showers are favourable for initiation of the disease by aeciospores.
Rust severity and pustules/plant increase progressively with an increase in the duration
of leaf wetness up to 24 h, at optimum temperature of 20oC.
Management:
Disease Cycle
The fungus that causes downy mildew survives in the soil and on pea trash and can be
seed-borne.
Infected seed can act as a primary source for systemic and local infections. The disease
can develop quickly when conditions are cold (5 - 15°C) and humid over 90 per cent for
4 - 5 days, often when seedlings are in the early vegetative stage.
Individual seedlings become infected and act as foci of infection from which the
disease spreads. Rain is the major means of spore dispersal and infection. Heavy dew will
promote sporulation.
Dry, warm weather is unfavorable for the disease. Systemic infection of plants can lead
to the disease developing late in the season if conditions are favourable.
Management
Varietal Selection: Growing a resistant variety is the most effective means of
controlling downy mildew in districts prone to this disease.
Chemical Control: Seed dressing with metalaxyl or oxadixyl (Group 4 systemic
phenylamide fungicides) can be effective. Seed treatments reduce the number of
seedlings with primary infection, thereby reducing the amount of air-borne spores that
cause secondary infection in the surrounding crop.
Crop Rotation: Extended crop rotations and destruction of infected pea trash will
minimize the risk of serious disease. Extended crop rotations allow spore numbers in the
soil to decline before sowing again to field peas. A break of at least 3 years between field
pea crops is recommended. Avoid sowing pea crops adjacent to last season’s stubble.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Citrus
Symptoms
Disease starts as water soaked large patches on the basal portions of the stem near
the ground level
First symptoms are dark staining of bark which progresses into the wood.
Bark in such parts dries, shrinks and cracks and shreds in lengthwise vertical
strips.
Bark at the base is destroyed resulting in girdling and finally death of the tree.
Later profuse exudation of gum from the bark of the trunk occurs. There may be a
considerable amount of gum formation in sweet oranges, but relatively little in
grapefruit.
Infection extends to crown roots.
Prior to death, the plant usually blossoms heavily and dies before the fruits
mature.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Favourable conditions
Prolonged contact of trunk with water as in flood irrigation; water logged areas and
heavy soils predispose the disease. Incidence is more in black soils than in light soils;
high water table leads to high incidence. The disease is severe in high rainfall areas.
Management
Preventive measures:
Selection of proper site with adequate drainage and high budding (30 to 46 cm or
above).
Provision of an inner ring about 45 cm around the tree trunk to prevent moist
soil. (Double ring method of irrigation)
Avoid irrigation water from coming in direct contact with the trunk.
Avoid injuries to crown roots or base of stem during cultural operations.
Use resistant sour orange rootstocks for propagating economic varieties
Painting Bordeaux paste or with ZnSO4, CuSO4, lime (5:1:4) to a height of about
60 cm above the ground level at least once a year.
Curative measures:
Scrape the diseased portion with a sharp knife.
Protect the cut surface with Bordeaux paste followed by spraying of 0.3% fosetyl-
AL reduces the spread.
Soil drenching with 0.2% metalaxyl and 0.5% Trichoderma viride commercial
formulation is also effective.
Symptoms:
Profuse gumming on the upper portions of the trunk, branches and twigs.
Infection starts at growth cracks or ridges at crotches.
Gum oozes out from the cracks developed on the diseased portion.
From bark, the infection spreads to wood which dries and becomes
discoloured.
Large limbs are killed and if left unchecked the whole tree may be killed in
course of time.
Sometimes branches break at the infected portion.
Favourable conditions
Reduced tree vigour, insect damage, malnutrition and old age predispose the disease.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management
The tress should be kept in a vigorous growing condition.
Wound in the bark especially on limbs and forks should be scraped and protected
with Bordeaux paste.
Gummed portions of affected bark should be removed and the cut surface
protected.
Spraying with 0.1% carbendazim on the affected limbs and forks is useful to
restrict the disease spread.
3) Dry root rot: Fungal complex (Fusarium sp., Diplodia natalensis and
Macrophomina phaseolina)
Economic Importance: Dry root rot is a major problem in all citrus growing areas of
Andhra Paradesh in both sweet orange and acid lime. It is also common in North
Arcot district in Tamil Nadu and in Mandarins in Wynad
Symptoms:
The disease is characterized by moist decay of root bark in the early stages. Later,
the bark becomes dry and shredded with hard dead wood underneath.
The affected trees show yellowing of foliage and bare necks.
The flowering is increased and the affected trees bear a heavy crop of small sized
fruits. The affected roots emit a foul odour and the tree finally dies.
Peeling of bark of the affected roots and formation of black sclerotia on the root
surface is also common
Favourable conditions
Excessive moisture, direct contact of water with trunk, poor aeration, heavy soils, and
frequent injuries to roots, excessive manuring at long intervals and close planting
favour dry root incidence. Lack of sufficient moisture or inadequate supply of
nitrogen may also lead to this disease. Defective soil, hard pan formation below the
second foot and unfavourable soil-air-moisture relationship in the subsoil leads to
inadequate oxygen at root zone which is primarily responsible for the incidence of dry
root rot.
Management:
Cut and destroy the diseased roots, if only one or two roots are affected and the
tap root and crown are still in good condition. The cut surface should be protected
with Bordeaux paste.
Avoid deep ploughing or digging which are likely to injure roots
Leaf mulch in the tree basins during the dry season helps in conserving the soil
moisture and thereby reduces disease incidence
Spray with Urea (4.5 kg in 450 litres of water) to reduce disease intensity
Drench the soil with 0.25 carbendazim + 0.25% Mancozeb at the rate of 1 litre per
m2 of the tree basin in early stage of infection
Apply 10 kg of neem cake followed by soil drenching with 0.5% Trichoderma
viride formulation + 0.2% copper oxy chloride in the early stages of infection
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms:
The disease attacks leaves, twigs and fruits.
The lesions on leaves in early stages consist of small, semi-translucent dots
which become sharply defined pustular elevations usually on the underside, flat or
somewhat depressed at the center. The opposite surface corresponding to the
warty growth shows a circular depression with a pink to red centre. In later
stages, leaves often become distorted, wrinkled, stunted and mis-shapened.
The twigs also develop similar lesions and the affected twigs are ultimately killed.
On the fruit, lesions consist of corky projections which often break into scab
affecting larger areas on the fruits. The surface becomes rough and distorted.
The market value of the fruits is considerably reduced, though the fungus rarely
affects the fruit flesh below the skin.
Favourable conditions
Young leaves are highly susceptible.
The fungus infects tissues only when the surface is wet and prefers temperature of
16 to 230C. The disease is a problem under low temperature and high humidity
conditions
Management:
The diseased leaves, twigs and fruits should be collected and destroyed
Spray with 0.3% COC or 1.0% Bordeaux mixture or 0.2% Difolaton or 0.2%
chlorothalonil at 15 days interval.
Symptoms:
Canker appears on leaves, twigs, petioles, branches, fruit stalks, fruits and thorns.
When it is severe, trunk and roots are also affected.
But the symptoms are most conspicuous on leaves, twigs and fruits.
The lesions appear as minute water soaked round, yellow spots which enlarge
slightly and turn brown, eruptive and corky.
On acid lime and sweet orange they are about 2 to 3 mm in diameter. These
pustules are surrounded by a characteristic yellow halo.
Canker lesions on the fruit do not possess the yellow halo as on leaves. Several
lesions on fruit may coalesce to form a patch. The crater-like appearance is more
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Favourable conditions: Free moisture for 20 minutes at 20-30°C initiates the disease.
Management
Prune out and burn all canker infected twigs before monsoon
Periodical spraying of bactericides along with an insecticide
Use canker tolerant varieties like “Tenali selection” and “Balaji”
Select seedlings free from canker for planting in main field
Spray Streptocycline (1g) + Copper oxy chloride (30g) in 10 litres of water at
fortnightly intervals for effective management of canker in citrus nurseries
Three sprayings of Streptocycline (1g) + Copper oxy chloride (30g) in 10 litres of
water at an interval of 20 days during rainy season is effective for leaf canker
Fruit infection can be prevented by two sprays of Streptocycline (1g) + Copper
oxy chloride (30g) in 10 litres of water at marble stage followed by another spray
30 days later
Control leaf miner when young flush is produced.
It affects all kinds of citrus plants but primarily orange, grapefruit and lime. Tristeza
symptoms consisting of a quick or chronic tree decline are particularly common and
severe on trees propagated on sour orange root stocks. The name “Tristeza” was
suggested to describe the sad appearance of the diseased citrus trees. Kagzi lime and
Nasnaran are indicator plants for CTV detection.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms:
Tristeza affected trees look chlorotic and sickly in the early stages. Gradually the
leaves drop and the defoliated twigs show die-back. The declining trees die
gradually but sometimes apparently healthy trees die suddenly.
Vein clearing or vein flecks (elongated translucent area) in young leaves of acid
lime is seen intermittently when viewed against light (characteristic symptom).
In sweet orange, the specific symptom of tristeza is honeycombing, a fine pitting
of inner face of bark in the portion of trunk below the bud union. In acid lime
which is highly susceptible to the disease, vermiform or linear pits appear in the
woody cylinder.
Tristeza infected citrus trees on sour orange rootstocks cause phloem necrosis at
the graft union
Diseased trees usually blossom heavily. Trees with stem pitting are stunted and
set less fruits. The fruits are of smaller size and of poor quality (insipid fruits). As
the fruits develop, the tree wilts partly or completely.
Grapefruit and acid lime are susceptible irrespective of root stock.
Pathogen: Tristeza is a highly flexuous filamentous virus 2000nm long and 10-12nm
in width. The virus is restricted to only phloem tissue and is a member of
Closterovirus group. CTV has ss +ve sense RNA of 20 K nucleotides as its genome.
Management:
Strict quarantine measures to be enforced
Use certified budwood free of CTV
Remove all diseased trees as and when the disease is noticed. Fresh plantings to be
taken with virus free materials on tolerant rootstocks. For sweet orange and
mandarin avoid susceptible root stocks.
For Andhra Pradesh, Maharashtra and Karnataka, Rangapur lime is
recommended as a root stock resistant to Tristeza. For the Punjab region,
Jattikhatti, Cleopatra mandarin and sweet orange are recommended as resistant
root stocks.
For acid lime, use seedling preimmunised with mild strain of tristeza virus (Cross
protection).
Periodic sprays of insecticides like Monochrotophos 0.05 % reduce s the
secondary spread of the disease in the orchard.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms:
Affected trees are stunted with pronounced leaf and fruit drop. Varied chlorotic
patterns on leaves are noticed which are persistent and cannot be corrected by zinc
sprays.
Reduction in leaf size is common. Many affected leaves show small circular
green islands within the chlorotic areas. Heavy leaf fall occurs with the onset of
summer. Often new flush may come out and leaves formed are short, upright and
chlorotic with green veins or with green blotches on the leaves.
Twig die-back occurs. Some branches in a tree exhibit severe symptoms whereas
others in the same tree are apparently normal.
Fruits show reduction in size, lopsided growth and oblique columella.
The rind surface exposed to sun appears yellow whereas the remaining portion
remains dull green. Diseased fruits are valueless owing to small size, distortion,
low in juice and soluble solids, high in acid and insipid taste.
Seeds are poorly developed, dark coloured and aborted.
Mode of spread:
The disease is transmitted through infected bud wood and citrus psylla, Diaphorina
citri. The disease also transmits from citrus to Periwinkle (Catharanthus roseus)
through dodder.
Management
Select certified disease-free seedlings.
Control psyllids with insecticides like dimethoate.
Use pathogen free bud wood for propagation.
Raise virus free plants through shoot tip grafting
500 ppm tetracycline spray though effective, requires fortnightly application
which is not economic.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Mango
Symptoms:
The disease can easily recognized by whitish or grayish powdery growth on the
inflorescence and tender leaves.
Generally the infection starts from the inflorescence and spreads downwards covering the
floral axis, tender leaves and stem. Leaves become twisted, curled and defoliate.
Infected floral parts are severely damaged and drop off. If the fruits are set, they do not
grow in size and may drop before attaining pea size. Fruits are sometimes malformed,
discolored due to severe mildew attack.
Because of poor fruits set and heavy flower and fruits drop, the loss due to the disease
may go as high as 70-80%.
Favourable conditions
Disease spread is favored by warm humid weather with cool nights.
Mode of spread:
Dissemination is by wind and the progress of the disease in the orchard is along the
direction of wind.
P.I: Through infected plant debris by conidia S.I: Wind borne conidia of Oidium
mangiferae.
Management
Can be controlled with two preventive sprays with wettable sulphur 0.3% once before the
flowers open and 2nd after the fruit set.
Dusting twice or thrice with fine sulphur will check the disease.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Spraying with Karathane 0.1% or cosan 0.1% before flowering and after fruit set (peanut
stage).
Resistant varieties: Neelum, Zardalu, Banglora, Torapari-khurd and Janardhan pasand
Disease cycle:
P.I: Mainly through previous season infected leaves, defoliated branches, mummified
flowers and flower brackets.
S. I: Mainly due to rain splash or wind driven rain water.
Management
Avoid over-crowding of orchards
Tree sanitation is important. Diseased twigs are to be pruned and burnt (along with fallen
leaves.)
Spray carbendazim or Topsin M (0.1%) or Chlorothalonil (0.2 at 14 days intervals until
harvest.
Before storage, treat the fruits with hot water (50-55°C), for 15 minutes or dip in
Benomyl solution (500ppm) or Thiobendazole (1000ppm) for 5 minutes or expose them
to ammonia and sulphur dioxide gases.
Symptoms:
There are two types of symptoms namely floral malformation and vegetative
malformation.
Vegetative malformation: There is a proliferation of infected tissue. The affected plants
develop excessive vegetative branches which are of limited growth, swollen and have
short internodes.
These dwarf branches are of various sizes which are often produced on the top of young
seedlings giving a bunchy top appearance. The axillary buds of dwarf branches are
unusually enlarged.
Vegetative malformation is more pronounced in young seedlings and seedling trees
than in grafted plants.
Floral malformation: The flowering panicles instead of coming out as a normal one
turns into just compact bunch of hard flowers. Individual flower is greatly enlarged and
has a large disc.
The inflorescence gets hypertrophied. The percentage of bisexual flowers in malformed
panicles is very low.
The malformed heads dry up in black masses and persist on the trees for a long time.
Disease cycle:
P. I: Through malformed inflorescence
S. I: Either by air borne conidia or by conidia carried by eriophid mite Aceria mangiferae
Management:
1. Use of disease free planting material and prophylactic spray of insecticides and
fungicides.
2. Pruning of diseased parts along with basal 15-20 cm apparently healthy portions.
3. Spray Captan (0.2%) or Benomyl (0.1%).
4. Spray napthelene acetic acid (NAA) 200 ppm during first week of October.
4. Bacterial canker
Symptoms
The disease attacks the leaves, leaf stalks, stem and fruits.
On the leaves disease first manifests itself as minute, water soaked irregular lesions,
black and is surrounded by chloratic haloes.
Due to vein limitations the spots become angular and result in cankerous patches,
which sometime dry up.
Sever infection results in defoliation. The bacteria also infects the fruits first showing
water soaked lesions, which later become dark brown to black and causes sever
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Etiology
Xanthomonas campestris pv.mangiferae-indicae (Patel et al.) Robbs et al.
It is a gram negative rod, motile by monotrichous flagella
Phylum:Proteobacteria
Class:GammaProteobacteria
Order:Xanthomonadales
Family: Xanthomonadaceae
Genus: Xanthomonas sp campestris: pv. mangiferae-indicae
Management
Use of clean planting and grafting material and Use of certified seedlings
Two sprays of streptocycline200-300ppm at 20days interval reduce fruit infection.
Dipping the fruits in 200ppm solution of agrimycin-100 is effective.
Mango verities like Bombay green, fazali, Jehangir and suvarnarekha are resistant.
Under high humid conditions these spots fuse, leaves turn yellow and drop down
prematurely.
Longitudinal cracks develop on petioles.
On green twigs, dark lesions of infection spread to inflorescence stalks.
When fruits are attacked, water soaked lesion develop and turn dark brown to black.
The affected fruits become yellow with deep cracks severely affected fruits are shed
prematurely.
Management:
Forthrightly spray of 1% B.M. or Agrimycin - 100 or Paushanycin or Plantomycin
(200ppm) or Streptomycin
Resistant variety: Bombay green
Mode of spread: Diseased leaves serve as primary inoculum. Scale insects and aphids,
Lecanium hemisphaericum, L. viride, L. nigrum, Hemilecanium imbricans and Pulvinaria
Psidii.
Management:
Controlling of plant hoppers by spraying Carbaryl (2g/lt) or Phosphomidon 0.03%
Spray dilute solution of starch or maida 5% (Boil 1 kg of maida or starch in 5 litres of
water, cool and dilute to 20 litres), which dries up and comes off in flakes, removing
along with it the sooty mold growth.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms:
The disease is characterized by red rusty spots on the leaves and young twigs
The spots are initially circular, slightly elevated and later coalesce to form irregular spots.
The upper surface of the spot consists of numerous unbranched filaments of the pathogen
which project through the cuticle. Some of the filaments represent the sterile hairs while
others the fertile ones
Initially the spots are greenish-grey in colour and variety in texture, but later on the
surface bears reddish-brown appearance.
Disease cycle: Common in close plantations. High moist conditions favour the
development of fruiting bodies.
P.I.- Zoospores.
Management:
Avoid close plantations
Spray Bordeaux mixture 1-2% or Fytolan / Blitox 0.5% or lime sulphur 0.1%
8. Loranthus
Symptoms:
Loranthus is a partial stem parasite. Loranthus seeds are disseminated by birds on to the
stems of the host.
Loranthus seeds do not require a host germination stimulus and will germinate
spontaneously.
The seedling radicle is negatively phototrophic and thus grows towards a dark surface
(often the host branch).
The first attachment structure formed is called a holdfast. The haustorium from the
holdfast eventually connects to the host xylem.
Parasite removes water and mineral nutrients from the host.
When in contact with the host cambium, the loranth haustorium induces the formation of
additional wood that enlarges into fluted columns.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management:
Pruning of affected branches
Periodic removal of mistletoes from infected branches and stems
Ethephon effectively controls mistletoes in some situations
Inject copper sulphate and 2,4-D into affected branches
Spray of diesel oil emulsion in soap water
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Grape
Losses in yield of fruits may be upto 40-60%. In addition to loss of yield, infected berries
tend to be higher in acid content than healthy fruits and are unsuitable for wine making.
Symptoms
The disease attacks the vines at any stage of their growth. All the aerial parts of the plant
are attacked. Cluster and berry infections usually appear first.
Floral infection results in shedding of flowers and poor fruit set.
Early berry infection results in shedding of affected berries.
Powdery growth is visible on older berries and the infection results in the cracking of
skin of the berries. Often infected berries develop a net-like pattern of scar tissues.
Powdery growth mostly on the upper surface of the leaves.
Malformation and discolouration of affected leaves. Leaf lesions appear late and doesn’t
cause much damage
Discolouration of stem to dark brown.
a. The first powdery mildew lesions are frequently found on the undersides of leaves
b. Very small orange to black spherical structures called cleistothecia develop on the upper and lower surfaces of leaves
c. Brown to black irregular blotches that can measure up to a few centimetres, follow the gradual degeneration of the fungus over
the course of the season
d. Berries turn ash grey colour and quickly become covered in spores, giving them a floury appearance.
e. At the end of the season, cleistothecia also appear on the berries
f. Affected berries dry out and may drop off
Favourable conditions
Cool dry weather
Maximum temperature in the range of 27-310C with R.H. upto 91% favour disease
incidence (November and December). Increase of R.H. by 1% increased disease
incidence by 2.4% and increase of temperature by 10C decrease the disease by 4.4%.
Management
Clean cultivation of vines or removal and destruction of all diseased parts
Dustings of vines with 300 mesh Sulphur (1st when new shoots are 2 weeks old, 2nd prior
to blossoming, 3rd when the fruits are half ripe).
Prophylactic spray with B.M. 1% or Lime sulphur at dormant stage delays development
of disease by decreasing initial inoculum.
Spray wettable sulphur @0.3% or karathane or calixin @0.1%
Morestan @0.03% sprayed at 4 days interval starting from last week of December to 1st
week of March
Grow resistant varieties like Chholth Red, Chholth white, Skibba Red, Skibba White, etc.
Symptoms
Symptoms appear on all aerial and tender parts of the vine. Symptoms are more
pronounced on leaves, young shoots and immature beries.
Irregular, yellowish, translucent spots on the upper surface of the leaves.
Correspondingly on the lower surface, dirty white, powdery growth of fungus appears.
Affected leaves become, yellow and brown and gets dried due to necrosis
Premature defoliation.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Favourable conditions
Optimum temperature : 20-22°C
Relative humidity : 80-100 per cent
Management
Collect and burn fallen leaves and twigs
Sanitation of the orchard
Vine should be kept high above ground to allow circulation of air by proper spacing
Pruning (April- may & September and October) and burning of infected twigs
Grow resistant varieties like Amber Queen, Cardinal, Champa, Champion, Dogridge and
Red Sultana
The disease can be effectively managed by giving 3-5 prophylactic sprays with 1%
B.M or Fosetyl -Al (Aliette) 0.2% or metalaxyl + mancozeb 0.3 to 0.4% or Azoxystrobin
or Dimethomorph
Chemical -5 sprays with 1% B.M.
1-Immediately after pruning of vines
2-When new flush formed (3-4 weeks after pruning)
3-Before buds open
4 -When bunches or berries have formed
5-During growth of shoots
It is especially serious on new sprouts during rainy season. Among various foliar diseases
of grapevine in India, anthracnose has longest spell spread over the period from June to
October
Symptoms
Visible on leaves, stem, tendrils and berries.
Young shoots and fruits are more susceptible than leaves.
Circular, greyish black spots or red spots with yellow halo appear.
Later the centre of the spot becomes grey, sunken and fall off resulting in a symptom
called ‘shot hole’.
Black, sunken lesions appear on young shoots.
Cankerous lesions on older shoots. Girdling and death of shoots occur.
Infection on the stalk of bunches and berries result in the shedding of bunches and berries
respectively.
Sunken spots with ashy grey centre and dark margin on fruits (Birds eye symptom). In
warm and wet weather pinkish spore mass develop in the centre of the spots
Mummification and shedding of berries.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
a. The fungus will cause small round spots which, as they age, give way to small holes (leaving a ‘shot-hole’ appearance)
b. During severe infections, the leaves shrivel up and drop.
c. Deep elongated cankers, greyish in the centre with a black edge
d. Inflorescences can turn yellow, brown, then dry out completely.
e. Deep spots, violet turning greyish in the centre, with a black edge
f, g. Severely infected berries dry up and drop prematurely
Etiology
Anamorph – Gloeorporium ampelophagum, produce hyaline, single celled conidia.
Teleomorph - Elsinoe ampelina, Produces hyaline 4 celled ascospores
Mode of spread and survival
Survives as dormant mycelium in the infected stem-cankers
Secondary spread is by means of conidia formed in the leaf and other plant parts which
are easily disseminated by wind and splashed rain. Continuous drizzle of rain for 2-3
days encourages the disease. No infection can take place in the absence of rain. Wind
associated with warm atmosphere (temp.) and heavy rains favour the disease spread.
Favourable conditions
Warm wet weather
Low lying and badly drained soils.
Anab-e-shahi is susceptible.
Management
Removal of infected twigs
Selection of cuttings from disease free areas and dipping them in 3% FeSO4 solution for
½ an hour before planting.
Spraying Bordeaux mixture 1% or COC@ 0.2% or [email protected]%.
Grow resistant varieties like Banglore blue, Golden muscat, Golden queen and Isabella.
Favourable conditions
High humidity
High rainfall and dew
Heavy dosage of N2 fertilizers
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management
Destruction of crop debris
Selection of disease free seed
ST with mancozeb@2g/kg seed
Foliar spray of [email protected]%
Disease cycle
P.I: Mainly from infected twigs. Bacterium survives in the soil on plant debris.
S.I Through wind splashed rain.
Management
Prune out and destroy infected plant debris
Spraying antibiotics like streptomycin 100 ppm along with copper fungicides
Symptoms
The presence of clustered, small, yellow to orange, powdery spores on the underside of
mature grapevine leaves. Small, dark spots also appear on the upper surface.
Under severe infection, the entire leaf surface is covered by sori and premature
defoliation occurs
The disease eventually lead to weakening of the vine due to poor shoot growth
Reduction in quantity and quality of fruit.
Disease cycle
P.I: Teliospores
S.I: Uredospores
GLR affects Vitis spp., including commercial and some ornamental grape varieties. It has
also been found on native Ampelocissus species
Management
Spray [email protected]% or dust sulphur@25Kg/ha
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Apple
Scabby spots on fruit begin as sooty, gray-black lesions and may have a white or red
halo
The lesions later become sunken and tan and may have spores around their margins
Infected fruit become distorted and may crack, allowing entry of secondary organisms
Severely affected young fruit may drop
Management
Clean cultivation
Resistant varieties: Emira, red free, Ambstraking, Ambroyal, Ambrich and Ambred
Spray [email protected]% or [email protected]% at short intervals after petal fall
Single application of [email protected]% at green bud stage followed by
[email protected]% at petal fall
Spray schedule
1st spray - Silver tip stage -0.2% captofol (or) 0.3% captan
IInd spray pink bud - 0.2% captan (or) 0.3% mancozeb
IIIrd spray at petal fall - 0.5% carbendazim
IVth spray - after 10 days - 0.2% captan
Vth spray - 15 days after - mancozeb 0.3%
Fruit set - 0.15% captafol
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management
Sanitation of orchard
Pre-bloom spray of lime sulphur (1:60)
Spray [email protected]% or Wettable S
Resistant varieties: Maharaja chunth and Golden Chinese (apple cultivars), Yantarka
Altaskya, Dolgoe (Crab apple cultivars)
Management
During winter prune out and burn blighted twigs, branches and cankers, and even
whole trees, at about 30cm below the point of visible infection
Disinfect the tools after each cut with 10% sodium hypochlorite
Insect control
Resistant varieties
Dormant sprays with copper sulphate or bordeaux mixture, however, bordeaux
mixture or streptomycin are the only effective blossom sprays
Management
Regulatory measures
Crop rotation with maize or other grain crops
Avoid injuries to roots or lower stem parts
Penicillin or vancomycin - partial control
Agrobacterium radiobacter (Strain K1026) (No gall) applied to fresh wounds.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Peach
Etiology
Mycelia are intercellular and not produce specific ascocarp.
Asci are produced (Open ascus) individually and measure 25to 40 x 8 to11 µm. Each
ascus bears eight ascospores of 3 to 7µm diameter.
Epidemiology
The disease is prevalent in areas where cool and misty spring weather prevails and the
dry hot weather hastens defoliation
Primary source of inoculum: Dormant mycelia in the affected stem newly formed
buds.
Secondary source of inoculum: Air borne conidia.
Management
Removal & burning of infected leaves and shoots reduce the spread of the disease
A dormant spray with Bordeaux mixture (1%) with an adhesive and a winter spray
with Bordeaux mixture (1%) before bud burst controls the disease.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Strawberry
Leaf spot
Common leaf spot of strawberry (also known as Mycosphaerella leaf spot, Ramularia leaf spot,
strawberry leaf spot, bird’s-eye spot, gray spotness, and white spot) is a common fungal leaf
disease that affects both wild and cultivated strawberries throughout the world. Common leaf
spot was once the most economically important strawberry disease, but the use of resistant
strawberry varieties/cultivars and improvements in methods for growing strawberries have
been effective in managing the disease and reducing its impact. Today, the disease is often a
cosmetic problem and typically has little impact on yield or fruit quality.
Symptoms
Symptoms of common leaf spot can occur on leaves, fruits, berry caps, petioles, and
runners. The most noticeable symptoms of the disease are small, round, necrotic (i.e.,
dead) spots on strawberry leaves.
Initially, these spots develop on the upper leaf surface and are deep purple to red in color.
The spots eventually develop tan, gray or almost white centers with distinct reddish-purple
to brown borders.
During warm, humid weather, uniformly rusty-brown spots without purple margins or light
colored centers may develop instead.
Spots can occur on the undersides of the leaves as well, but these spots tend to be less
vibrant in color.
As the disease progresses, spots enlarge in diameter and may merge together, in extreme
cases leading to leaf death.
Spots on berry caps, petioles, and runners resemble those produced on upper leaf surfaces.
Shallow, black spots may develop on infected fruits, and are often surrounded by brown or
black, leathery tissue.
Disease cycle
Common leaf spot is caused by the fungus Mycospharella fragariae, which can enter a garden
on infected strawberry plants or via windblown spores from nearby strawberries.
Once introduced into a garden, the fungus is spread predominantly by splashing water from
rain or sprinklers used for watering. M. fragariae is most active when temperatures range from
65°F to 75°F, with periods of high rainfall and humidity. M. fragariae survives the winter on
dead strawberry leaves and other plant parts, and is moved to new foliage in the spring by early
season rains.
Management
Use certified disease-free nursery stock. Examples of resistant varieties include ‘Crimson
King’, ‘Earliglow’, ‘Glooscap’, ‘Ogallala’, and ‘Ozark Beauty’.
Plant strawberries in full sunlight, in well-drained soils, and with proper spacing to
optimize air circulation and create a drier environment that is less favorable for the common
leaf spot pathogen.
Once plants are in the ground, avoid overhead watering (i.e., DO NOT use a sprinkler) as
this will splash the common leaf spot pathogen from plant to plant, and provide a wet
environment that is more favorable for the fungus to infect. Instead, use a drip or soaker
hose for watering.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
At the end of the growing season, remove strawberry plant debris to minimize sites where
the fungus can survive the winter. Deep bury, burn (where allowed by local ordinance) or
hot compost this material.
Use captan, myclobutanil or copper as the active ingredient. Use copper-containing
fungicides only prior to flowering. If you decide to use a myclobutanil-containing product,
alternate applications of this product with applications of a second fungicide containing
another active ingredient.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Arecanut
Major diseases
1. Mahali disease -Phytophthora meadii (=P. arecae)
2. Bacterial leaf stripe: Xanthomonas campestris pv. arecae
3. Anabe roga (disease): Ganoderma lucidum
4. Yellow leaf disease: Phytoplasma
5. Bud rot - Phytophthora arecae
6. Stem bleeding -Thielaviopsis paradoxa
7. Inflorescence die back – Colletotrichum gleosporioides
1. Mahali/koleroga
Causal organsim: Phytophthora meadii (=P. arecae)
In areas receiving heavy rain fall, mahali (heavy devastation) or koleroga (kole=rotting, roga
=disease) is most dreaded disease. Butler in 1906 first recorded this disease from Mysore.
Lesli,C.Coleman (1910’s) who worked extensively on this disease and developed
management practices to manage the disease which are still working satisfactorily.
Symptoms
Characteristic symptoms include rotting and excessive shedding of immature nuts from
the trees.
The first sign of the disease is on the nuts, on which water soaked lesions usually
develop towards the base. Because of this watery rot, the disease is locally called as
“Neerugole”.
Later leads to discoloration, discoloration starts browning then leads to deep browning,
later dropping of nuts takes place..
The fallen nuts show the felty, white mass of mycelium of the fungus which soon
envelops the entire surface. Infected nuts loose their luster. This type of symptoms
with boost like growth of the fungus , as also locally called as “Busurugole”.
The disease gradually spreads among the bunch ultimately covering the entire bunch
wherein they rot and shed from the bunches.
Fruit stalks and rachis of inflorescence are also affected. They are lighter in weight
which deteriorate and become unsuitable for chewing.
Very often, the top of the affected trees may also dry resulting in withering of leaves
and bunches.
Etiology
The mycelium is inter or intra - cellular, coenocytic but forms septa in older stages.
Haustoria are finger like, occasionally branched and sparsely produced.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
The sporangiophores are irregularly branched and the sporangia are pyriform to
elliptical.
Oospores are the sexual spores which are also act as dormant spores that survive for
about 4-5 years.
Epidemiology
o
The optimum temperature favourable for the fungus is 18-22 C
Relative Humidity of more than 95% is congenial for the development of disease.
Sporangia of the fungus have been caught successfully in aeroscope slides at a height of
10-11m .
The fungus infects the nuts readily but not the older nuts. Heavy rainfall, wind, low
temp, alternate sunshine and rainfall favours the disease.
Management:
Clean cultivation
Destruction of affected trees.
Collection and burning of fallen nuts.
Spray Bordeaux mixture 1% to the bunches at least two times at an interval of 45
days. The first spray should be given immediately after the first few monsoon
showers. If the monsoon prolongs, a third spray is essential.
Covering the bunches with polybags gives a complete control.
The lesions are covered with abundant bacterial exudates on the lower surface. The
exudate is creamy white and slimy.
On drying, it forms a waxy film or creamy white or yellowish flakes or fine granules
or irregular yellowish masses.
In the advanced stages, the lesions may measure 1cm or more wide and several
centimeters long involving the midrib also.
The affected midrib and veins of the leaflet get discolored and turn black.
All the leaflets of a leaf may be affected resulting in complete or partial blighting of
the leaf and in severe cases the entire crown may get killed, particularly in case of
seedlings.
Etiology
It is soil borne, rod shaped, gram negative bacteria, monotrichous, genetic material DNA
reproduced by binary fission.
Epidemiology
Temperature 26 to 280C, Relative humidity 85-90%, intermittent rainfall, presence of
susceptible host favour the disease.
Management
Early identification and eradication.
Use healthy planting materials.
Antibiotics like tetracycline and its formulations are effective as prophylactic and
curative treatments at 500 ppm concentration.
Stem injection of antibiotics has longer residual effect than foliar spray. Streptocycline
0.05% or copper oxychloride 0.3% spray can also be given.
Symptoms
Above ground
Yellowing and browning of outer whorl of leaves. As the disease advances the inner
whorl also exhibit the same symptom.
Leaf dries at later stage of the disease, droops and hangs around the stem.
The impact is the flowers, and nut size reduction and dropping.
In severe or advanced stages, drooping of all the leaves and their dropping leaving
only the stem without leaves.
Discolouration of vascular bundles can be seen.
On the trunk
Stem bleeding and oozing of gum takes place upto the height of 5m as the disease
advances.
Below ground level - on roots
The roots of the infected plant become brittle, discololured and dry.
Sporophores and fruiting bodies can be seen on the stem portion at the collar region
mostly after the death of the tree which gives the name “Anabe Roga (Mushroom
like)”.
Etiology
The fungus is heterothallic and weak parasite.
Vegetative spores are the Chlamydospores.
Conidia are round, thin walled. Sexual spores are basidiospores
Source of inoculums
Primary source of inoculum: Chlamydospore and dormant mycelia survive in the soil
and infected roots.
Secondary source of innoculum: Air borne basidiospores.
Epidemiology
Neglected plantations
Sandy loam soils
High plant population density
Summer stressed plantations
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management
Proper management of the garden is the best way to check the occurrence of the
disease. Improve the drainage.
Drench the root zone of the affected palm with 0.3% Calixin at quarterly intervals@
15-20 ltrs per palm+root feeding of calixin (125ml/palm) during January, March, July
and October.
Apply 2 kg neem cake per palm per year.
Phytosanitory measures like cutting and burning of the dead palms along with bole and
roots should be followed strictly.
Isolate affected palms by digging trenches 60 cm deep and 30 cm wide around, one
metre away from the base and drench with Captan (0.3%), Calixin (0.1%) or Copper
oxychloride (0.3%).
Remove and destroy all severely affected palms and stumps of dead palms.
Drench the soil with 1% Bordeaux mixture before planting healthy seedlings.
Discourage growing of collateral hosts of fungus such as Delonix regia and Pongamia
glabra in the vicinity of gardens.
Avoid flood irrigation and water flowing from infected palms to healthy palms.
Management
True Mangala seedlings and South Canara variety showed tolerance to this disease. The
hybrid Saigon×mangala yielded max number of nuts with minimum disease intensity.
Palms which received higher dose of potassium and magnesium recorded minimum
disease intensity.
Use of Chlorotetracyclin hydrochloride (Aureomycin) and tetracycline chloride
(achromycin) through root feeding and stem injection had no ameliorative effect on the
disease.
Maintain trees in good vigour.
Tolerant varieties like True Mangala and south Kanara
NPK@100:40:140/palm/year
Addition P 800g/palm/year
Application of potassium and magnesium
Integrated management of orchard
5. Bud rot
Causal organism: Phytophthora palmivora
Symptoms
The fungus Phytophthora palmivora. P meadii causing koleroga in bunches also pass on
to the buds and cause rotting.
The first symptom of the disease is the discoloration of the spindle from the natural
light green color to yellow and then brown.
Infection spreads to young leaves which rot rapidly. As the infection spreads inside the
bud the growing point of the stem also rots resulting in the death of the palm.
The spindle slumps and can be drawn out with a gentle pull.
The outer leaves then become yellow, droop and drop off one by one leaving a bare
stem. Secondary organisms colonize the rotting bud and convert it into a slimy mass
which would emit a foetid smell.
Etiology
The mycelia are aseptate with intercellular mycelium and the haustoria.
Zoospores are the asexual spores borne in sporangia.
Oospores are the sexual spores borne in oogonium.
Primary source of inoculum: oospores.
Secondary source of inoculum: zoospores.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Epidemiology
This organism require cool weather condition, temperature requirement is 18-20º c,
relative humidity is 98-100%, require cloudy weather, intermittent rainfall & high
density plantation. It occurs in severe form in heavy rainfall tracts of Karnataka.
It generally occurs in monsoon season.
Fresh infection during November onwards becomes severe during succeeding months.
Management
Soil application of Trichoderma reduces the inoculum in soil.
Remove the infected tissue completely and treat the wound with Bordeaux paste.
Spray Bordeaux mixture (1%) to the crown of healthy palms which are in the vicinity
of the affected palm. Remove koleroga affected bunches and destroy them.
6. Stem bleeding
Causal organism: Thielaviopsis paradoxa (de Seyenes) Hohn.
Symptoms
Both the young and old plants are affected but young palms are highly susceptible.
Symptoms appear on the basal portions of the stem as small discolored depression during
initial stages.
Later the spots coalesce and cracks develop on the stem which eventually produces
hollows upto varying depths along the infected portion.
Crown of affected adult palms get reduced in size followed by reduction in yield.
Finally a dark brown liquid oozes out from cracks.
Source of inoculum
Primary source of inoculum: Dormant mycelia.
Secondary source of inoculum: Air borne conidia.
Epidemiology
More serious in kharif season and also more serious in case of poor drainage areas.
Management
Improving the drainage may help in minimizing the disease incidence.
Root feeding with proper chemical.
Application of hot coal tar or Bordeaux paste is effective in reducing the disease.
Symptoms
Die back of inflorescence is associated with low fruit set. About 60% of palms in the
state of Karnataka and Kerala are infected by this disease causing severe shedding of
buttons.
Disease appears on the rachillae of the male flowers, then in the main rachis as
brownish patches which soon spread from tip downwards covering the entire rachis
causing it wilting. The female flowers of the infected rachis are shed.
The fungus also infects the developing embryo inside the female flowers, which
eventually shrivels up showing a brown discoloration.
Under severe conditions the fungal infection proceeds from tip downwards producing
the condition known as die-back.
Concentric rings of light pink coloured conidial mass of the pathogen appear on the
discolored portions of the infected inflorescence.
Etiology
Mycelium is septate, asexual spores are the conidia borne in acervulus.
Ascospores are the sexual spores borne in Perithecium.
Primary source of innoculum: Dormant mycelia.
Secondary source of innoculum: Conidia.
Epidemiology
The disease is prevalent throughout the year, but is most serious during the dry
period (Feb-May).
Temperature requirement is 28-32ºC with relative humidity of 90-92% and
presence of weak host.
Management
Remove affected inflorescence immediately.
Spray Zineb (4 g in 1 litre of water) or Mancozeb (3 g/l) twice, once just after female
flowers are set and again 15-28 days later.
Aureofungin sol at 50 ppm concentration is also effective in controlling the disease.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Cocoa
Symptoms
Appearance of brown spots on the pod.
The discoloration and brown spots spreads over the whole pod.
Internal tissues of diseased pods become brown.
Infected beans become discoloured.
Source of inoculum
Primary source of inoculum is the oospore.
Secondary source of inoculums is zoospores and sporangia.
Epidemiology
Closer spacing between trees and damp locality accompanied by cool damp weather
favor the rapid spread of the disease.
Management
Periodically remove the infected pods.
A site with relatively low rainfall and good drainage is recommended.
Spray 1 per cent Bordeaux mixture with on set of monsoon and also frequent
intervals. The spray should be mainly directed at the pods and bearing branches.
Provide frequent drainage and regulate shade to increases aeration.
Pseudomonas fluorescens (Pf1) liquid formulations @ 0.5% as soil and foliar spray
(3 times per year- June, October & February) was found to be effective in reducing
the Cocoa Pod rot and Stem canker.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Cardamom
Pathogen:
Initially Phytophthora nicotianae (Barda de Hann) var. nicotianae Waterhouse was
reported to be the causal agent of this disease.
The CdMV (Cardamom Mosic Virus) genomes are single-stranded linear positive-
sense RNA.
Disease cycle and epidemiology:
It is transmitted by banana aphid Pentalonia nigronervosa.
Clones from infected gardens, seedlings raised in the vicinity of infected plantations,
voluntary seedlings collected from infected plants and few infected zingiberaceous hosts
form the primary source of disease introduction to cardamom plantations.
Entry of the virus also occurs in contiguous and nearby plantations upto 1000 m from the
external inoculum source.
Management
Use healthy planting material which reduces the spread of the disease.
Periodic surveillance of the plantations should be done at least twice a year to detect the
virus infection and infected plants may be removed immediately.
Spray Mancozeb 0.2 % or Copper oxychloride 0.2 % or Bordeaux mixture 1%.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms:
The symptoms start as water soaked lesions on the lower surface of the leaves (Plate 1a)
and these lesions later enlarge rapidly, involving 25-70 per cent of the leaf lamina (Plate
1b).
With the onset of south-west monsoon during may –June, runner shoots arising from the
base of the vine are also infected.
The leaves later become flaccid and droop and the plants show die-back symptoms.
The foot rot infection occurs as wet patch at the collar region of the vine resulting in
varying degree of rotting of the main stem (Plate 1c).
There is yellowing and gradual drying of the foliage leading to sudden death of the plant
and hence the disease is also called quick wilt (Plate 1d).
Plate1a. Water soaked symptoms on leaves Plate 1b. Characteristic lesions on leaves
Plate 1c. Lesions on the runners Plate 1d. Symptoms of quick wilt
Plate-1. Symptoms of Phytophthora foot rot of pepper.
Pathogen:
The disease is caused by Phytophthora palmivora (Butler) Butler but now it is changed to
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
P. capsici Leonian.
Mycelium is hyaline, branched 3.3-8.6 µm wide and non-septate but few septa are found
in case of old hyphae, typically hyphal branches arise at right angles, often variously
swollen and tuberous and of abnormal diameter.
Sporangia are rarely produced or almost absent in culture, the sporangia are hyaline, ovoid
to pyriform or sometimes round to lemon shaped, non-pedicillate with a predominant,
hemispherical papilla at the apex.
The zoospores are reniform to oval, biflagellate and remain motile for 20-30 minutes, then
shed flagella and become encysted and germinate by means of germ tubes.
Oospores are formed abundantly in aerial as well as submerged mycelia in the medium.
The oogonia are hyaline, circular to spherical, the oogonial stalk is encompassed by
persistant amphygynous antheridium.
The oospores are circular to spherical, the oospores are found to germinate either by germ
tubes or by the rupture of oosporic walls.
The fungus does not produce chlamydospores.
Management:
Use healthy planting material.
Removal of infected vines from the plantation is essential to reduce the inoculum buildup.
The movement of soil through farm implements from diseased to healthy gardens may
also be prevented.
Application of soil amendments like neem cake, cotton seed and groundnut meal (250
g/m2) is also useful in managing the disease.
Two sprays of Bordeaux mixture (5:5:50) during the pre monsoon and mid monsoon
period reduce the aerial infection.
To minimize the soil borne inoculum, drenching of soil around the vines with copper
oxychloride (0.3%). Fungicides like metalaxyl + mancozeb (0.25%) or cymoxanil +
mancozeb (0.25%) can also be used for spraying.
Soil application of bioagents like Trichoderma virens and T. harzianum @ 5x 105 cfu/g
inoculum has also been found effective in the management of this disease.
Different species of pepper like Piper colubrinum, P. arboretum and P. sarmentosum have
been found resistant while cvs. like Narayakodi, Kallu valley, Uthirankotta and Balankotta
were tolerant to this disease.
Pathogen:
The disease is caused by Fusarium solani Sacc. f.sp. piperi.
Mycelium is septate and hyaline at first and becoming cream coloured with age, however,
some isolates produce blue or red pigment.
Micro conidia are ellipsoidal, straight to curved, one to two celled and hyaline.
Macro conidia are hyaline, 3-5 septate, falcate having gradually pointed and curved ends
and appear on sporodochia.
Chlamydospores, both rough and smooth walled, characterized by thick walls are terminal
or intercalary.
Management:
Application of neem cake @ 1kg/vine reduce M. incognita population under field
conditions.
Apply Phorate (3 g a.i./vine) application twice a year for the management of both
nematodes.
Mycorrhizal fungi Glomus mossae, G. fasciculatum, Gigaspora margarita and
Acaulospora laevis also show varying degree of root knot suppression.
Piper colubrinum is resistant to both root knot and burrowing nematode.
3.ANTHRACNOSE
The disease is also known as “Pollu‟. Spike shedding due to this disease can go upto 10 per
cent. In early infection, there is up to 77 per cent weight loss of berries while late infection
causes 56 per cent infection.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms:
The symptoms on young leaves and spikes appear as small brown specks which are
surrounded by yellow halo (Plate-3a).
In severe form, defoliation and spike shedding may also occur.
Small cracks develop on the berries after the infection has been established, thus reducing
the quality of the produce.
The infection on tender berries causes darkening of the pericarp and affects their
subsequent development (Plate-3b).
With time, these dry up resulting in chaffey berries, hence the name „pollu‟ which means
the hollow berry.
Favourable conditions
The disease is mainly noticed in nurseries during June- September and is caused by
Sclerotium rolfsii.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management
Selecting fields that are free of S. rolfsii.
Close plant spacing and over-irrigation promote disease development and should be
avoided.
Injury during cultivation should be avoided as much as possible.
Deep plowing can be used to bury debris and sclerotia of S. rolfsii.
Soil application of antagonistic like Trichoderma spp.
Soil and foliar application of Bordeaux mixture 1%.
Sanitation, use of healthy cuttings, good drainage, proper irrigation.
Remove and destroy wilted plants treat that place and surrounding vines with fungicidal
solution then replace with healthy seedling.
Carboxin 37.5 + Thiram 37.5WP - Vitavax Power 2g/lit → 1- 1.5 lit/plant
Application of FYM with Trichoderma harzianum
Apply neem cake 100 – 150 g/plant.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Rubber
1. Powdery mildew: Oidium heveae
Causal organism: Oidium heveae
Symptoms
White, cottony, hairy or powder-like borders are seen along the lesions.
The shiny filamentous colonies of Oidium are clearly visible on both sides of the
affected, freshly-fallen leaves.
Severity of powdery mildew disease is commonly seen during and after over
wintering or during flushing of the tree.
Etiology
This fungus is an obligate pathogen and can not be grown in culture.
It produces thin and membranous characterized by oval or barrel shaped conidia or
oidia borne in chains on short conidiophores. The mycelium is ectophytic, septate
having subepidemial haustoria.
Management
Spraying wettable Sulphur (0.2%) and Carbendazim (0.1%)
In mature trees, the pathogen causes dropping of premature leaves resulting defoliation
and hence the disease is also called as ’Phytophthora leaf fall’.
Etiology
The fungus belongs to the Phylum Oomycota, Family Pythiaceae and grows
abundantly on V-8 agar.
The colonies are white, aerial, and cottony in culture.
The sporangia are characterized by lemon-shaped and doubled papillate structures
which measure 34.5 – 57.5 x27.5 -49.0 mm in size under 100x and oospores with 22 -
28 mm.
Management
Prophylactic spray with Bordeaux mixture (1%) and Zinc sulphate (0.2%) at cropping stage.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Turmeric
Disease cycle
P.I: The fungi survive in soil and infected rhizomes as oospores
S.I: Spreads through irrigation water as zoospores
Management
Crop rotation with non-hosts
Grow turmeric in light soils with good drainage
Use disease free rhizomes for planting
Rhizomes should be dipped in [email protected]/l or Bordeaux mixture@1% solution
for 40 minutes
Drench the soil at root region with captan@2 g or [email protected] g or metalaxyl@1 g
per liter in the initial stages of the disease
Turmeric varieties, PCT-13 and PCT-14 are resistant to this disease.
Disease cycle
P.I: Infected plant debris
S.I: Air borne conidia
Management
Remove and destroy infected plant debris
Treat rhizomes with [email protected]% solution
Spray [email protected]% or [email protected]%. during Aug-Dec along with
[email protected] ml/lt
Avoid excess shading
Tolerant varieties: TS-2, TS-4, TS-9, TS-88
Favourable conditions
Temperature of 21-230C with 80% R.H.
Management
Collect and destroy diseased leaves
Spray [email protected]% or [email protected]% at 20 days interval
Resistant varieties: China (Curcuma domestica) and Jaweli (C. amada)
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Coriander
STEM GALL Protomyces macrosporus
It is the most important disease of this crop causing considerable yield losses.
Symptoms:
The disease is systemic in nature and manifests in the form of tumour like swellings on all
aerial parts of the plants.
The galls are soft and fleshy when young, later becoming hard and woody as they grow
old.
The peduncle as a whole appears abnormal with outgrowths or malformation along with
hypertrophied flowers and fruits.
Pathogen:
Fungus responsible for this disease is Protomyces macrosporus Unger.
Hyphae are intercellular, closely septate and broad, branching is irregular, scattered cells in
the hyphae swell, form ellipsoidal or globose bodies, which later develop in to
chlamydospores.
As the chlamydospores mature, a thick, hyaline and three-layered wall measuring 50 to 60
µm in diameter surrounds them.
The mycelium of the fungus is only found in the tumours although the resting spores of the
fungus cause systemic infection.
Management
i) The disease affects less in the early and late sown crops. Sowing crop around 16 October and
16 November gave minimum yield losses.
ii) Use of clean and healthy seed and follow suitable crop rotation.
iii) Use resistant cvs./ lines like JD 1, G-5365-91, Pant Haritma, UD 20, Rcr 41, Pant-1, CIMAP
2053.
iv) Seed treatment with captan/ thiram (0.3%) followed by their foliar sprays.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Potato
1. LATE BLIGHT
Late blight is the most destructive disease of potato throughout the world. It was first
recorded in the beginning of nineteenth century in the Andes Mountains of South America.
The fungus moved from this place to Europe around the year 1842 and established in Ireland
where it caused severe epidemic in 1845-46, resulting in famous Irish famine. Four million
people were directly affected by this epidemic and many (approx. 1.5 Million) among them
faced death with millions migrating to other parts of the world. Since then, the disease has
been reported from almost all parts of the world wherever potato is grown. In India, the
disease was first reported from Nilgiri Hills in between 1870 and 1880. Since then, it is
appearing in plains as well as in hills regularly. In Himachal Pradesh, disease was first
reported from Kumarsain of Shimla District by Butler (1903).
Symptoms:
The symptoms of the disease appear on leaves, stem and tubers.
Initially small water-soaked lesions develop near the tips and margins of the leaves which
rapidly grow into large, brown to purplish black, necrotic lesions under favourable weather
conditions (Plate 1a).
During morning hours, whitish downy growth of the pathogen consisting of sporangiophores
and sporangia can be seen on the edges of the lesions mostly on the underside of the leaves.
Light brown to dark brown lesion appear on stem and petioles which may elongate later and
girdle the affected parts (Plate 1b.)
Since the disease is polycyclic in nature, the entire crop in the field may be killed in one or
two weeks and field give blighted appearance (Plate 1c).
The tubers may get infected by rain washed sporangia from the diseased foliage.
The infected tuber show irregular, small to large, slightly depressed areas of brown to
purplish skin which extend deep into the internal tissue of the tubers (Plate 1d).
The infected tuber tissue which is firm and dry in the beginning is often invaded by
secondary pathogens, mainly bacteria both in the field or poorly ventilated storage places
resulting in to soft rot of tubers.
Pathogen:
The disease is caused by Phytophthora infestans (Mont.) de Bary.
The mycelium is coenocytic, endophytic, hyaline, branched and intercellular.
Sporangiophores arise from the internal mycelium through stomata and are slender, hyaline,
sympodially branched, indeterminate, relatively thick walled, septate having side branches
with swollen base (Plate 2).
Sporangia develop on the tip of the sporangiophores and are hyaline, thin walled, lemon
shaped, distinctly papillate.
On maturity, the sporangium turns to the side, growth of the sporangiophore continues
which looks to have zigzag growth with characteristics swellings at the nodes.
P. infestans is heterothallic for sexual reproduction and involves two mating types namely
A 1 and A 2.
In India, although A 1 mating type is of common occurrence, prevalence of A 2 type has
been recorded in Shimla Hills after 1984.
Antheridia and oogonia are produced after A 1 and A 2 mating types come in close contact.
Antheridia are amphygynous while oogonia are spherical.
Oospores are thick walled and develop after fertilization.
Forecasting:
Several methods of late blight forecasting have been developed for better disease
management through proper planning of spray programme.
These are primarily based on record of temperature and rainfall or relative humidity and
predict the probability of the late blight development assuming the presence of inoculum.
“BLITECAST”, a forecasting model is being used in North-eastern U.S.A. for timing
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
fungicide application.
Such disease prediction rules have also been developed in Netherlands (Dutch Rules) and
England (Beaumont Rules).
In India, CPRI people achieved complete success in predicting outbreaks of late blight in the
hills. According to them:-
i. the 7 day moving rainfall (30 mm for Shimla, 28.9 mm for Ootacamund and 38.5 mm for
Shillong) and mean temperature of 23.9o C or less continues for 7 days, the disease would
appear within 3 weeks and if
ii. hourly temperature ranging between 10-20o C associated with 80 per cent or more
relative humidity continues for 18 h for 2 consecutive days, the blight would appear within a
week.
Management:
Use healthy seed and cull piles near cold stores should be destroyed.
High ridges and proper earthing up prevents tuber infection.
Restrict irrigation during cloudy days.
Use resistant varieties like Kufri Giriraj.
Give timely application of fungicides like mancozeb/ chlorothalonil/ propineb (0.25%) as
prophylactic sprays (1st week of November for main crop in plains and IIIrd week of June in
hills) and repeat at weekly intervals.
Repeat sprays promptly after rain. Use metalaxyl + mancozeb or cymoxanil + mancozeb
(0.25%) only when disease risk is likely to be severe and favourable weather conditions
persist.
Avoid the use of formulations containing metalaxyl alone.
Digging of tubers should be done after 2-3 weeks of dehaulming.
2.EARLY BLIGHT
Symptoms:
The symptoms first appear on older leaves as dark brown oval or angular spots or lesions
surrounded by chlorotic zone, which may extend much beyond the lesion due to the
presence of toxin “alternaric acid” produced by the pathogen (Plate 3).
Under favourable climatic conditions, they enlarge rapidly, become irregular and may
involve entire part of the leaf lamina.
Concentric ridges appear on the necrotic tissue giving them target board appearance, lesions
on leaf coalesce together and give blight appearance.
Dark brown lesions are produced on stem and petioles, which break at the point of infection.
On the tubers, the lesions are slightly dark, sunken and round to irregular in shape, with time
infected tubers show dry rot symptoms.
Pathogen:
The fungus responsible for this disease is Alternaria solani Sorauer.
The mycelium is septate and pale to olivaceous brown.
Conidiophores arise singly or in small fascicles, through stomata from the mycelium present
in the dead centres of the spots.
Conidia are usually solitary, obclavate, oblong to ellipsoid, tapering to a beak almost of the
same length or even longer as that of the conidial body.
Conidia are muriform, pale to golden or olivaceous brown having 9-11 transverse and 0 to
few longitudinal septa.
No perfect stage of the fungus has been recorded.
Management:
Various cultural practices like removal and destruction of diseased haulms from the infected
field after harvest, use of healthy seed tubers for planting and proper fertilization of the
plants should be followed.
With the initiation of the disease, spray the crop with mancozeb (0.25%) or chlorothalonil
(0.2%) and repeat at 10-14 days interval.
Resistance source is available with Solanum phureja and S. chacoense which can be
exploited for breeding resistant cultivars.
Cv. Kufri Sindhuri provides good resistance against this disease in plains.
3. BLACK SCURF
Black scurf causes qualitative damage as it decreases the quality and market value of the
tubers both for table as well as seed purpose.
Symptoms:
Stem canker and blight phase and the scurf phase are the two distinct phases of the disease.
In stem canker phase, the growing tips of sprouts show browning.
Sunken, circular or elongated brown necrotic spots may also be observed on the sprouts.
Severely affected sprouts are killed.
Later, when shoots emerge, similar necrotic lesions are observed on the stem which may
extend downwards and may completely girdle the stem.
The most prominent symptom of black scurf is the presence of black crust on tubers due to
the formation of sclerotia of the fungus (Plate 4).
The pathogen produces a large number of sclerotia superficially on the surface of growing
tubers.
These sclerotia may be hard or spongy forming a black crust of scurf on the tuber surface.
These are normally seated on the skin and do not cause any damage to the tuber inside.
Black scurf phase is more common than stem canker in India.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management:
Planting of healthy and disease free tubers is helpful in reducing the incidence of the
disease.
Two to four years rotation with cereals, brassicas and legumes is helpful for the
management of this disease.
The increase in organic matter content of the soil helps in reducing the population of the
fungus through enhanced activity of the antagonist microorganisms.
The normal unsprouted tubers should be dipped in carbendazim (0.1%) or Monceren 25
SC (0.25%) for 10 minutes.
The seed after treatment should be dried under shade by spreading on the floor of the cold
store.
4. POTATO WART
The disease is quite serious in temperate regions of the world. In India, the disease
was first reported by Ganguli and Paul (1953) from Darjeeling and is presently restricted to
that area only due to restrict domestic quarantine on this disease.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms:
All the underground parts except roots are attacked.
The plant cells multiply rapidly at the infection site and produce hypertrophied tissue
masses resulting into wart type symptoms on the tubers and beads like projections on the
stems or stolons varying in size from small protuberances to large intricately branched
structures (Plate-5 a &b ).
Warts are normally soft, pulpy, spherical and similar in colour to tubers.
The colour may change to green on exposure to sunlight.
Sometimes whole tuber may be covered with warts.
Sometimes secondary microorganisms invade the wart tissues causing their
decomposition.
Management:
Since the pathogen is soil borne, its eradication is very difficult.
Strict domestic quarantine measures enforced in India have helped to restrict the disease to
Darjeeling district only.
Follow crop rotation with non-host crops for 8-10 years.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Some potato lines viz., Rondo, Edina, Mira from European countries have shown
considerable resistance to wart.
Varieties developed by CPRI, Shimla like Kufri Jyoti, Kufri Sherpa, Kufri Jeevan and
Kufri Muthun have demonstrated resistance to late blight as well as wart.
5. BROWN ROT
Symptoms:
Both above and underground plant parts are affected.
There is a sudden wilting and death of the infected plants or collapse of one or more
branches is observed.
Wilting appears during July in the hills about two weeks after the onset of monsoon rains
(Plate 1a).
Many wilted plants also show stem rot at soil level.
Greyish brown discolouration appears through the stem of affected tubers (Plate 1b).
Cross-section of such tubers reveals a distinct brown discolouration in the vascular ring.
A slight pressure on the cut tuber causes oozing of typical grayish white bacterial slime
out of the vascular ring.
Vascular browning is a characteristic symptom of the disease.
In North-eastern hills, lenticels infection of potato tubers in the form of water-soaked
lesions is quite common.
A high temperature regime (28-30o C) and relatively high soil moisture are favourable for
wilt development.
The bacteria multiply rapidly inside the water-conducting tissue of the plant, filling it with
slime.
This results in a rapid wilt of the plant, while the leaves stay green.
If an infected stem is cut crosswise, it will look brown and tiny drops of yellowish ooze
may be visible.
Management:
It is difficult disease to manage as the commercial cultivars are highly susceptible and
chemical control is not feasible.
The reduction of the initial inoculums is of prime importance to manage bacterial wilt.
Use of disease free seed is important for avoiding introduction of this disease to new
fields.
In disease prone areas, plant whole tuber.
Follow wheat-maize rotation at least for 2-3 years.
Application of stable bleaching powder @ 12 kg/ ha has been found to reduce bacterial
wilt by 80 per cent when applied in furrows at the time of planting.
6. COMMON SCAB
Symptoms:
Symptoms of scab are generally seen on tubers and are categorized as shallow and deep
pitted.
In shallow scab, the affected tubers show superficial roughened areas, sometimes raised
about but often slightly below the skin of the tubers.
The lesions of scab consist of corky tissue which is the result of abnormal proliferation of
the cells of tuber epiderm due to invasion by the pathogen.
The lesions may vary in shape and size and the color is brown.
In deep pitted scab, the lesions are dark brown or almost black and measure 3-4 mm or
more in depth surrounded by hard corky tissue.
They may join together involving entire surface of the tuber.
Quite often, multiple types of symptoms such as slightly brownish roughening of tuber
skin, proliferated lenticels with hard corky deposition, concentric series of wrinkled layers
of cork around central black core, raised rough and corky pustules and deep pits
surrounded by hard corky tissue are produced.
Russet scab in the form of superficial encrustation is also becoming quite common in the
state.
Pathogen:
The disease is caused by a bacterium Streptomyces scabies (Thaxter) Waksman and
Henrici.
The mycelium of the pathogen is slender, branched with few or no cross walls.
The spores are cylindrical or ellipsoid produced on special hyphae that develop cross walls
from tip and spores are pinched off.
The S. scabies is gram positive and aerobic bacteria.
Management:
As the disease is both tuber and soil borne, it is difficult to control it.
However, some management practices have been adopted to check this disease.
Healthy and blemish free seed tubers should be selected for sowing in order to reduce the
primary source of inoculum.
Green manuring and cultivation of certain legumes before planting potato has been
emphasized as important cultural practices in controlling common scab.
Green manuring probably increases the activity of certain actinomycetes and
other bacteria which are antagonistic to S. scabies.
Soil moisture is important factors in the development of disease, it has been exploited for
minimizing the losses.
Successful control of potato scab can be achieved by frequent irrigations of the field at
weekly intervals from tuberisation until maturity.
The tubers can be disinfected by dipping them for 10 minutes in Emisan (0.25%).
VIRAL DISEASES
1. LEAF ROLL VIRUS (POTATO LEAF ROLL VIRUS)
Symptoms
There is rolling of upper leaves.
Infected leaves remain upright and turn pale yellow in colour.
Plants produced from infected tubers show rolling of lower leaves and stunting of plants
with upright habit (Plate 1).
Rolled leaves are leathery, stiff and brittle. Marginal interveinal chlorosis of leaflets is
visible on upper leaves.
Virus characters
Genome: Positive sense ssRNA virus
Family: Luteoviridae
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Genus: Polerovirus
Species: Potato leafroll virus
Management
Disease free seed tubers for planting
Aphid control
Management:
Always use virus free certified seed from reliable sources.
Rouge out infected plants as soon as these are first noticed in early crop period.
Keep the aphid population under check by spraying insecticides like Rogor or Metasystox
@ 250 ml/acre or apply 5 kg of Thimet 10G/acre at first earthing up.
Cut the haulms in 4th week of December when aphid infestation starts (20 aphid /100
leaves) and leave the tubers in soil to mature till the end of February.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Note
Potato virus Y (PVY) is a Potyvirus, causes stipple streak. The necrotic strain generally
causes mild foliage symptoms, but necrosis in the leaves of susceptible potato varieties.
Potato virus S (PVS) is a Carlavirus, if plant infected early in the season, show a slight
deepening of the veins, rough leaves, more open growth, mild mottling, bronzing, or tiny
necrotic spots on the leaves. PVS is transmitted by aphids non-persistently.
Potato virus X (PVX) is the type member of the Potyvirus family of plant viruses. Plants
often do not exhibit symptoms, but the virus can cause symptoms of chlorosis, mosaic,
decreased leaf size, and necrotic lesions in tubers.
PVX can interact with PVY and PVS to cause more severe symptoms and yield loss than
either virus alone. The source of this virus is infected tubers.
Spread:
PVY is mechanical and aphid transmitted
PVS is transmitted by aphids, including Myzus persicae, the green peach aphid. It is also
mechanically transmissible, and transmissible through tubers.
PVX is transmitted mechanically, not by an insect vector. Tobacco, pepper, and tomato can
also serve as hosts of PVX.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Cucurbits
1) Downy mildew – Pseudoperonospora cubensis
Host range: Musk melon, Sponge gourd and Bitter gourd etc.
Symptoms
Yellow, angular spots appear on upper surface of leaves
The corresponding lower surface of these spots shows a purplish downy growth in
moist weather
The spots turn necrotic with age
The diseased leaves become yellow and fall down
Diseased plants get stunted and die
Fruits produced may not mature and have a poor taste
Disease cycle
P.I: Collateral hosts or fungus surviving in plant debris
S.I: Wind borne sporangia or splashing rain water
Management
Destruction of cucurbitaceous weeds around field
Spray [email protected]% or [email protected]%
Spray [email protected]% at 10 days interval
Symptoms
Whitish or dirty grey, tiny powdery growth on foliage, stems and young growing
parts
The superficial growth ultimately covers the entire leaf area
The diseased areas turn brown and dry. This leads to premature defoliation and death
Fruits remain undeveloped and are deformed
Disease cycle
P.I: Collateral hosts or through Cleistothecia
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Symptoms
Leaves curl downwards and become mottled, distorted, wrinkled and reduced in size
Stunting and rosetting of young leaves
Fruits are often misshapen, mottled, warty and reduced in size
Fruits may be bumpy or deformed in late infections
Management
Rogue out infected plants
Eliminate perennial weed hosts
Vector control by spraying monochrotophos or phosphamidon, 1.5 ml per liter of
water
Symptoms
Leaves will have abnormal colours
Leaves show wilting, Leaves are yellowed or dead
Stems show internal discoloration, Stems also show stunting or resetting and wilt
Whole plant shows dwarfing
Whole plant will be dead
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Management
Soil application of bio-agents like Trichoderma sp, Pseudomonas fluorescens, Purpureocillium
lilacinum (Paecilomyces lilacinus).
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Favourable conditions
Warm humid weather with rains or heavy dew
Management
Select disease free bulbs for planting
ST with thiram @3g/kg seed
Spray [email protected]% or [email protected]%
Favourable conditions
Wet soils with a temperature of 260 C
Management
Resistant varieties: Nasik red, Pusa Ratna, Pusa Red
Protection of bulbs from rains after harvest
Dry bulbs properly before storage by hot air at 37 – 480C
Spray zineb or captan @0.2% before harvest of crop
Favourable conditions
Extended periods of leaf wetness from dew formation, rainfall or overhead irrigation during
bulb formation and development can result in severe leaf blighting.
Management
Resistant varieties like Arka Kalyan can be used
A fungicide spray program with Tebuconazole, Hexaconazole @0.1% and Mancozeb and
Avatar (Hexaconazole + Zineb) @0.2% can provide good protection.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Chilli
Symptoms
Pre-emergence damping off: Seedlings disintegrate before they come out of soil
surface. This is known as pre-emergence damping-off which results in poor field
emergence / poor seed germination.
Post-emergence damping off is characterised by development of disease after
seedlings have emerged out of soil surface but before the stems are lignified.
Lesion formation at collar region
Infected areas appear brown and water soaked
Plants shrivel and collapse as a result of softening of tissues
Infected stems become hard, thin (Wire stem symptoms) and infected seedlings
topple. Disease appear in patches both in nursery and field beds.
Disease cycle
P.I: Oospores in soil or plant debris
S.I: Zoospores through irrigation water
Favourable conditions
Heavy rainfall
Excessive and frequent irrigation
Poorly drained soil and close spacing
High soil moisture with temp around 25-30o C
P. aphanidermatum, prefer temp above 200 C
P. debaryanum, P. ultimum, prefer cool temp (<200 C)
Management
Raise nursery in light soil with proper drainage
Burning farm trash on the surface of the beds.
Sowing seed on raised beds of 6-8” high (15cm)
Using low seed rate of 650 g/cent.
Seed dressing with Argosan or ceresan or Thiram or captan @ 2-3 g/Kg.
Soil drenching with 1% Bordeaux mixture or COC@ 0.3% or [email protected]%
Biocontrol with Trichoderma viride and Trichoderma harzianum
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
2) Anthrcnose, Die-back and fruit rot – Colletotrichum capsici (Tel: Glomerella cingulata)
Symptoms
December - October in transplanted crop
Small, circular to irregular, brownish black scattered spots appear on leaves
Severely infected leaves defoliate
Infection of growing tips leads to necrosis of branches from tip backwards
Necrotic tissues appear grayish white with black dot like acervuli in the center
Shedding of flowers due to the infection at pedicel and tips of branches
Fruit symptoms
Ripe fruits are more liable for attack than the green ones
Small, circular, yellowish to pinkish sunken spots appear on fruits
Spots increase along fruit length attaining elliptical shape
Severe infection result in the shrivelling and drying of fruits.
Such fruits become white or greyish in colour and lose their pungency.
On the surface of the lesions minute black dot like fruiting bodies called ‘acervuli’
develop in concentric rings and fruits appear straw coloured
The affected fruits may fall off subsequently. The seeds produced in severely
infected fruits are discoloured and covered with mycelial mat.
Pathogen: The mycelium is septate and grows both inter and intracellularly in the host
tissue. The asexual fruiting bodies, acervuli contain many rigid, brown coloured, 1-5
septate setae. A large number of conidia are borne on conidiophores in each acervulus
which are falcate, unicellular, hyaline having a normally truncated base.
Disease cycle
P.I: Infected seeds and diseased crop debris
S.I: Conidia dispersed by rain splash and wind
Favourable conditions
Temp, 280 C with RH more than 97%
Humid weather with rainfall at frequent intervals
Management
Collect and destroy all infected plant parts
Collect seeds only form fruits without infection
Removal and destruction of Solanaceous weed hosts and infected plant debris
Seed treatment with captan or Thiram 3-4g/kg
Spray thrice with [email protected]% or [email protected]%. just before flowering, at fruit
formation stage and 15 days after second spray.
Resistant varieties: G3, G4, B61, Lorai, etc.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Disease cycle
P.I: Dormant mycelium in the infected crop debris.
S.I: Air-borne conidia
Favourable conditions
Cool dry weather favours conidial germination
High RH favours disease development
Management
Spraying wettable [email protected]% or Dinocap or Carbendazim or Tridemorph 0.1%.
Disease cycle
P.I: Dormant mycelium in infected plant debris, infected seeds and volunteer plants
S.I: Wind borne conidia.
Management
ST with carbendazim@2g/kg seed
Spray [email protected]% or [email protected]% at 15 days interval
5) Fusarium wilt: Fusarium oxysporum f.sp.capsici
Symptoms
Fusarium wilt is characterised by wilting of the plant and upward and inward rolling of
the leaves.
The leaves turn yellow and die.
Generally appear localised areas of the field where a high percentage of the plants wilt
and die, although scattered wilted plants may also occur.
Disease symptoms are characterised by an initial slight yellowing of the foliage and
wilting of the upper leaves that progress in a few days into a permanent wilt with the
leaves still attached.
By the time above - ground symptoms are evident, the vascular system of the plant is
discoloured, particularly in the lower stem and roots.
Pathogen
Mycelium is grayish white. Microconidia are formed singly, hyaline and cylindrical. Macro
conidia are cylindrical to falcate. Chlamydospores are globose to oval and rough walled.
Management
Use of wilt resistant varieties.
Drenching with 1% Bordeaux mixture or Blue copper or Fytolan 0.25% may give
protection.
Seed treatment with 4g Trichoderma viride formulation or 2g Carbendazim per kg seed
is effective.
Mix 2kg T.viride formulation mixed with 50kg FYM, sprinkle water and cover with a
thin polythene sheet. When mycelia growth is visible on the heap after 15 days, apply
the mixture in rows of chilli in an area of one acre.
6) Murda complex
Symptoms
Pale yellow, curling, puckering of interveinal areas, shortening of internodes, reduction in
size bushy appearance, stunted growth, no fruit formation, or deformed fruits
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Thrips-upward curling
Mites-downward curling with elongation of petioles, copper like metallic shining on lower
surface of leaves
Viruses-curling, filiform of leaves, rat tail symptoms
Management
Seed treatment with Imidacloprid (5g/kg)
Nursery should be rised under insect proof net
Before sowing Carbofuran3G 25g/bed should be applied to the soil
Barrier crop with Maize or sorghum
Insecticide spray with Imidacloprid 17.8SL (0.3ml/l) or Thiomethoxam25WG (0.3g/l) or
Acephate 75SC (1g/l)
White fly: Triazophos 1.5ml/l
Mites: Fenazaquin 10% EC (Magister) 2.0ml/l, Spiromesifen 22.9% WSC (Oberon)
0.75ml/l
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Rose
Management
Collect and destroy infected plant debris
Four sprays with wettable [email protected]% or [email protected]% or [email protected]% at 10
days interval
Resistant varieties: Ashwini, Ambika, Angeles, American pride, Surabhi
Management
Affected parts should be collected and destroyed
Spray Tridemorph @0.025% or benomyl @0.1% at weekly intervals starting with
the sprouting of the plants till new foliage appears.
Shade and extensive irrigation should be avoided.
Resistant varieties: Bebe bune, coronado ,Grand opera, sphinx.
Radiance - escape infection due to waxy surface
Management
Diseased twigs should be carefully removed and destroyed
After pruning the cut end should be protected with chaubattia paste
Spray [email protected]% or [email protected]% or [email protected]% in early
September and late October
Resistant varieties: Blue moon, Red gold, Summer queen, etc.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Jasmine
1) Rust – Uromyces hobsonii
Symptoms
Leaves, stems and inflorescence are affected
Blisters or tumors and other abnormalities may be produced on the infected plant
parts
Infected portions become hypertrophied
Orange coloured pustules on both surfaces of leaf but predominantly on lower
surface
Chlorosis & defoliation of leaves under severe conditions
Yellow or orange coloured cankers on stems and twigs
Splitting of bark of affected branches and subsequent death of branches
Infected flower buds are swollen and deformed
Flower production is highly reduced
Disease cycle
P.I: Teliospores in infected plant
S.I: Wind borne aeciospores
Pathogen
Autoecious rust (Demicyclic rust/ Opsis rust)
Uredial stage is absent
Pustules are initially yellow (aeciospores) and later turn dark (teliospores)
Favourable conditions
Rust initiates in June- July and persists till March
Management
Remove and destroy affected plants or plant parts to avoid further spread.
Spray Oxy-carboxin (plantavax) or Mancozeb @0.2%
Dust sulphur (20-25kg/ha) or spray tridemorph (0.05%) or triadimefon (Bayleton) @
0.05%
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Marigold
1. Alternaria blight Alternaria alternata
Symptoms
Circular to irregular tan to brown/purplish spots develop on leaves and stems. These can vary in
size, color, and number, depending upon the pathogen. It also leads to flower blight at later
stages.
Management
Avoid overhead irrigation.
Efforts to maximize plant vigor by fertilizing and watering are helpful.
It is also helpful to pick and remove symptomatic leaves as soon as they develop.
Applications of fungicides like chlorothalonil and thiophanate-methyl.
Spray with Dithane M-45 fungicide @ 0.2% at fortnightly intervals starting from the first
appearance of disease symptoms.
Management
Good sanitation practices including grooming the plants and removing spent or senescing
flowers can minimize the potential for infection.
Avoid overhead irrigation. It is also important to avoid wetting the flowers when watering and
crowding plants.
Adequate spacing between the plants can promote good air circulation.
Control can also be achieved with the use of fungicide sprays applied as soon as symptoms are
visible with iprodione, chlorothalonil, and thiophanate-methyl.
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Chrysanthemum
Pathogen:
Mycelium is septate and pale to olivaceous brown in colour.
Conidiophores arise singly or in small fascicles through stomata from the mycelium
present in the dead centres of spots.
Conidia are olivaceous brown, smooth having transverse and few longitudinal septa.
Disease cycle and epidemiology
The pathogen(s) overwinter in infected plant debris.
Warm and humid climatic conditions favour the development of the disease.
Management:
Collect and destroy the infected plant debris.
Apply mancozeb (0.25%) or chlorothalonil (0.2%) as foliar sprays as the disease starts
appearing.
Tebuconazole (0.1%) and tebuconazole 50% + trifloxystrobin 25%WG (0.05%) were
effective
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD
Diseases of Tuberose
1. Wilt complex/Stem Rot: Meloidogyne sp. and Sclerotium rolfsii
Symptoms
The disease symptoms are preceded by the appearance of prominent spots of loose green
colour due to rotting which extend and cover the entire leaf. The infected leaves get
detached from the plant.
More or less round sclerotic, brown spots are formed on and around the infected leaf. As a
result, the infected plant becomes weak and unproductive.
The disease symptom is preceded by the appearance of prominent, coarse, mycelial masses
on the leaf surface or near the soil level.
Management
Drenching with Pseudomonas fluorescens 2g/litre of water
Application of Thimet or Furadan (20 kg/ha), Furadon @ 2 g/plant or carbofuran @ 2-5
kg/ha, neem @ 1 tonne/ha controls nematode infestation.
The disease can be controlled by drenching the soil around the stem with brassicol @ 1 %
or Zineb (20%) at the rate of 30 kg per hectare.
The incidence can be minimized by reducing soil moisture or planting at wider spacing (45
cm X 30 cm).
Soil drenching with ystemic fungicides viz., hexaconazole, propiconazole, tebuconazole at
0.1% found effective
Management
The disease can be controlled by the spray of Bordeaux mixture (0.4%), Zineb (0.5%) or
Mancozeb (0.2%) or Iprodione (0.2%) at 10 days interval.
Spray of iprodine +carbendazim 0.1% at 10 days interval starting the first spray at disease
appearance was found effective
Spray with azoxystrobin (0.1%) at 15 days interval
Systemic fungicides viz., hexaconazole, propiconazole, tebuconazole at 0.1% found effective
Diseases of Crops and Their Management- II PAT 303 (2+1), UASD