Path 365

Course title: Diseases of Field and Horticultural
Crops and their Management -II
Course : PATH 365 Credit: 3(2+1) Semester-VI
Lecture 1, 2 & 3
By
(Matinkhan A. Atar)
Assistant Professor, Plant Pathology
College of Agriculture, Bhanashiware
Wheat crop diseases and Their Management
Disease Causal organism

 1. Rust
 a. Black stem rust........Puccinia graminis f.sp. tritici
 b. Brown leaf rust……..Puccinia recondiata f.sp. tritici
 c. Yellow stripe rust….. Puccinia strifmis f.sp. Tritici
 2. Loose smut............Ustilago tritici
 3. Karnal bunt........... Neovossia indica
 4 Powdery mildew.....Erysiphe graminis var. tritici
 5. Alternaria blight....Alternaria triticina/Bipolaris sorokiniana
 6. Ear cockle........ Anguina tritici
1. Wheat rust
A. Black stem rust........Puccinia graminis f.sp. tritici
❑Symptoms:
➢Symptoms are produced on almost all aerial parts of the wheat plant but are most
common on stem, leaf sheaths and upper and lower leaf surfaces.
➢Uredial pustules (or sori) are oval to spindle shaped and dark reddish brown (rust)
in colour. They erupt through the epidermis of the host and are surrounded by
tattered host tissue.
➢The pustules are dusty in appearance due to the vast number of spores produced.
Spores are readily released when touched.
➢As the infection advances teliospores are produced in the same pustule. The colour
of the pustule changes from rust colour to black as teliospore production progresses.
If a large number of pustules are produced, stems become weakened and lodge.
➢The pathogen attacks other host (barberry) to complete its life cycle. Symptoms are
very different on this woody host.
➢ Other spores are Pycnia (spermagonia) produced on the upper leaf surface of
barberry which appears as raised orange spots.
➢ Small amounts of honeydew that attracts insects are produced in this structure.
Aecia, produced on the lower leaf surface, are yellow. They are bell-shaped and
extend as far as 5 mm from the leaf surface
Black stem rust :
The pustules may be abundant and
produced on both leaf surfaces and
stems of host plants.
HOSTS: Wheat, barley and common
Barberry (Berberis,Mahoberberis,
and Mahonia spp.)
Microscopically
urediospores
spores are
covered with
fine spines
Teliospores of Puccinia graminis

tritci
B. Brown
or leaf rust - Puccinia triticina (P. recondita)
❑Symptoms:
➢The most common site for symptoms is on leaf blades, however, sheaths, glumes
and awns may occasionally become infected and exhibit symptoms. Uredia are seen
as small, circular orange blisters or pustules on the upper surface of leaves.
➢Orange spores are easily dislodged and may cover clothing, hands or implements.
When the infection is severe leaves dry out and die. Since inoculum is blown into a
given area, symptoms are often seen on upper leaves first.
➢As plants mature, the orange urediospores are replaced by black teliospores.
➢Pustules containing these spores are black and shiny since the epidermis does not
rupture.
➢Yield loss often occurs as a result of infection by Puccinia recondita f. sp. tritici.
Heavy infection which extends to the flag leaf results in a shorter period of grain fill
and small kernels.
Brown or leaf rust Rusty-red urediospores
C. Yellow or stripe rust - Puccinia striiformis
❑Symptoms
➢Symptom Mainly occur on leaves than the leaf sheaths and stem. The first sign of
stripe rust is the appearance of yellow streaks (pre-pustules), followed by small,
bright yellow, elongated uredial pustules arranged in conspicuous rows on the
leaves, leaf sheaths, glumes and awns.
➢ Bright yellow pustules (Uredia) appear on leaves at early stage of crop and
pustules are arranged in linear rows as stripes.
➢Pustules are yellow in colour in the beginning later on become dull black brown.
➢ The stripes are yellow to orange yellow.
➢The teliospores are also arranged in long stripes and are dull black in colour.
of urediospores
yellow‐orange masses
❑Etiology:
➢Urediospores:
Uredospores are stalked, oval, unicellular, brown, thick walled with 4-
round equatorial germ pores measuring outer layer 25-30 µm 17-20 pm. The spore
wall is thick with echinulate outer layer.
➢Teliospores
The teliospores (Fig. 4.60B) are stalked, spindle-shaped, thick and smooth-
walled with round or pointed apex, 2-celled and slightly constricted at the septum.
Spores are chestnut brown in colour and measure about 15-20 µm x 40-46 µm.
➢Basidiospores
Basidiospores are unicellular, thin-walled and very small. After discharge
from basidium by explosive mechanism, they are disseminated by air current. The
basidiospores can survive for a few days. They can infect only the leaves of alternate
host, the barberry, otherwise they die.
➢Pycniospores
The pycnium produce receptive hyphae and haploid, unicellular,
uninucleate pycniospore of single mating type either of + or – type. Within few days,
the growing mycelium becomes aggregated under the epidermis and forms a
yellowish flask-shaped structure, called Pycnium or Spermogonium
➢Aeciospores :
The aeciospores are unicellular, binucleate (n + n), thin-walled and orange
in colour. The young aeciospores are polyhedral in shape, but becomes globose with
maturity
❑Diseaes Cycle:
The life cycle is same for all these rust except their choice of hosts i.e.
1. Black stem rust : Beberies, mohonia acauifolia
2. Brown or leaf rust : Thalicirum polygamum
3. Yellow or stripe rust: Bromus juponicus.
❑Disease cycle in India:

In India, all these rusts appear in wheat growing belt during Rabi
crop season. Uredosori turn into teliosori as summer approaches. The
inoculum survives in the form of uredospores / teliospores in the hills
during off season on self sown crop or volunteer hosts, which provide an
excellent source of inoculum. In India, rust cycle is incomplete due to non
availability of alternate host.
❑Diseaes Cycle: A. Black stem rust Puccinia graminis f.sp. tritici
2. Brown or leaf rust
Management of wheat rust:
A. Black stem rust
•Mixed cropping and crop rotation
•Avoid excess nitrogen
•Sulphur dusting @ 35-40 kg/ha
•Mancozeb @ 2g/lit
•Resistant varieties
Lerma Rojo, Safed Lerma,
Sonalika and Chotil
B. Brown or leaf rust :
•Mixed cropping with suitable crops.
•Avoid excess dose of nitrogenous fertilizers.
•Spray Zineb at 2.5 kg/ha or Propiconazole @ 0.1 %.
•Grow resistant varieties like PBW 343, PBW 550, PBW 17
C. Yellow or stripe rust:
•Mixed cropping and crop rotation
•Avoid excess “N”
•Sulphur dusting @ 35-40 kg/ha
•Mancozeb @ 2g/lit
•Resistant varieties
Lerma Rojo, Safed Lerma,
Sonalika and Choti
2. Loose smut (Ustilago tritici)
Symptoms
➢Generally, diseased plants are indistinguishable from the healthy plants before
heading but diseased plants produce heads earlier than healthy plants.
➢Terminal symptom in all the varieties is the production of black powder in place of
wheat grains in the ears. Almost every ear of the diseased plant is converted into
black powder.
➢The black powder is a mass of olive-green microscopic spores of the smut fungus.
➢When spores are blown to flowers of healthy plants, they germinate on the female
organ (Ovary), stigma and lead to infection of the developing seed.
➢The smut fungus thus reaches in the mature grain and remains dormant there until
germination of the grain.
➢From superficial examination at harvest time, infected grains are sown in the
following season; the fungus inside the seed becomes active as the germination starts.
➢The fungus grows inside the plant first behind the growing point, keeping pace with
apex of the growing shoot.
➢As the ear formation starts, there is an accumulation of the fungus in the floral
parts, which are completely destroyed due to formation of the black powder.
Symptoms of loose smut
❑Etiology:
The spores are olive brown, lighter on one side, spherical or oval, 5-9 µm in
dia. They readily germinate in water. Each spore (Teliospores) produces four celled
mycelium. Germination of spores take place in moist condition by germ tube. The
pro-mycelium cells fuse to the germ tube that enters the ovary and stigma
established in the embryo and remain dormant until seed germinate.
❑Disease Cycle of loose smut of wheat:
The disease is internally seed borne and systemic. The infected grains can
not be distinguished apparently from healthy grains. The pathogen remains
dormant with in the mature grain. When such seed are sown, the dormant
mycelium becomes active and grows keeping pace with the growing tip of the host.
Secondary spread is by teliospores which are wind borne.
Management:
•Hot Water Treatment (54°C for about
10 min).
•Treat the seed with Vitavax @ 2g/kg
seed before sowing.
•Burry the infected ear heads in the soil,
so that secondary spread is avoided.
•Growing Resistant Varieties Viz, Np
710, Np 120, and Pb 90, Raj 2296, K-
8027, K-8251, HW-657, HW-240, Raj-
6276, VL-646, VL-719.
3. Karnal bunt (Neovossia indica)
Symptoms:
➢Karnal bunt attacks durum wheat, rye, and triticale, a hybrid of wheat and rye.
Despite its preference for a common crop, Karnal bunt can be extremely difficult to
diagnose in the field for many reason.
➢First, not all kernels on a plant head will be infected, and thus infected plants are
not as readily identifiable. This distribution is the reason for Karnal bunt's being
referred to as partial bunt.
➢Another factor which makes Karnal bunt difficult to readily diagnose in the field is
the fact that most infected kernels do not show symptoms prior to maturity.
➢In an ear only few grains are infected. A portion of the grain is converted into black
powdery mass. The black powder which gives foul smell due to presence of Tri-
methyl amine is a mass of thick walled dark brown spores of the fungus known as
teliospores.
➢The fungus is both seed borne and soil born and the infection occurs at flowering
time by airborne sporidia.
❑Etiology:
The spores are dark brown, smooth walled measuring 20-49 µm requires a
long lasting period, sporidia are produced in large number on short stout basidium.
The primary sporidia are needle shaped, secondary sporidia are sickle shape
❑Disease cycle
Karnal bunt was reported as a soil borne disease by Mitra (1931), but now it
is considered as an air borne disease. The fungal spores are also transferred by means
of equipment, tools or by man moving from milling places. The spores remain viable
for several years in soil (Bonde et al. 2004), wheat straw and farm yard manure. Soil
or seeds are primary sources of inoculum. Environment plays a key role in disease
progression. Teliospores germinate at suitable temperature (15–25oC) and humidity
in the soil. This condition generally dominates during February to March in North
Indian plains (Dumalasová & Bartoš 2009, Rush et al. 2005)
On germination, each teliospore produces promycelium which bears 110–185
primary sporidia at its tip. The primary sporidia are sickle shaped and were regarded
as infective entities. Now it is well known that secondary sporidia (allantoid and
filiform) play an important role in the disease cycle of the pathogen. The allantoid
sporidia are pathogenic while filiform sporidia increase the inoculum by division on
host/soil surface. The sporidia are mostly binucleate and on 169 germination produce
a germ-tube that penetrates the developing grain through stigma or ovary wall.
Infection takes place mainly at the time of anthesis. Generally, the grains are
moderately affected but in severe conditions whole grain may be infected
❑Management of Karnal bunt (Neovossia indica)
1. Deep ploughing during summer
2. Crop rotation
3. Use of resistant varieties is the most effective method for controlling the disease.
E.g. PBW 502 and N-75-3 and N-75-5 are partially resistant
4. The incidence of Karnal bunt can be effectively reduced by the application of
foliar fungicides between late boot and flowering. Some effective fungicides are
Propioconazole, Agrozim and Bavistin (carbendazim) and Bayleton (triadimefon).
5. Integration of propiconazole with bioagent fungus (Trichoderma viride) gives
almost complete control.
6. The temperature of the soil rises considerably by practices of polythene mulching
and wheat straw burning after mechanical harvesting.
4 Powdery mildew (Erysiphe (Blumeria )graminis var. tritici)
Symptoms:
➢Powdery mildew appears as fluffy, white powdery growths of fungal
spores on the leaf surface
➢Symptoms progress from lower to upper leaves.
➢ Under severe disease pressure as the season progresses, the fluffy, white
powdery growth can also affect stems and heads.
➢Fungal colonies eventually enlarge and merge together.
➢The area surrounding the lesion and on the reverse side of the leaf turns
yellow to brown.
➢Older infections on leaves and heads turn grey and can develop black
fruiting bodies, called cleistothecia, which appear as black specks.
➢Moderate to severe infections can result in leaf death.
➢Young, succulent growth such as new tillers is usually more susceptible
than older plant tissues.
➢ A powdery mildew infected crop will appear yellow from a distance,
similar to a crop suffering from water logging or nutrient deficiency.
Therefore, close examination is needed.
❑Etiology:
Powdery mildew, caused by Blumeria graminis f. sp. tritici (syn. Erysiphe
graminis). The mycelium can cover the plant surface almost completely, especially
the upper sides of leaves. It is asexually produced conidia and sexually formed
ascospores (produced from cleistothecia). Ascocarp is dark brown, globose
with filamentous appendages, asci oblong. ascospores hyaline, ellipsoid, 20–30 x
10–13 µm in size. Anamorph produces on hyaline conidiophores catenate conidia of
oblong to cylindrical shape, not including fibrosin bodies, 32–44 x 12–15 µm in size.
Haustoria are palmate.
❑Disease cycle:
Each mildew infection produces masses of tiny, white spores. These are
readily blown about by the wind, spreading the disease. The fungus needs a high
humidity but not rain or dew to infect the plant. Development of powdery mildew is
greater at mild temperatures (15-22°C) and in lush crops. Rain suppresses
development for up to five days. Hence, the disease usually occurs during drier
winters in most areas.
Mildew symptoms usually appear five to seven days after infection. The fungus can
multiply quickly and crops can become heavily diseased within four to five weeks of
the first signs of the disease. The disease most likely carries over from one season to
the next on the stubble. Mildew from one cereal (eg. barley) will not infect other
cereals (eg. wheat)
❑Disease cycle of P M of wheat
❑Management:
➢Controlling the disease involves eliminating conducive conditions as much
as possible by altering planting density and carefully timing applications &
rates of N2.
➢Milk has long been popular with home gardeners and small-scale organic
growers as a treatment for powdery mildew. Milk is diluted with water
(typically 1:10) and sprayed on susceptible plants at the first sign of
infection, or as a preventative measure, with repeated weekly application
often controlling or eliminating the disease.
Another way to control wheat powdery mildew is breeding in genetic
resistance, using "R genes" (resistance genes) to prevent infection. Eg.
KAMAL, LAL Bahadur, MP 1142, NP 852, NP 792, NP 818, NW 2036, NI
5439, NIAW 301, PBW 226, PBN 51, PV 18, Raj 4037, RAJ 2184, Sonaora
64,Sagarika, UP 215, UP 368, UP 1109, UP 2382,VL 829,VL 401,VL 616, WL
2265,WH 291,WG 377,WH 542, NARMADA 195.
➢Spray Wettable Sulphur 0.2% or Carbendazim @ 500 g/ha
➢One spray of propiconazole (Tilt 25 EC) @ 0.1 % at ear head emergence or
appearance of disease (whichever is earlier) is recommended for the
powdery mildew prone areas.
5. Alternaria blight (Alternaria triticina / Bipolaris sorokiniana)
❑ Symptoms:
➢The disease appears when wheat plants are 7-8 weeks old and becomes
severe when the crop is mature.
➢ Small, chlorotic, oval shaped lesions appear. These lesions become
irregular in shape.
➢The chlorotic borders of the lesions may become diffuse and turn light to
dark brown in color. Lesions are difficult to distinguish from spot.
➢Infection usually starts on the lower leaves, but symptoms can be found on
all plant parts.
➢As the disease progresses, several lesions coalesce to cover large areas,
resulting in the death of the entire leaf. In some cases the leaf starts drying
up from the tip, prematurely, when lesions appear.
➢Black powdery conidia may cover the lesions at this stage under moist
conditions.
➢The lowermost leaves are the first to show the signs of infection; the
fungus gradually spreads to the upper leaves. In severe cases, similar
symptoms are produced on the leaf sheath and stem, as well as the awns and
glumes if spikes are infected at the pre-anthesis stage. If the spike is infected
this early, seeds do not form.
➢ Infection at the dough stage of seed development results in glume
infection, ear infection and seed infection. Heavily infected fields present a
burnt appearance and can be identified from a distance (Prasada and
Prabhu, 1962; Prabhu and Prasada, 1966; Singh, 1990)
❑Symptomps of alternaria on wheat crop
❑Etiology:
Mycelium initially hyaline,
becoming olive-buff to deep olive-
buff, branched, septate, 2-7 µm wide.
Conidiophores similar to mycelium
in colour, septate, unbranched or
occasionally branched, erect, broader
towards the distal end, on the host
single or fasciculate, emerging
through stomata, amphigenous,
geniculate or straight, length
variable, between septa 17-28 × 3-6
µm.
Conidia acrogenous, borne singly or in chains of 2-4, smooth, irregularly ovoid, both
ends rounded, or ellipsoid, or conical-ellipsoid, gradually tapering into a beak; beak
(a secondary conidiophore) concolorous with the main conidial body, straight, 20-37
× 3-7 µm. Spore body pale brown to dark olive-buff, becoming darker with age,
verrucose, transverse septa 1-10, longitudinal septa 0 -5, constricted at septa, varying
in size; length including beak 15-89 µm, width 7-30 µm.
❑Disease cycle:
The fungus overwinters largely as seed-born spores. These asexual spores
multiply in the soil and transfer primary inoculum to susceptible plant leaves through
direct soil contact or by soil that is splashed onto the lowest leaves in rainfall or
irrigation. At this point, the polycyclic nature of A. triticina is evident when conidia,
the secondary inoculum are produced. Conidia germinate in temperatures between
20-25 degrees C and with 10 hours of water film on the leaves or 48 hours of
humidity greater than 90% . Conidia germinate, producing 2-4 germ tubes, each with
an appressorium and penetration peg. Hyphae infect via direct penetration and
proliferate inter- and intra-cellularly. Hyphae reach the deep mesophyll tissue within
72 hours of inoculation. Mycelium will spread to the epidermis and parenchyma
tissue but not so deep as to infect the vasculature. Leaf tissue thickness becomes
greatly reduced and chloroplasts of infected cells grow larger and irregularly shaped.
Mycelium will produce conidiophores which extend out of host tissue stomata and
bear conidia either singly or in chains. These conidia serve as secondary inoculum for
further infections within the season. Lesions appear between 2-5 days after
inoculation. Infections in the seed head produce spores for the next season. Conidia
in leaf and stem tissue can survive in debris, but its viability is greatly reduced when
left on top of the soil surface or in hot, wet environments; their survival is limited to 2
months on the soil surface and 4 months when buried
Management of alternaria blight of wheat:
➢Seed borne infection can be controlled by treating seed with Vitavax @ 2.5 g/kg of
seed.
➢Apply adequate fertilizers and irrigation.
➢Alternaria leaf blight can also be controlled by Zineb or Dithane M-45. The
fungicides may be sprayed as described for rust but mix the urea at 2-3 % with Zineb
for first and second sprays.
6. Ear cockle (Anguina tritici)
❑Symptoms
❖On Plant
➢Affects all growing stages.
➢Growth of the plant reduces.
➢The ears of diseased plants do not emerge properly.
➢The awns are twisted and the ear is also very much twisted.
➢Infected seedlings are more or less severely stunted and show characteristics rolling
and twisting of the leaves.
➢ A rolled leaves often traps the next emerging leaf and inflorescence within it and
causes it to become bent or badly distorted
➢Base of the stem are enlarged, bent and generally stunted.
➢Plants show spreading nature and tents towards more tillering.
❖On Infected ears/kernels
➢The affected ears are shorter and broader with very short or no awns on the glumes.
➢The affected ears are greener than the healthy ones, and galls shed off the ear more
readily than kernels.
➢Diseased head may have one, few or all of its kernel turned into nematode galls.
➢Galls are shiny at first but turn brown or black as the head matures.
➢ Mature galls are hard, dark, rounded and shorter than normal wheat kernels.
❑Symptoms of ear
cockle
❑Etiology:
➢Pathogen is large nematode about 3.2 mm long and 120micrometer in diameter.
➢Host: specific to wheat
➢Nematode lays eggs and produces all its juvenile stages and adults in seed galls.
❑Disease cycle :
➢Seed gall nematode contains 1000 to 3000 larvae in a seed.
➢Galls fallen to ground softens during warm, moist weather and release infective
second stage juveniles.
➢The juveniles swim upward on the leaves through film of water and feed ecto-
parasitically on leaves.
➢When the inflorescence begins to form, the juveniles enter the flower primordia and
produce the third and fourth stage juvenile and adults.
➢Each infected flower primodium becomes a seed gall and may contain 80 or more
adults
❑Management:
➢Use only healthy seed from healthy crop.
➢Cleaning of contaminated seeds by sieving or floating in water.
➢Crop rotation for 2.3 yrs such as barley or oat.
➢Hot water treatment of seed, first soaking seed in cold water for 4-5 hours and
treating at 54°C.
➢Soil application of nematicides such as Nemaphos, Aldicap@ 10 kg a.i/ha.
Thank You
Lecture 4 & 5
By
(Matinkhan A. Atar),
M.Sc. Agri., NET
Sugarcane Diseases and Their
Management :
Diseases Causal organism
1.Red rot : Glomerella tucumanensis
2. Smut : Ustilago scitaminea
3.Wilt :Fusarium moniliforme, Cephalosporium
sacchari
4. Grassy shoot : Mycoplasma like organism
5.Ratoon stuntting : Leifsonia xyli subsp. xyli
6. Pokkah Boeng : Fusarium moniliforme var subgluinans
Sheldo
1.Red rot : Perfect stage Glomerella tucumanensis
Imperfect stage: Colletotrichum falcatum
❑Symptoms:
➢ The affected canes exhibit leaf colour change, from green to orange and
then to yellow in the third or fourth leaf. Then the leaves start drying from
bottom to top.
➢ If the fungal spores enter the leaf sheath through the leaf midrib, then
reddish spots can be seen on the back side of the leaf midrib also.
➢ The external symptoms appear only after16 - 21 days after infection and
drying of entire cane takes another 10 days time.
➢ When the affected cane is split opened, the inner region is reddish in
colour with intermittent white tinges across the cane length.
➢ Sometimes, the pith inside the cane is filled with blackish brown liquid
and exhibited alchohol odour.
❑Symptoms of red rot of sugarcane:
Reddish lesion on leaf midrib Orange to yellow leaf Inner region with reddish colour
❑Etiology:
➢The mycelium of the fungus grows both inter- and intracellularly in the
parenchymatous cells of the host tissue. The hyphae are colourless, slender,
freely branched and septate. Acervuli appear just above or below the nodes
along the depressions or ridges.
➢They are black velvety bodies, develop in clusters. Acervuli are cuspidate with
irregularly arranged setae.
➢ Aseptate conidiophores 20µ long and 8µ wide, on which one-celled falcate
conidia are borne. Conidia are 16 to 48µ long and 4 to 8µ broad. They bear large
oil globule in the centre. Chlamydospores are terminal or intercalary.
❑Disease Cycle of red rot of sugarcane:

The sets may harbor the fungus and thus perpetuate the disease
from season to season. The fungus may also persist in the soil on diseased
clumps and dry leaves left in the field after the harvest. The primary source
of infection is planting material, plant debris and chlamydospores.
Secondary infection through conidia spread through irrigation water,
cultivation tools and implements, wind borne inoculums.
❑Management strategies:
❖Cultural method:
➢The best way to control red rot is to select setts for planting from healthy plants
in a disease- free area.
➢The red rot affected field must be rotated with rice for one season and other
crops for two seasons.
➢Growing of recommended resistant and moderately resistant varieties viz., Co
86032, Co 86249, CoSi 95071, CoG 93076, CoC 22, CoSi 6 and CoG 5.
❖Physical method:
➢Removal of the affected clumps at an early stage and soil drenching
with Carbendazim 50 WP (1 gm in 1 litre of water)
➢The cut ends and entire setts should be dipped in a fungicide solution, such as
one per cent Bordeaux mixture.
➢If the disease is noticed in the field, the leaves and canes should be collected
and destroyed by burning.
❖Chemical method:
➢Adopt sett treatment with Carbendazim before planting (Carbendazim 50 WP
(0.5 gm in 1 litre of water) or Carbendazim 25 DS (1gm in 1 litre of water) along
with 2.5 kg of Urea in 250 litre of water
➢Use fungitoxic chemicals like Bavistin, Benomyl, Topsin and Aretan at 0.1 per
cent for 18 min. at 52ºC for dipping setts which gave almost complete
elimination of rot infection
2. Smut (Ustilago scitaminea):
Symptoms:
➢Affected plant produce a whip like black shoot ( 25 – 150 cm) from the
growing point of the canes.
➢At first the mass of smut powder on this outgrowth is covered with thin
silvery membrane made up of host epidermis. It soon ruptures exposing
dense black powdery mass consisting of smut spores.
➢Whip covered by translucent silvery membrane enclosing mass of black
powdery spores.
➢Initial thin canes with elongated internodes later become reduced in
length.
➢Profuse sprouting of lateral buds with narrow, erect leaves especially in
ratoon crop
❑Etiology :
The fungal mycelium spores (teliospores) are echinulate, light brown and
spherical, measuring 6.5 – 8.5 µ in diameter.
They germinate readily in water, producing 2-3 celled promycelia.
Sporidia arise terminally or laterally and are hyaline, thin walled, single celled
and elliptical to linear.
❑Disease Cycle of smut of sugarcane:
➢Sugarcane smut is disseminated via teliospores that are produced in the
smut whip. These teliospores located either in the soil or on the plant,
germinate in the presence of water.
➢The primary transmission of the disease is through diseased seed pieces,
while the secondary transmission is through windblown spores.
➢In addition, spores or sporidia, present in or on the soil surface, are also
carried to different fields through rain or irrigation water.
❖Cultural method:
➢Growing of resistant and moderately resistant varieties viz., Co 86249, CoG
93076, CoC 22, CoSi 6 and CoG 5
➢Discourage ratooning of the diseased crops having more than 10 per cent
infection
➢Cajanus cajan can be grown as a companion crop between rows of
sugarcane, and the secondary spread of the disease is substantially reduced
❖Physical method:
➢Treating the seed setts with Areated Steam Therapy (AST) at 50 ºC for 1
hour or in hot water at 50 ºC for 30 minutes or at 52 ºC for 18 minutes
➢Roguing of smut whips with gunny bags/polythene bag and dipped in
boiling water for 1 hour, and diseased clums must be uprooted and burnt
❖Chemical method:
➢Sett treatment with fungicides viz., Triadimefon @ 1gm in 1 litre of water
or Carbendazim @ 1gm in 1 litre of water for 10 minutes.
➢Spray on infected stools with a small amount of a 10% solution of
roundup, using a small hand held sprayer.
➢In severe cases spray the entire block with glyphosate (360 G/L) at 5-7
lit/ha
3.Wilt :Fusarium moniliforme, Cephalosporium sacchari
❑Symptoms:
➢ The first symptoms of the disease become apparent only when the plant has
grown for about 4-5 months.
➢Then gradual yellowing and drying of foliage, shrinkage/withering of canes.
➢If the affected canes are cut and examined, the pith will be Light to dark
purplish or brown discolouration of ground tissue, pithiness and boat shaped
cavities in the middle of the internodes.
➢A characteristic disagreeable odour is also associated with this disease.
➢Often a cottony white mycelium is seen in the pith region
Reddish discolouration Yellowing of leaves Shrinkage of cane

in cane
❑Etiology:
The fungal mycelium is hyaline, septate and thin walled. The conidiophores are
simple or branched and produce single celled, hyaline, oval to elliptical
microconidia. Macroconidia are straight with 3-5 septae measuring 27-73 × 3.4-5.2
mm. Blastoconidia are either straight, sickle shaper or pike shaped with 2-3 septae.
Moreover will be found as elliptical cell shaper structure with 1.-43x3.0-4.5 mm in
size
Disease cycle of wilt:
➢The fungal mycelium is abundant in the infected canes.
➢The hyphae are hyaline, thin walled and septate.
➢They produce numerous microconidia on simple or branched, lateral or terminal
hyphae, but NO macroconidia are produced.
➢Conidia readily germinate to produce single germ tubes.
➢The fungus is transmitted from place to place through the infected seed setts.
➢When the diseased setts are planted, the eyes may fail to develop or often the
shoots arising from the eyes may wilt, due to the infection spreading to the shoots.
➢Root formation in such setts may be very poor. The fungus can also survive in soil
as a saprophyte for 2-3 years.
➢Near-neutral and alkaline soils are favoured by the fungus. The perfect stage is not
known.
❖Cultural method:
➢Selection of healthy seed setts from disease-free area for planting
➢Grow resistant varieties like Co 617 and B.P.17 are more resistant than
other varieties
➢Crop rotation, managing root borer, avoiding prolonged drought and
water logging and hygienic practices.
❖Chemical Method:
➢Dipping the setts in 40 ppm of boron or manganese, or spraying the plants
with either of these minor elements reduces the disease intensity.
➢sett treatment with fungicide like Bavistin, 0.1 per cent before planting
➢Apply carbendazim @ 2gm/lit of water at the root zone area and same as
follow at 15 days interval
4. Grassy shoot : Mycoplasma like organism
❑Symptoms:
➢The disease appears nearly two months after planting.
➢The disease is characterised 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 with premature proliferation of auxillary
buds. Cane formation rarely occurs in the affected clumps, if formed, thin
with shorter internodes having aerial roots at the lower nodes.
➢The buds on such canes usually papery and abnormally elongated.
Profuse tillering Whitining of leaf Grassy shoot Reduced inter nodal

length
❑Etiology:
➢The disease is caused by a phytoplasma.
➢Two types of bodies are seen in ultrathin sections of phloem cells of
infected plants. The spherical bodies of 300-400 nm diameter
and filamentous bodies of 30-53 mm diameter in size.
➢ Mycoplasma cells are physically small – less than 1 µm – and they are
therefore difficult to detect with a conventional microscope.
❑Disease cycle :
➢The primary spread of the phytoplasma is through diseased setts and
cutting knifes.
➢The pathogen is transmitted secondarily by aphids viz., Rhopalosiphum
maydis, Melanaphis sacchhari and M. idiosacchari.
➢Sorghum and maize serves as natural collateral hosts.
❑Management strategies
❖Cultural method:
➢Growing resistant varieties viz., Co 86249, CoG 93076 and CoC 22
➢Avoid ratooning if Grassy Shoot Disease incidence is more than 15 % in the
plant crop
➢If disease symptoms are visible within two weeks after planting, such
plants can be replaced by healthy plants.
➢Uprooted infected plants need to disposed of by burning them.
❖Physical method:
➢Rogue out infected plants in the secondary and commercial seed nursery.
➢Treat the setts with aerated steam at 50°C for 1 hour to control primary
infection.
➢Treating them with hot air at 540C for 8 hours and spraying twice a month
with aphidicides.
❖Chemical method
➢Spray dimethoate @ 1ml in 1 litre of water to control insect vector
➢Apply pesticide methyl-demeton @ 2ml/lit of water for controlling aphid
5.Ratoon stuntting : Leifsonia xyli subsp. Xyli
❑Symptoms:
➢The affected plants are stunted, the stunting being most severe in stubble
and ratoon crops.
➢In infected stocks, the presence of pin head like orange coloured dots of
bacteria on the internal soft tissue in the nodal region
➢The setts taken from diseased plants germinate poorly and the few shoots
that are emerged grow very slowly.
Stunted growth Orange pin head dots

on inter node
❑Etiology:
➢The organism that causes RSD is a small aerobic bacterium named Leifsonia
xyli subsp. xyli. The genus of this pathogen was previously called Clavibacter.
➢The pathogen ( Clavibacter xyli sub sp. xyli) is a RLO known to be present
in the xylem cells of infected plants. They are small, thin, rod shaped
or coryneform (0.15 to 0.32µm wide and 1.0-2.7µm long) and Gram positive.
Disease cycle:
The RSD pathogen is primarily transmitted through seed cane taken
from diseased plants. Because symptoms of the disease are not readily visible,
the bacterium may be spread unknowingly from one area to another. Stalks in
potential seed fields can be randomly sampled and serologically assayed to
determine RSD incidence. The RSD pathogen can also be readily transmitted by
knives and mechanical harvesting machines that become contaminated with the
bacteria in the juice from diseased stalks. Transmission by harvesting machinery
is very significant.
Cane-chewing animals such as rodents may be capable of transmitting
the pathogen when they gnaw on a diseased stalk and then on a healthy one.
Not much is known about this means of transmission or its significance.
According to reports, the pathogen survives in the soil after harvest to re-infect
healthy plants (Bailey and Tough 1992). However, the extent of infection
by Leifsonia xyli subsp. xyli surviving in the soil is not known.
❖Cultural method:
➢Select healthy setts for planting.
➢Field should maintain at proper sanitation.
➢Ungerminated setts should be removed and fill the gap with new setts
which should be treated before planting.
❖Mechanical method:
➢Treat the setts with hot water at 50°C for about 2 hours this gives 100 per
cent control. A temperature higher than this would kill the cane and lower
temperature than the specified enables the pathogen to survive.
➢Aerated steam therapy eliminates the pathogen from the infected canes.
Use of disinfectants to clean seed cutting tools which would reduce the
chance of spread of pathogen from the infected to healthy setts.
❖Chemical method:
➢Chemical disinfectants that may be used on cane cutting knives includes,
Lysol, Dettol, ethanol, Mirrol and Roccal. Atleast 5 minutes of contact with
the cutting surface is needed to assure disinfection.
6. Pokkah Boeng : Fusarium moniliforme var subgluinans sheldo
❑Symptoms:
➢The characteristics symptoms of Pokkah Boeng disease are the appearance
of chlorotic patches towards the base of the young leaves,
➢ in acute cases disease shows distortion of stalk with external and internal
cut like lesions and rotting of apical part of stalk.
➢Under field conditions, the disease may develop many variations from the
general symptoms, but the final result is usually a malformed or damaged
top and stalk.
➢The base of affected leaves is often narrower as compared to normal
leaves.
➢ Knife cut symptoms of the disease were reported in varieties CoS767,
CoC671, CoC8014, Co1158, CoS8315 and CoS 8436.
➢Development of disease symptom in four phases was observed namely
chlorotic phases I and II, top rot and knife cut phase (Fig 1).
➢ The apical leaves may also show pronounced wrinkling and twisting
depending upon the susceptibility of varieties and existing climatic
conditions also malformed or damaged top and stalk due to this disease.
➢The symptoms of Pokkah boeng disease were mainly two types i.e.,
chlorotic phase and acute phase of top rot and knife cut (fourth phase) of
this disease in Maharashtra.
❑Symptoms images :
❑Etiology:
➢Fusarium moniliforme showed di erent colour for its mycilium pale
white, pink and purple mycilium and for pigmentation of metabolites also
during the growth on artificial medium
➢the growth of conidia range from 9.3-29.7 µm in length and 2.7-6.0 µm in
width; mycelium width of ranged in between 1.75-7.00 µm.
➢ Mycelium of F. moniliforme was generally dense in delicately floccose to
felted with powdery appearance due to formation of macro conidia.
❑Disease cycle:
Transmission and viability of pathogen Basically it is an air-borne
disease and primarily transmitted through the air-circulation and secondary
infection takes place through the infected setts, irrigation water, splashed
rains and soil. The pathogen (F. Moniliforme) can survive for 12 months in the
plant debris under natural conditions and can remain viable for more than
10 months under laboratory conditions.
❑Management:
➢Planting of healthy seed material/use of resistant verities
➢wider spacing planting of sugarcane is necessary to facilitate the plant
protection operations.
➢Canes showing ‘top rot’ or ‘knife cut’ should be rouged out from the fields
as they are shown
➢Spraying of different fungicides like Bavistin (1 gm/lit. of water) or Blitox
(0.2%) or Copper oxychloride or 0.3% Dithane M-45 (3 gm/L of water) are
the effective for reducing the Pokkah Boeng disease
Thank You
Course title: Diseases of Field and
Horticultural Crops and their Management -
II
Lecture 4 & 5
By
M.Sc. Agri., NET
Sunflower Diseases and Their Management :
1. Sclerotinia stem rot : Sclerotium rolfsii

2. Alternaria blight : Alternaria helianthi
3. Rust : Puccinia helianthi
4. Downey mildew : Plasmopara halstedii
1. Sclerotinia stem rot : Sclerotium rolfsii
❑ Symptoms :
▪ Typical Symptoms
➢Initial symptoms of the disease are noticed 40 days after sowing.
➢Sickly appearance of plants can be noticed from a distance and a row effect can be
observed in heavily infested soil. Later the entire plant withers and dies.
➢White cottony mycelium and mustard-seed-type sclerotial bodies are conspicuous
on the affected stem near soil level
▪ General symptoms
➢ Initial symptoms are visible during pod development.
➢ Leaves will and turn gray-green before turning brown, curling and dying.
➢ It is important to observe stems and pods for white mycelium and sclerotia to
differentiate Sclerotinia stem rot from other stem and root rot diseases. Since
blossoms are infected first, early stem or pod water-soaked symptoms often
initiate near colonized flowers.
➢ In a few days diseased stem areas are killed and become tan and eventually
bleached.
➢ This bleached stem will have a pithy texture and will shred easily.
➢ Infected plant parts generally will have signs of the fungal pathogen as white,
fluffy mycelium during humid conditions and sclerotia on the surface of or
embedded in the stem tissue.
➢ Although stem and pod infection usually occurs about 6 to 14 inches above
the soil line, some basal infection also may be found.
❑Etiology:
Sclerotia of S. rolfsii most commonly produce a mushroom-like fruiting body
termed an apothecium. One or several apothecia can emerge from a single
sclerotium. Apothecia are fleshy-colored discs measuring 4-8 mm in dia. They
produce ascospores as a result of a sexual process, with ascospore. Ascospores are
hyaline (clear or non-pigmented), unicellular and thin-walled.
❑Disease cycle :
The fungus survives in the field as sclerotia in the soil and in plant debris.
Sclerotia may survive for a period of up to four to seven years in the soil. Infection
occurs during the flowering stage when there is high rainfall and cool
temperatures. Wet soil results in the production of apothecia (small, mushroom-
like, fruiting bodies) from germinating sclerotia. Apothecia form and release
spores into the air, which are windborne and can infect the sunflower head during
wet weather. Wounds on the back of the sunflower heads may become infection
sources and initiate head rot.
❑Management:
➢Collection and destruction of plant debris
➢Seed treatment with Trichoderma viride @ 4 g/kg seed and soil application
of Trichoderma viride @2.5 kg/ha, mixed with 50 kg FYM or in conjunction with
organic amendments such as castor cake or neem cake or mustard cake @ 500 kg/
ha.
➢Seed treatment with 3 g Thiram + Carbendazim is recommended.
2. Alternaria blight : Alternaria helianthi
❑Symptoms:
➢The fungus first produce brown spot on the leaves and later spread on the
stem, sepal and petals.
➢The lesion on the leaves are dark brown with pale margin surrounded by
yellow halo.
➢The spots later enlarge in size with concentric rings and become irregular
in shape. Several spots coalesce to show bigger irregular lesion leading to
drying and defoliation.
➢Severe reduction in seed and oil yield reported.
➢The most affected components are number of seeds per head and the seed
yield per plant.
➢The disease also affects the quality of sunflower seeds by affecting
germination and initial vigour of the seedlings.
❑Symptoms:
❑ Etiology :
➢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 pale grey-yellow to pale brown, muriform, having many
transverse septa and 1 -2 longitudinal septa.
❑Disease cycle
The fungus survives in the infected host tissue and on weed hosts. The
fungus is also seed borne. The secondary spread is mainly through wind
blow conidia
❑Management
➢Occurrence and severity of the disease depends on the season and
planting dates. Mid-September planting of sunflower remains free from the
disease.
➢Remove and destroy infected plant debris.
➢Rogue out weeds at periodical intervals.
➢Treat the seed with Thiram 6 gm/kg.
➢Foliar spray with 0.3 per cent Mancozeb four times at an interval of 10
days controls the disease.
3. Rust : Puccinia helianthi
❑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.
➢The disease is autoecious rust. The pycnial and aecial stage occur on
volunteer crops grown during off-season.
❑Etiology:
The disease is autoecious rust produce uredial and telial stages on the
leaves.
➢Aceiospores: they are orange, typical, ellipsoidal and finally echinulate.
➢Uredospores: they are brown and vary from subglobose to ovate. The wall
of spore is smooth, chestnut brown. The spores are pedicellate.
➢Teleiospore: bi-celled and black in colour.
➢Basidospores: Infect sunflower to produce pycnia of + or – types
➢Pycniospores: they small, oval, hyaline and appear as shining viscous
mass.
❑Disease cycle:
➢The pathogen survives in the volunteer sunflower plants and in infected
plant debris in the soil as teliospores.
➢The disease spreads (Secondary) by wind-borne uredospores from
infected crop.
❑Management
➢Use of tolerant and resistant varieties (Modern, EC684142 and Surya)
➢Crop rotation should be followed.
➢Previous crop remains should be destroyed.
➢Removal of crop residues
➢Spray Mancozeb at 2kg/ha.
4. Downey mildew: Plasmopara halstedii
❑ Symptoms:
The disease spreads rapidly through seeds.
Symptoms of the disease are evident as seedling damping off, systemic
infection, local foliar lesions and basal root or stem galls.
➢Damping off: seedlings are killed before or soon after the emergence due
to subterranean infection by the downey mildew fungus. Affected plants
dry and become windblown.
➢Systemic infection: plants carrying systemic infection are severely
stunted and flowering the upper leaves become entirely chlorotic. The
stems become britle. Flower heads of infected plants remain errect, become
small in size, remain sterile and produce no seeds or only few seeds are
produced on such heads.
➢Local foliar lesions: small angular greenish-yellow spots appear on
leaves as a result of secondary infection. The spots may enlarge and
coalesce to infect a large part of the leaf. The fungal growth becomes visible
at lower surface of the diseased area.
➢Basal root or stem galls : the root infection may result in formation of
galls at the base of the plants of primary roots.
❑Symptoms:
❑Etiology:
Mycelium non-septate. Sporangiphore are typically branched at right angles.
Produce brownish, thick walled, resting sexual oospores. Microscopic
observation revealed the monopodial branching sporangiphore at near right
angles, with 5-6 terminal branches 6-10 µm long & bearing single elliptic
papillate zoosporangia 15 -25 X 12-16 µm .
❑Disease cycle:
➢Primary source : The disease is seed and soil borne.
The oospores in the residues of the previous sunflower crop or oospores
have been reported to remain dormant up to 14 yrs.
➢Secondary source: secondary infection may be caused by the zoosporangia
produced in great numbers on systemically infected plants by wind.
❑Management:
➢Practice a five-year or longer crop rotation between sunflower crops with
non hosts such as corn and small grains.
➢Choice of planting sites and disposal of infected crop residues also give a
fairly good control.
➢Seed treatment with Metalaxyl or Apron at the rate of 3 g per kg of seed
has been found to give effective control.
Lecture 8 & 9
By
M.Sc. Agri., NET
Mustard crop Diseases, Symptoms, Etiology, Disease cycle and
Their Management

1. Alternaria Blight Spot : Alternaria brassicae
2. White Rust : Albugo candida
3. Downy mildew : Peronospora parasitica
4. Sclerotinia Stem Rot : Sclerotinia sclerotiorum
1. Alternaria Blight Spot : Alternaria brassicae
❖ Symptoms:
➢The disease attacks on the lower leaves as small circular brown necrotic spots
which slowly increase in size.
➢Many concentric spots coalesce to cover large patches showing blightening and
defoliation in severe cases.
➢Circular to linear, dark brown lesions also develop on stems and pods, which are
elongated at later stage.
➢Infected pods produce small, discolored and shriveled seeds.
❑Etiology:
The conidia are dark brown and smooth-walled, up to 60 x
14µm. The conidia are cylindrical to oblong in shape and are muriform and
produced in chains of 8-10 spores. They are firmly attached to conidiophore
that are olive-brown, septate, and growing to an upper range of 100-200 µm,
although this overall length may vary. Conidia are borne in continuous,
chain-like structure.
❑Disease cycle:
➢The disease is externally and internally seed born.
➢The pathogen survives through spores (conidia) or mycelium in diseased
plant debris or weed.
❑Management
➢Crop rotation helps reduce disease carryover but does not eliminate
airborne spores from another field.
➢Clean seed to remove shrunken seed that may be infected with black spot
and have low viability.
➢Use seed with high germination (over 90%). Swath badly infected crops
early to minimize shattering losses and seed shrinkage due to black spot.
➢seed treatment with Thiram + Captan (1:1) 0.3% and four sprays of Zineb
(0.25%) were found quite effective to control Alternaria disease.
2. White Rust : Albugo candida
❖ Symptoms:
Symptoms are produce on all parts excepts roots. Symptoms appears as
result of two types of infection.
❑Local infection :
➢White to creamy yellow pustules of variable size & shape appears on the
leaves, stem and inflorescence. Pustules merge from to form large patches.
The pustules after host epidermis ruptured, become powdery appearance.
(give white rusty appearance)
➢Tan-yellow spots develop on the upper leaf surface opposite the pustules.
❑Systemic infection :
➢Pustules may also form on the pods. Infected flowers develop a "staghead"
in which the flowers are sterile, malformed and green, and various flower
parts may be thick and club-shaped and greatly enlarged.
➢Young stem and flower organs infected stimulate hypertrophy and
hyperplasia resulting abnormal enlargement of infected organs.
➢Most turnip or Polish varieties of canola as well as brown and oriental
mustard are susceptible.
➢Yield losses are about 1% for each 1% of staghead observed in a field. Yield
losses in Manitoba are usually less than 10%
White rust symptoms on mustard
❑Etiology:
Mycelium is endophytic, branched, hyline and having knob shaped
haustoria. Sporangiophores in the beginning are sub epidermal and are
clavate and simple. Lateral wall of sporangiophore is thickened but laterally
they are free from the sporangia, which form in a basipetal chain. The
sporangia of Albugo germinate by zoospore or by germ tubes depending on
the temperature. When zoospore are produced, the sporangia extrude 4-12
zoospore.
❑Disease cycle:
➢ The pathogen survives through oospores in affected host tissues and soil.
➢Secondary infection is carried out by sporangia and zoospores which
produce new infection
Management
➢The use of resistant varieties is considered to be the best and cheapest
method of managing the plant disease. (DRMRIJ-12-14, DRMRIJ 12-39,
DRMRIJ-12-48, DRMRJA 35, DRMRIJ 12-44, DRMRIJ 12-26, DRMRIJ 12-28 and
DRMRIJ 12-40)
➢Use at least a three year crop rotation & Control volunteer canola and
susceptible mustard-type weeds in the rotation.
➢Two Spraying propiconazale 25EC (0.5%), or metalaxyl 8% or mencozeb
64% wp (0.2%), 15 day interval gives effective control.
3. Downy mildew : Peronospora parasitica
❑ Symptoms:
➢Young seedlings are more susceptible than adult plants and can die from
downy mildew if infected when young.
➢The first observable symptom is small, light green-yellow lesions on the
upper leaf surface, later showing on the under surface
➢ Grayish white irregular necrotic patches develop on the lower surface of
leaves.
➢Later under favourable conditions brownish white fungal growth may
also be seen on the spots.
➢A mealy growth on the underside of the leaf, corresponding to yellowing
of the upper surface of the leaf
➢The bottom sides of leaves develop a fluffy or downy appearance from
sporulation during cool, moist conditions.
➢Old lesions become necrotic and translucent after invasion by secondary
saprophytes.
➢ Seedlings may be killed or develop dark brown vascular systems from
severe infections, but older plants are rarely killed.
➢The most conspicuous and pronounced symptom is the infection of
inflorescence causing hypertrophy of the peduncle of inflorescence and
develop stag head structure.
Disease symptoms
❑Etiology:
P. parasitica has a coenocytic mycelium which ramifies in the intercellular
spaces of the host and forms haustoria which penetrates the cells of infected
tissues (Channon 1981). Infection of the host plant can either occur asexually
(from conidia borne on definite conidiophores) (Tommerup 1981) or sexually
(from oospores in the soil)
❑Disease Cycle
The fungus is both soil and seed-borne and can persist in the soil for a long
time. Infection is favoured by cool, wet weather and under ideal conditions,
new infections can develop in as little as 3 to 4 days. The fungus is related to
white rust with specialised spores (oospores) probably responsible for
primary infections. Conidial spores produced on the underside of the
infected leaf are then responsible for the secondary spread of the disease.
❑Management:
➢Eradicate cruciferous weeds (wild mustards, etc.) that may harbor the
fungus.
➢Manage irrigation to reduce periods of high humidity.
➢Seed treatment with Metalaxyl 35 SD (Apron) at 6 g/kg of seeds.
➢Spray the crop with 0.2 % Ridomil or 0.1% Karathane as soon as the
symptoms are noticed and repeat the spray two to three times at 10 days
interval
4. Sclerotinia Stem Rot : Sclerotinia sclerotiorum
❑ Symptoms:
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.
Yield loss of 10 to15% has occurred in Saskatchewan, Manitoba and North
Dakota; occasionally losses of 50% have occurred in Manitoba
❑ Symptoms Sclerotinia Stem Rot :
Typical symptoms of stem rot observed on mustard in the Sclerotinia stem rot at the base of the stem
survey areas
Embedded Sclerotia in Pod & Stem

❑Etiology:
S. sclerotiorum (Lib.) de Bary is necrotrophic fungal pathogen in the
Ascomycota and Order Helotiales produce fluffy white mycelium on and in
infected plant parts. This mycelium aggregates itself into sclerotia, there are
four stages in its life cycle: sclerotium, apothecium, ascospore, and
mycelium (Hieu, 2007). Fungal sclerotia has been reported to be of two
types i.e. myceliogenic and carpogenic. One or several apothecia can
emerge from a single sclerotium. Apothecia are fleshy-colored discs
measuring 4-8 mm in dia. They produce ascospores as a result of a sexual
process, with ascospore. Ascospores are hyaline (clear or non-pigmented),
unicellular and thin-walled
❑Sclerotinia stem rot disease cycle:
(A) Sclerotia of Sclerotinia sclerotiorum survive in the soil. (B) Under cool, wet
environmental conditions sclerotia germinate to produce apothecia. (C) Apothecia
produce sexual spores called ascospores, which are forcibly discharged from the
apothecium into the air. (D) Ascospores colonize senescing flowers and infection
can spread into the stem at the node. (E) Signs of S. sclerotiorum include sclerotia
and tufts of white mycelium. Symptoms can include bleached stem lesions, wilt,
lodging and plant death resulting in no seeds or poor pod fill. (F) Sclerotia form in
and outside stems and pods and are dropped to the soil during harvest
Management
➢Use crop rotation; do not plant highly susceptible crops more than once in
four years, including dry edible beans, sunflowers, 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.
➢Reduce humidity and high-moisture periods within the plant canopy and
field.
➢Field flooding during warm temperatures destroys sclerotia.
➢Seed treatment with T. viride @4g/kg or P. fluorescens @ 10g/ kg of seed or
Carbendazim or Thiram 2g/kg of seed.
➢Spot drenching with Carbendazim 1g/lit or P. fluorescens / T. viride 2.5
kg/ha with 50 kg FYM.
Lecture 10
By
M.Sc. Agri., NET
Gram (Chick pea)crop Diseases, Symptoms,
Etiology, Disease cycle and Their
Management.
1. Wilt : Fusarium oxysporum f.sp.ciceri

2. Grey mould : Botrytis cineria
3. Ascochyta blight : Ascochyta rabiei
1. Wilt : Fusarium oxysporum f.sp.ciceri
❖ Symptoms:
➢The disease can affect the crop at any stage.
➢Leaves eventually take on a dull-yellow colour, wilt and the plant collapses
and dies.
➢The field symptoms of wilt are dead seedlings or adult plants, usually in
patches.
➢In some cases there may be leaf vein clearing before wilt begins.
➢At seedling stage, 3-5 weeks after sowing, whole seedlings collapse and lie
flat on the ground with dull green leaves and shrunken stem.
➢Dark drown or dark discoloration of the internal the xylem tissues stain
dark-brown to almost black are visible.
➢At adult stage, drooping of petioles, rachis and leaflets and finally entire
plant occurs.
❑Etiology:
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 conidiophore, are thin walled, 3 to 5septate, fusoid and pointed at
both ends. Chlamydospores are roughwalled or smooth, terminal or
intercalary, may be formed singly or in chains.
❖ Symptoms of Gram wilt:
Vascular wilt and yellowing field
Vascular discolouration
❑Disease cycle
The disease is seed and soil borne. The primary infection is through
chlamydospores in soil, which remain viable upto next crop season. The
secondary spread is through irrigation water, cultural operations and
implements.
❑Management Strategies:
➢Deep summer ploughing
➢Follow crop rotation measures continuously.
➢Always use disease free seeds.
➢Avoid sowing when temperatures are high.
➢Follow 6-year crop rotations with sorghum
➢Apply FYM 10-15 cart load/ha.
➢Seed treatment with T. viride @4g/kg or P. fluorescens @ 10g/ kg of seed or
Carbendazim or Thiram 2g/kg of seed.
➢Spot drenching with Carbendazim 1g/lit or P. fluorescens / T. viride 2.5
kg/ha with 50 kg FYM.
➢Seed treatment with Carbendazim at the rate of 1g/kg of seed /
➢Seed treatment with Thiram + Carbandizm @ 1g+2g per kg of seed.
2. Grey mould : Botrytis cineria
❖ Symptoms:
➢Lack of pod setting is the first indication.
➢Under favourable conditions, foliage shows symptoms and plants often die
in patches.
➢Shedding of flowers and leaves, covered with spore mass can be seen.
➢Lesions on stem are 10-30 mm long and girdle the stem fully.
➢Tender branches break off at the point where the gray mold has caused
rotting.
➢Affected flowers turn in to a rotting mass.
➢Lesions on the pod are water-soaked and irregular.
➢On infected plants, the pods contain either small, shriveled seeds or no
seeds at all.
Stem infection caused by botrytis.
Seed discolouration caused by botrytis infection

❑Etiology :
➢CONIDIOPHORES produced from mycelium or sclerotia, usually formed in
tufts, 750 µm to over 2 mm long, smooth-walled, grey-brown to brown, 18-23
µm wide in the lower part, hyaline to pale brown and branched in the upper
part; each branch ended with a hemispherical or spherical swelling, 5-12 µm
diam, having minute sterigmata (s), i. e., spore-bearing projections.
➢CONIDIA are two types: macro- and micro-conidia.
• Macroconidia globose, ellipsoidal, or egg-shaped, smooth, hyaline to pale
brown, usually with a protuberant hilum, 8-14 x 6-9 µm.
• Microconidia not observed.
➢SCLEROTIA shield-like, lenticular to irregular, brown to black, 0.2-0.5(15)
mm diam, consisting of densely packed medulla and a pseudoparenchymetous,
dark brown to black cortical layer of cells, 5-10 µm diam.
❑Disease Cycle
The fungus survives on infected seed, as a saprophyte on decaying
plant debris and as soil-borne sclerotia. The disease is often established in
new areas by sowing infected seeds. Masses of spores are produced on
infected plants. These fungal spores can be carried from plant to plant by air
currents and spread the disease rapidly. Once a crop has become
established, the warm, humid conditions under the crop canopy provide
ideal conditions for infection and spread of the disease.
❑Disease cycle of botrytis grey mould in chickpeas
➢Avoid excessive irrigation and vegetative growth.
➢Intercrop with linseed.
➢Avoid excessive irrigation. Use compact varieties.
➢Deep summer ploughing Reduce plant density and increase in air passage
between the plants.
➢Seed treatment with Carbendazim + Thiram (1:1) @ 3g/kg of seed is
recommended or Spray the crop with Captan 5 - 6 kg/ha at 15 days
interval./Spray of Carbendazim @ 1.5g/lit of water is recommended./Spray
Mancozeb @3 g/lit of water
3. Ascochyta blight : Ascochyta rabiei
❑Symptoms:
➢All above ground parts of the plant are infected.
➢ On leaf, the lesions are round or elongated, bearing irregularly depressed
brown spot and surrounded by a brownish red margin.
➢Similar spots may appear on the stem and pods.
➢ The spots on the stem and pods have pycnidia arranged in concentric
circles as minute block dots.
➢When the lesions girdle the stem, the portion above the point of attack
rapidly dies.
➢ If the main stem is girdles at the collar region, the whole plant dies.
❑Etiology:
The fungus produces hyaline to brown and septate
mycelium. Pycnidia are spherical to sub-globose with a prominent
ostiole. Pycnidiospores are hyaline, oval to oblong, straight or slightly curved
and single celled, occasionally bicelled.
❑Symptoms images:
Symptoms of leaf infection
Ascochyta blighted patches occur within a crop

Symptoms of pod infection as the disease spreads from infected plants to
surrounding healthy plants
❑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 pycnidiopores (conidia). Rain splash
also helps in the spread of the disease.
❑ Management
➢Remove and destroy the infected plant debris in the field.
➢Intercrop with wheat, barley, mustard
➢Follow crop rotation with cereals.
➢Exposure of seed at 40-50˚C reduced the survival of A. rabiei by about 40-70
per cent.
➢Treat the seeds with Thiram 2g or Carbendazim 2 g or Thiram +
Carbendazim (1:1 ratio) at 2 g/kg.
➢Spray with Carbendazim at 500 g/ha or Chlorothalonil 1kg/ha.
Lentil crop Diseases, Symptoms, Etiology,
Disease cycle and Their Management.
1. Rust : Uromyces viciae-fabae
2. Wilt : Fusarium oxysporum f.sp. lentis
1. Rust : Uromyces viciae-fabae
❑ Symptoms:
➢Rust pustules can be seen on leaf blade, petiole & stem.
➢Rust starts with the formation of yellowish-white pycnidia and aecial cups
on the lower surface of leaflets and on pods, singly or in small groups in a
circular form.
➢Later, brown uredial pustules emerge on either surface of leaflets, stem and
pods.
➢Pustules are oval to circular and up to 1 mm in diameter. They may
coalesce to form larger pustules.
➢In severe infections leaves are shed and plants dry prematurely, the
affected plant dries without forming any seeds in pods or with small
shrivelled seeds.
❑ Etiology:
➢Pycniospores:
Pycnia (spermogonia) and the spore form pycniospore (spermatia).
Pycnia were small, flask shaped and produced on the upper as well as lower
surface of leaves and possess flexuous hyphae and nectar drop at the mouth.
➢Aeciospores
Designates aecia (aecidia) with aecisopores. Aeciospores were round to
angular or elliptical with fine warts, yellowish in colour and 14-22 m in dia.
➢Uredospores
Uredospores are light brown, spiny, elliptical, single called, pedicillate,
20-30 x 18-26 mm and possess 3-4 germ pores.
➢Teliospores
Teleutospores were subglobose, ovate or elliptical, single called,
pedicillate, thick walled with flattened apex and 25-38 x 18-27 mm in diameter.
They were light brown with papillate apex.
➢Basidiospores:
Basidia with basidiospores. The teleutospore germinates and forms a 4-
celled basidium on which four, single celled hyaline basidiospores were formed.
❑Disease Cycle:
➢Uromyces viciae-fabae is an autoecious fungus.
infected crop
❑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, oxycarboxinthiram,
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
2. Wilt : Fusarium oxysporum f.sp. lentis
❑ Symptoms:
➢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
shrivelled.
❑ Wilt of lentil :
❑ Etiology:
The pathogen is known to produce three kinds of asexual spores; micro
conidia, macro conidia and chlamydospores. Microconidia are usually single
celled, ovoid or kidney-shaped and hyaline. Macroconidia are usually 2-7 celled,
long with pointed apical cell and notched basal cell. Chlamydospores are single
celled, oval or spherical shaped and thick walled, formed singly in macroconidia
or apical or intercalary in the hyphae.
❑ Disease cycle
implements
❑ Management:
➢Ploughing of the field during summer.
➢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.
➢Following crop rotation with cereal crops which are not affected by wilt pathogen.
➢Using antagonistic microflora like B. subtilis, T. harzianum, T. viride @ 4 g/kg seed etc
➢ 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.
Crops and their Management -I
Lecture 11,
By
M.Sc. Agri., NET
Linseed crop Diseases, Symptoms, Etiology, Disease cycle
and Their Management.
1. Alternaria bud blight : Alternaria lini
2. Rust : Melampsora lini
3. Powdery mildew : Oelium lini
1. Alternaria bud blight : Alternaria lini
❑Symptoms:
➢The disease appears from seedling stage to seed setting stage
➢Alternaria lini cause a brown and black target like lesion on the leaf and
buds.
➢The disease symptoms initially appear as light brown to black dots like
spots on stem and leaves.
➢ Lesions can cover the whole leaf surface and lead to curled and dried of
bud of linseed which cause failure of flower to open during the day
➢Minute dark brown to black spots appeared near the base of calyx, which
enlarged later, differed in colour and spread all over the bud passing in to
the pedicle the symptoms were same as reported
➢the leaf spot and black bud disease, pathogen (Alternaria lini) has been
found to parasitize the leaves, floral organs and buds causing seedling
blight leaf spot and black bud.
➢ The most common symptoms of this disease were leaf spot and black
bud. The affected buds in most of the cases were completely replaced by
fungal mycelium and conidia.
➢The affected capsule may contain deformed, discoloured and blighted
seeds.
Symptoms on Leaves of Linseed Plants Symptoms on Buds of Linseed Plants
❑Etiology:
➢Hyphae Septate, branched, hyaline later turning to pale then olive grey.
The mycelial width was 3.0 – 5.3 µm.
➢Conidiophores Septate, erect, branching or non-branching geniculte, olive
buff to dark olive buff, 21.5 – 100.5 µm wide.
➢ Conidia Conidia are formed simply or in branches chain, consisting 02-10
spores, smooth or verculose, linear to obclavate, dark olive to buff in colour,
provided with 1-7 cross and 1-5 longitudinal septa and often with short
conical or cylindrical beak, light brown to dark olive buff, measuring 1.5-45.6
x 7.0 – 3.5 µm in size, beaks usually light colour measuring 3.5-18.0 µm x 3.0
– 65. µm.
❑Disease Cycle :
Primary inoculum :
Seed seems to be the main source of primary inoculum as the
pathogen was effectively transmitted from infected seeds to the emerging
seedlings. Infected linseed stem debris, volunteer linseed plants and the
weed Veronica agrestis were also sources of primary inoculum for the
infection of linseed crops by A. linicola.
Secondary spread :
Conidia of A. linicola were mainly dispersed by the wind (air-borne
conidia).
❑Management:
➢ Seed treatment (ST) with T. viride (4 g/kg seed).
➢Seed treatment (ST) with thiram (3 g/kg seed)
➢ Two foliar sprays (FS) of mancozeb (0.25 %) at 15 days intervals.
2. Rust : Melampsora lini
❑ Symptoms:
➢The leaves are the first to show the symptoms and gradually all the aerial
parts of the plant get infected.
➢ Large, orange coloured pustules generally appear on the leaves. Small
pustules are initially surrounded by chlorotic areas.
➢Little necrosis of the leaves is at first observed but it grows, becomes more
general and the leaves prematurely die.
➢The pustules on the leaves are uredopustules containing uredospores.
➢Uredopustules may also appear on stems.
➢While the uredopustules on leaves are round and small, those on stems are
elongated and irregular.
➢Teleutopustules are generally produced on stems and rarely on leaves, if
they have not been shed prematurely.
➢ Orange yellow uredopustules are often surrounded by reddish-brown
teleutopustules.
➢The contents of telial pustules do not break the epidermis of the host and
remain buried subepidermally appearing glossy.
Flax rust on leaf & Stem
Uredia and telia on flax boll

❑Etiology:
The causal organism, Melampsora lini, is an autoecious rust as all
it’s the four stages (pycnial, aecial, uredial and telial) occur on the linseed
plant. However, the pycnial and aecial stages of die fungus have not been
observed in India. In this country, the disease is a concern of only uredial
and telial stages.
The mycelium of the fungal pathogen is septate, branched, dikaryotic, sub-
epidermal and intercellular.
➢Uredospores: The uredia (sing, uredium) are orange-yellow coloured,
scattered or in groups, usually rounded on leaves but elongated on the
stems. Each uredium contains uredospores and paraphyses. The
uredospores are binucleate, ovate, possessing fine warts and indistinct germ
pores on their wall, and measuring 15-25 x 13-18 µm.
➢Teleutospores: The telia (sing, telium) are irregularly elongate, reddish-
brown in colour. The teleutospores are sessile, cylindrical, unicellular,
reddish-brown in colour, measure 42-80 x 8-20 µm, and are arranged in
palisade-like manner.
Disease Cycle:
➢The primary infection in the plains of our country is not carried out by any
inoculum perennating locally; it is caused by the uredospores produced on
hills. The uredospores are blown-down to plains by wind, fall onto the
surface of the host, germinate and cause infection.
➢Secondary infection:The uredospores produced as a result of primary
infection get disseminated by wind, insects and other sources and cause
secondary infection on the healthy plants.
Management strategies:
➢The only sure measure for the control of this disease is the use of resistant
varieties. E.g.NP (RR) 9, 10, 56, 95, 218, 279B, 279K3, 368, 381, 389, 415, 501.
➢ Seed treatment to inactivate the teleutospores in hilly areas has been
suggested.
➢ Avoidance of excessive nitrogenous manures, which favour lush growth, is
recommended.
3. Powdery mildew: Oelium (Oidium) lini
Symptoms:
➢A greyish white powdery growth on young, leaves (tips).
➢The disease appears after mid of January at the time of capsule formation or
seed setting.
➢The powdery growth was observed on entire plant. The capsules were also
covered with powdery mass
➢Powdery white appearance that starts as small spots and can eventually cover
leaves, stems, flowers, and even entire plants.
➢Infections can cause discoloration or loss of leaves and also deformed leaves
and other plant parts.
➢Early infections may cause complete defoliation of flax plants.
❑Etiology:
It is asexually produced conidia and sexually formed ascospores (produced
from cleistothecia). Ascocarp is dark brown, globose with filamentous
appendages, asci oblong. ascospores hyaline, ellipsoid, 20–30 x 10–13 µm in
size. Anamorph produces on hyaline conidiophores catenate conidia of
oblong to cylindrical shape, not including fibrosin bodies.
❑Disease cycle:
Primary infection by Each mildew infection produces masses of tiny,
white spores (conidia). These are readily blown about by the wind,
spreading the disease.
❑ Management Strategies:
➢Plant varieties with greater resistance to powdery mildew when available.
➢Give plants extra spacing and grow in areas with more sun.
➢Prune plants near the ground and any overly dense areas of foliage to
allow better airflow.
➢Avoid over-fertilizing plants with nitrogen. Consider using a slow-release
fertilizer and avoid applying nitrogen late in the growing season when
infections are more common.
➢Remove infected parts of plants and all debris around them. Infected parts
and debris should be destroyed. When pruning infected plants, your
pruning tool should be disinfected after each cut with a bleach and water
solution (1 part bleach to 4 parts water).
➢Overhead watering can help wash powdery mildew spores off of plants.
This is best done in the morning so excess moisture can dry faster during
the heat of the day.
➢The disease can be controlled by spray of sulfex @ 3 kg/hectare in 1000
litres water.
➢Application of systemic propiconazole (0.1%) recorded minimum disease.
Lecture 11,
By
M.Sc. Agri., NET
Pea crop Diseases, Symptoms, Etiology, Disease cycle and
Their Management.
1. Downy mildew : Peronospora pisi Sydow
Peronospora viciae
2. Powdery mildew : Erysiphe phoygoni
3. Rust : Uromyces fabae
4. Wilt : Fusarium oxysporum f. pisi
1.Downy mildew: Peronospora pisi Sydow OR Peronospora viciae
❑ Symptoms:
➢Yellow to brown scattered patches of discoloured areas appear on the upper
surface of the leaflets and stipules.
➢Simultaneously with this, downy growth in patches of variable size are visible
on the under surface corresponding with the lesions of the upper surface.
➢The downy coating is whitish when young, but the colour gradually turns
greyish-violet with age.
➢This growth is composed of branches sporangiophores, arising from the
mycelium of the fungus which has entered within the leaf tissues. Sporangia are
borne at the tips of the ultimate branches.
➢The infected leaflets and stipules become reduced in size with their margins
curled downwards.
➢ The infected areas gradually develop into elongated blotches, and often to
irregular spots.
➢With the spread of infection, blotches also appear on the pods.
➢When young, the blotches on the pods are pale-green, more or less elliptical to
irregular, but gradually the blotches turn dark to bright-brown, mottled with
light-green islands.
➢Blotch followed by the green island effect is a typical symptom of the disease.
➢Seeds lying corresponding to the infected tissues of the pods abort and
become very much reduced in size.
❑Etiology:
Mycelium consists of aseptate branched hyaline hyphae. The hyphae
produce branched, finger- shaped haustoria.
The sporangiophores arise directly from the internal hyphae.
They are dichotomously 2 to 10 times branched at acute angles, ultimate
branchlets acute and more or less reflexed. The sporangia are nearly oval but
narrowed a little below, greenish-yellow to pale-violet in mass and 22 to 27µ
by 15 to 19µ in dia. The oospores are roundish, light-brown having a thick
epispore marked by a large, raised reticulation. They measure 26 to 43µ, in
dia.
❑Disease Cycle :
➢Primary inoculum :
The primary cycle, when infection starts in the leaflets and stipules
from the inoculum produced by the germination of oospores of previous
year; and.
➢Secondary spread :
The secondary cycle, when the pods become infected from the
sporangia produced by the primary cycle. The discoloured patches on the
leaflets and stipules denote successful infection. Host penetration is through
stomata by the germ tube produced by sporangial germination.
❑Management:
➢The destruction of previous year’s plant debris
➢ Following crop rotation of two or three years are very effective control
measures.
➢Deep tillage to bury crop residues.
➢Use tolerant cultivars.
➢Use metalaxyl for seed treatment.
2. . Powdery mildew : Erysiphe phoygoni
❑ Symptoms:
➢It is characterised by a white powdery growth on the leaves, stems and
pods.
➢ First symptoms appear on the leaves in the form of white floury patches
on both sides of leaves.
➢ The disease then spreads to other green parts of the plant such as tendrils,
pods, stems etc.
➢ The patches on the leaves originate in the form of minute discoloured
specks from which powdery mass radiates on all sides.
➢In the advanced stages of the disease large areas of the host get coveted
with white floury patches.
➢ Infected plants impart dirty appearance.
➢In extreme severe infections the infected leaves are shed leaving stem
devoid of the leaves..
➢ Affected seeds become brown.
➢ Water stress accelerates mildew development. Warm days and cool nights
favour disease development.
➢The fungus is seed-borne. It causes considerable damage and may result
up to 20-30 % losses in pod number
❑Etiology:
The fungus is an obligate parasite having septate, hyaline, profusely
branched superficial mycelium sending finger shaped haustoria to the host
cells.
oblong to cylindrical shape, not including fibrosin bodies, 32–44 x 12–15 µm
in size.
❑DISEASE CYCLE OF POWDERY MILDEW
➢ Primary source of infection-Infected debris
➢ Secondary source of infection-wind blown conidia
➢Fungus survives in summer leftover debris.
➢Seed is not considered as main source of inoculum.
➢Avoid late planting.
➢ After harvest, collect the plants left in the field and burn them.
➢ Grow resistant varieties like JP-83, PM-2, JP-4, and JRS-14.
➢ By formulation of wettable Sulphur such as Sulfex and Thiovit at 3 kg/ha.
➢ 0.03 % Calixin followed by Karathane (0.2%) and Bavistin (100 ppm)
Symptoms:
➢Pea rust is characterized by the appearance of two types of symptoms in
India. Early symptoms develop on abaxial side of older leaves and form
round to oval aecidia.
➢Initially aecidia form creamy white to light yellow to bright orange colored
pustules on the leaf and stem.
➢These pustules further developed and spread to other parts of the plants.
An aecidia is a cluster of several small cups like structure on the plant.
Aeciospores released from the aecial cups are deposited as yellow powder.
➢Small aecidial pustules are mostly confined to the leaf. However it can be
seen on stem also.
➢Uredial pustules developed on both the surface of leaf but mostly confined
to the stem.
➢They appear as powdery light brown pustules. The ruptured epidermis on
infected portion of host exposes black to brown powdery mass.
➢Telial symptoms appear after aecial/uredial infection late in the same
season or on the part of plant leading to senescence.
➢Grain size is significantly reduced in badly infected genotype and colour of
the grain becomes dull.
❑Etiology:
➢Pycniospores:
➢Aeciospores
Designates aecia (aecidia) with aecisopores. Aeciospores were round
to angular or elliptical with fine warts, yellowish in colour and 14-22 m in
dia.
➢Uredospores
Uredospores are light brown, spiny, elliptical, single called,
pedicillate, 20-30 x 18-26 mm and possess 3-4 germ pores.
➢Teliospores
pedicillate, thick walled with flattened apex and 25-38 x 18-27 mm in
diameter. They were light brown with papillate apex.
➢Basidiospores:
Basidia with basidiospores. The teleutospore germinates and forms a
4-celled basidium on which four, single celled hyaline basidiospores were
formed.
❑Disease cycle:
infected crop
➢Cultural practices viz., planting time, planting geometry, intercropping
and row spacing.
➢Use of foliar fungicides as Hexaferb and Dithane M-45 give best control.
effective.
❑Symptom
➢Symptom of the disease is more pronounced in 3 to 5 week old plants. In
young seedlings, cotyledons droop and wither.
➢Yellowing of lower leaves and stunting of plants.
➢The xylem vessels develop brown discoloration and get distorted.
➢Leaflet margins curl downward and inward.
➢The stem may be slightly swollen and brittle near the soil.
➢Internal woody stem tissue often is discolored, turning lemon brown to
orange brown.
➢Externally, the root system appears healthy; however, secondary root rots are
likely to occur on plants wilted for long periods.
➢Eventually, wilted plants may die.
❑Etiology:
➢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 conidiophore, are thin walled, 3 to
5septate, fusoid and pointed at both ends.
➢Chlamydospores are roughwalled or smooth, terminal or intercalary, may
be formed singly or in chains.
❑Disease cycle
implements.
➢Avoid early sowing in badly infested areas.
➢Seed treatment with T. viride @4g/kg or P. fluorescens @ 10g/ kg of
seed or Carbendazim or Thiram 2g/kg of seed.
➢Spot drenching with Carbendazim 1g/lit or P. fluorescens / T.
viride 2.5 kg/ha with 50 kg FYM.
Lecture 13-14,
By
M.Sc. Agri., NET
Cotton crop Diseases, Symptoms, Etiology, Disease cycle and Their
Management.
1. Root rot : Sterile Stage: Rhizoctonia bataticola (Taub.).
Imperfect Stage: Macrophomina phaseolina (Tassi).
2. Wilt : Fusarium oxysporum f. vasinfectum
3. Anthracnose :Colletotrichum gossypii
4. Black arm :Xanthomonas axonopodis pv. malvacearum
5. Dahiya diseases or :Imperfect stage. Ramularia areola Atk.
Grey mildew Perfect stage. Mycosphaerella areola.
6. leaf curl :Cotton leaf curl viruses (CLCuV)
7. 2-4-D injury :
1. Root rot : Sterile Stage: Rhizoctonia bataticola (Taub.).
Imperfect Stage: Macrophomina phaseolina (Tassi).
❑ Symptoms:
The pathogen causes three types of symptoms viz., seedling disease, sore-shin and
root rot.
➢Seedling disease Germinating seedlings and seedlings of 1-2 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, later turning dark 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.
Initially, all the leaves droop suddenly and die with in 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.
Wilting and plant death caused by the cotton Root rot caused by cotton root rot fungus
root rot fungus.
Growth of cotton root rot fungus on root and Fresh spore mat of cotton root rot fungus
base of stem.
❑Etiology:
The fungal hyphae are septate and fairly thick and produce black,
irregular sclerotia which measure 100 m 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, and other cultural operations.
❑Management
➢Treat the seeds with Trichoderma viride @ 4g/kg or Pseudomonas
fluorescens @ 10g/kg of seed.
➢Treat the seeds with Carboxin or Thiram at 5 g or Carbendazim at 2g/kg.
➢Spot drench with 0.1% Carbendazim or 0.05% Benomyl.
➢Apply farm yard manure at 10t/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.
2. Wilt : Fusarium oxysporum f. vasinfectum
❑ Symptoms:
➢The disease affects the crop at all stages.
➢The earliest symptoms appear on the seedlings in the cotyledons which turn yellow and then
brown.
➢The base of petiole shows brown ring, followed by wilting and drying of the seedlings. In young
and grown up plants, the first symptom is yellowing of edges of leaves and area around the veins i.e.
discoloration starts from the margin and spreads towards the midrib.
➢The leaves loose their turgidity, gradually turn brown, droop and finally drop off.
➢Symptoms start from the older leaves at the base, followed by younger ones towards the top,
finally involving the branches and the whole plant.
➢The defoliation or wilting may be complete leaving the stem alone standing in the field. Sometimes
partial wilting occurs; where in only one portion of the plant is affected, the other remaining free.
➢The taproot is usually stunted with less abundant laterals
➢Browning or blackening of vascular tissues is the other important symptom, black streaks or stripes
may be seen extending upwards to the branches and downwards to lateral roots.
➢In severe cases, discolouration may extend throughout the plant starting from roots extending to
stem, leaves and even bolls.
➢ In transverse section, discoloured ring is seen in the woody tissues of stem. The plants affected
later in the season are stunted with fewer bolls which are very small and open before they mature.
❑Etiology:
Macroconidia are 1 to 5 septate, hyaline, thin walled, falcate with tappering ends.
The microconidia are hyaline, thin walled, spherical or elliptical, single or two
celled. Chlamydospore 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 OF WILT
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 wind and irrigation water.
MANAGEMENT
➢Treat the acid delinted seeds with Carboxin or Carbendazim at 2 g/kg.
➢Remove and burn the infected plant debris in the soil after deep summer
ploughing during June-July.
➢Apply increased doses of potash with a balanced dose of nitrogenous and
phosphatic fertilizers.
➢Apply heavy doses of farm yard manure or other organic manures. Follow
mixed cropping with non-host plants.
➢Grow disease resistant varieties of G. hirsutum and G. barbadense like
Varalakshmi, Vijay Pratap, Jayadhar and Verum.
➢Spot drench with Carbendazim 1g/litre.
3. Anthracnose :Colletotrichum gossypii
❑Symptoms:
➢The pathogen infects the seedlings and produces small reddish circular spots
on the cotyledons and primary leaves.
➢ The lesions develop on the collar region, stem may be girdled, causing
seedling to wilt and die.
➢In mature plants, the fungus attacks the stem, leading to stem splitting and
shredding of bark.
➢The most common symptom is boll spotting. Small water soaked, circular,
reddish brown depressed spots appear on the bolls.
➢ The lint is stained to yellow or brown, becomes a solid brittle mass of fibre.
➢The infected bolls cease to grow and burst and dry up prematurely.
❑Etiology:
The pathogen forms large number of acervuli on the infected parts.
The conidiophore 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 seeds for about a year. The pathogen also perpetuates 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
❑Management
➢Treat the delinted seeds with Carbendazim /Carboxin/ Thiram /Captan at
2g/kg.
➢Remove and burn the infected plant debris and bolls in the soil.
➢Rogue out the weed hosts.
➢Spray the crop at boll formation stage with Mancozeb 2kg or Copper
oxychloride 2.5 kg or or Carbendazim 500g/h
4. Black arm :Xanthomonas axonopodis pv. malvacearum
❑ Symptom
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 cause 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 and 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 infection on mature bolls lead to premature bursting.
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.
Angular leaf spot Vein necrosis Boll rot
❑Etiology:
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.
❑Disease cycle
The bacterium survives on infected, dried plant debris in soil for
several years. The bacterium is also seed-borne and remains in the form of
slimy mass on the fuzz of seed coat. The bacterium also attacks other hosts
like Thumbergia thespesioides, Eriodendron anfructuosum and Jatropha
curcus 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.
❑Management
➢Delint the cotton seeds with concentrated sulphuric acid at 100ml/kg of
seed.
➢Treat the delinted seeds with carboxin or oxycarboxin at 2 g/kg or soak the
seeds in 1000 ppm Streptomycin sulphate overnight.
➢Remove and destory the infected plant debris.
➢Rogue out the volunteer cotton plants and weed hosts.
➢Follow crop rotation with non-host crops.
➢Early thinning and early earthing up with potash.
➢Grow resistant varieties like Sujatha, 1412 and CRH 71.
➢Spray with Streptomycin sulphate +Ttetracycline mixture 100g along
with Copper oxychloride at 1.25 Kg/ha
5. Dahiya diseases or Grey mildew :Imperfect stage. Ramularia areola Atk.
Perfect stage. Mycosphaerella areola.
❑Symptom
➢The disease usually appears on the under surface of the bottom 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 vein lets.
➢On the upper surface, the lesions appear as light green or yellow green
Specks.
➢A frosty or whitish grey 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.
➢White or grey powdery growth may occur on the upper surface also. The
infection spreads to upper leaves and entire plant may be affected. The
affected leaves dry up from margin, cup inward; turn yellowish brown and fall
of prematurely.
Whitesh grey powdery growth
❑Etiology:
The pathogen produces endophytic septate mycelium. Conidiophores
are short, hyalineand 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 flattend 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 pathogen survives during the summer in the infected crop
residues. The perennial cotton plants and self-sown cotton plants also
harbour 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.
❑ 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 Carbendazim at 500g/ha, repeat after a week.
➢Grow the resistant varieties like Sujatha and Varalakshmi.
6. leaf curl :Cotton leaf curl viruses (CLCuV)
Symptoms:
➢Two types of symptoms are associated with Cotton leaf curl virus-infected
cotton. A typical, severe upward or downward leaf curl symptom
accompanied by foliar discoloration and mosaic is commonly reported in
most African countries and in India and Pakistan.
➢Downward and upward curling of leaves and thickening of veins and
enation on underside of leaves are the characteristic symptoms of the
disease.
➢In serve infection all the leaves are curled and growth retarded.
➢Boll bearing capacity is reduced
❑Etiology :
➢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 white fly 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.
7. 2-4-D injury :
The chemical 2, 4-dichlorophenoxyacetic acid, more commonly known as
2,4-D, is classed as a "broad spectrum post emergence selective herbicide’’ used for
control of herbaceous annual decoct weeds, but crops like cotton, tomato tobacco
are extremely sensitive to 2-4-D, which cause harmful damage to crops (Cotton).
Symptoms of 2,4-D Injuries
1. Injuries to Leaves:
➢Leaves are greatly modified.
➢They become narrow and deeply lobed.
➢Scorching, rolling and puckering of leaves which hamper normal photosynthesis in
plants. As result of 2,4-D Injuries there can be elongation of leave giving string like
slender appearance.
2. Disruption of phloem tissues and dislocation of normal translocation of food
materials-so plant look like wilted.
3.Growth ceases-Alteration of nucleic acid.
4.Blocking of gaseous exchange between leaf and atmosphere so ultimately plant die.
5. Malformation is also observed on crop.
❑Management :
➢Spray 2 % Urea may show little recovery.
➢Take nescesary precaution during 2-4 weedicide spraying.
Lecture 15, 16 & 17
By
(Matinkhan A. Atar), NET
Mango fruit crop diseases and Their
Management
Disease Causal organism

1. Die back : Lasiodiplodia theobromae
2. Anthracnose : Colletotrichum gloeosporioides
3.Mango-malformation : Fusarium moliliforme var. subglutinans
4. Bacterial blight : Xanthomonas campestris pv.
mangiferaeindicae
5. Powdery mildew : Oidium mangiferae
6. Spongy tissue : Physological disorder
7. Red rust : Cephaleuros virescens
8. Pink diseases : Erythricium salmonicolor
9. Loranthus : Loranthus falcatus(Parasitic plant)
10. Stone graft Mortality: Fusarium oxysporium
11. Lime induced chlorosis
1. Die back: Lasiodiplodia theobromae
(Botryodiplodia theobromae)
❑ Symptoms:
➢Die back is one of the serious diseases of mango.
➢The disease on the tree may be noticed at any time of the year
but it is most conspicuous during October-November.
➢The disease is characterized by drying of twigs and branches
followed by complete defoliation, which gives the tree an
appearance of scorching by fire.
➢Initially it is evident by discoloration and darkening of the
bark. The dark area advances and extends outward along the
veins of leaves.
➢The affected leaf turns brown and its margins roll upwards. At
this stage, the twig or branch dies, shrivels and leaf falls. This
may be accompanied by exudation of yellowish brown gum.
❑Etiology:
The mycelium produced dark brown to black conidia. Immature
conidia are subovoid or ellipsoid, thick-walled, hyaline, aseptate and
one-celled, turning dark brown, two-celled and with irregular
longitudinal striations when at maturity. The size of mature conidia
averaged 26.6 ± 0.51 μm long and 12.9 ± 0.28 μm wide
❑Disease cycle/perpetuation:
Diseased twigs bearing fruiting bodies are the main source of
perpetuation and survival of the pathogen and thus serve as initial
inoculums for next season
➢Pruning of the diseased twigs 2-3 inches below the affected portion
and spraying Copper Oxychloride (0.3%) on infected trees controls
the disease.
➢The cut ends of the pruned twigs are pasted with Copper
Oxychloride (0.3%).
2. Anthracnose: Colletotrichum gloeosporioides
Perfect stage : Glomerella cingulata
Symptoms:
➢It is of widespread occurrence in the field and in storage.
➢The disease causes serious losses to young shoots, flowers and fruits
under favorable climatic conditions (high humidity, frequent rains
and the temperature range of 24- 32°C).
➢The disease produces leaf spot, blossom blight, withered tip, twig
blight and fruit rot symptoms.
➢Tender shoots and foliage are easily affected which ultimately cause
die back of young branches.
➢Older twigs may also be infected through wounds, which in severe
cases may be fatal. Black spots develop on panicles. Severe infection
destroys the entire inflorescence resulting in failure of fruit setting.
➢Young infected fruits develop black spots, shrivel and drop off.
➢ Fruits infected at mature stage carry the fungus into storage and
cause considerable loss during storage, transit and marketing.
❑Etiology :
Mycelium is septate. Acervuli develop
profusely in diseases parts of plants. The
conidia in mass are pinkish but hyaline
indiviually. Conidia are straight, cylindrical or
oval, hyaline single celled with round ends
sometime contain one or two oil globules
❑Disease cycle /perpetuation:
➢Infected plant parts (diseased twig, leaves and fruits) are primary
source of infection.
➢Secondary spread through air-borne conidia
➢The diseased twigs should be pruned and burnt along with fallen
leaves.
➢Spray P. fluorescens (FP 7) at 3 weeks interval commencing from
October at 5g/like on flower branches.
➢Spraying twice with Carbendazirn (Bavistin 0.1%) at 15 days
interval during flowering controls blossom infection.
➢Spraying of copper fungicides (0.3%) is recommended for the
control of foliar infection.
➢Postharvest disease of mango caused by anthracnose could be
controlled by dip treatment of fruits in Carbendazim (0.1%) in hot
water at 520C for 15 minutes.
3.Mango-malformation: Fusarium moniliforme var.
subglutinans
❑Symptoms:
➢Three types of symptoms: bunchy top phase, floral
malformation and vegetative malformation.
➢In bunchy top phase in nursery bunching of thickened small
shoots, bearing small rudimentally leaves. Shoots remain short and
stunted giving a bunchy top appearance.
➢In vegetative malformation, excessive vegetative branches of
limited growth in seedlings. They are swollen with short internodes
forming bunches of various size and the top of the seedlings shows
bunchy top appearance.
➢In malformation of inflorescens, shows variation in the
panicle. Malformed head dries up in black mass and persist for long
time.
➢Secondary branches are transformed into number of small leaves
giving a witches broome appearance
Etiology :
➢Micro conidia are one or 2 celled, oval to fusiform and
produced from polyphialides.
➢Macro conidia are rarely produced. They are 2 -3 celled
and falcate.
➢ Chlamydospores are not produced.
❑Disease Cycle/Perpetuation:
Malformed inflorescences and vegetative growth serve as
sources of pathogen conidia, which reach infection sites by at least
three different routes:
(i) aerial dissemination via wind;
(ii) via contaminated bud mites (A. mangiferae); or
(iii) via infected host materials that fall into the funnel-like structure
of the apical buds.
➢Diseased plants material should be destroyed
➢Use of disease free planting material
➢Incidence reduced by spraying 100-200ppm NAA during October.
➢Pruning of diseased parts along the basal 15-20 cm apparently
healthy portions.
➢This is followed by the spraying of Carbendazim (0.1%) or Captafol
(0.2%).
4. Bacterial blight : Xanthomonas campestris pv. Mangiferaeindicae
❑Symptoms:
➢The disease is noticed on leaves, leaf stalks, stems, twigs, branches
and fruits, initially producing water soaked lesions, later turning into
typical canker.
➢On leaves, water soaked irregular satellite to angular raised lesions
measuring 1-4 mm in diameter are formed. These lesions are light
yellow in colour, initially with yellow halo but with age enlarge or
coalesce to form irregular necrotic cankerous patches with dark
brown colour.
➢On fruits, water-soaked, dark brown to black coloured lesions are
observed which gradually developed into cankerous, raised or flat
spots. These spots grow bigger usually up to 1 to 5 mm in diameter,
which covers / almost the whole fruit.
➢These spots often, burst extruding gummy substances containing
highly contagious bacterial cells.
Etiology :
➢It is Gram stain negative
bacterium
➢Cell type – straight rods
➢Size : 0.4 – 1.0 µm wide X 1.2 –
3.0 µm long
➢Motility : motile by a single
polar flagellum
❑ Disease cycle :
➢Primary infection: In lesions on plant parts and can also survive for
long periods in diseased plant tissues.
➢Bacterium spread through irrigation water and or wind splashed
rain and also by mechanically cause of secondary infection.
❑ Management strategies:
➢Diseased plants material should be destroyed
➢Use of disease free planting material
➢Three sprays of Streptocycline (0.01%) or Agrimycin-100 (0.01%)
after first visual symptom at 10 day intervals and monthly sprays of
Carbendazim (Bavistin 0.1%) or Copper Oxychloride (0.3%) are
effective in controlling the disease.
5. Powdery mildew : Oidium mangiferae
❑Symptoms:
➢The characteristic symptom of the disease is the white superficial powdery
fungal growth on leaves, stalks of panicles, flowers and young fruits.
➢The affected flowers and fruits drop pre-maturely reducing the crop load
considerably or might even prevent the fruit set.
➢The fungus parasitizes young tissues of all parts of the inflorescence, leaves
and fruits.
➢Young leaves are attacked on both the sides but it is more conspicuous on
the grower surface. Often these patches coalesce and occupy larger areas
turning into purplish brown in colour
❑Etiology:
The mycelium is ectophytic, branched with haustoria and hyaline.
Conidia are borne in chains on short conidiophores. They are
hyaline. Single celled pathogen is an obligate parasite.
❑Disease Cycle of P. M. of Mango:
➢Primary infection through dormant mycelium on the tree.
➢Secondary infection takes place through air borne conidia
❑ Management strategies:
➢Dusting the plants with fine sulphur (250-300 mesh) at the rate of
0.5 kg/tree.
➢The first application may be soon after flowering, second 15 days
later (or) spray with Wettable sulphur (0.2%), (or) Carbendazim
(0.1%),(or) Tridemorph ( 0.1%),(or) Karathane (0.1%).
6. Spongy tissue: Physological disorder
➢ Spongy tissue is common only in the Indian subcontinent, especially in South
India. This malady is observed in several varieties of mango, but it is severe and
common in the ‘alphonso’ variety.
➢It is a major problem in Alphonso, where a pulp patch fails to ripen. This malady is
caused due to inactivity of ripening enzymes due to high temperature, convective
heat and post harvest exposure to sunlight.
➢Spongy tissue in mangoes cannot be detected unless the mango is cut open. The
area affected will appear white and soft, like a sponge.
➢ But it is difficult to indentify from the outside and hence the rot spreads, making
the mangoes inedible. When the rotten mangoes are stored along with other
mangoes, the rot spreads to other mangoes too. This has been the cause for decrease
in the quality and also in production of mango in India.
Causes:
Several researches conducted have shown that spongy tissue formation in mangoes
is caused by the shift of the seed to germination mode inside the fruit. Germination is
the process by which a seed develops into a plant. During this stage, the seed
requires nutrients to develop. So when the seed inside the mango shifts into
germination mode, it sucks the nutrients from the surrounding fleshy part of the
fruit, making it appear white and spongy. Hence as the fruit ripens, the patch
affected by this malady can be seen clearly.
Since the spot is devoid of nutrients, it begins to rot (identified by the appearance of
black colour). If identified earlier, the particular patch can be removed and the rest of
the mango can be consumed
Control:
➢Harvesting the fruit when it is three-fourth matured instead of waiting for it to
mature fully, and then storing it in a cool place, will prevent any rotting.
➢Use of mulching and post harvest exposure to low temperatures between 10-15 C
for 10-18 hours has been useful in reducing the malady.
❖Symptoms of spongy tissue development in Alphonso mango fruits:
A. Spongy uncut fruit, B. X-ray image of Spongy fruit,
B. C. Spongy cut fruit and D. Spongy fruit with air cavities.
7. Red rust: Cephaleuros virescens
❑Symptoms:
➢The disease is characterized by initial green coloured patches, as and when
disease advances the organism turns red rusty spots on the leaves and young
twig.
➢The spots are initially circular, slightly elevated and later coanesce to form
irregular spots.
➢The upper surfaces of the spot consist of numerous, unbranched filaments,
which project through cuticle.
➢Some of the filaments represent sterile hairs while others the fertile ones.
➢Spores mature, fall off and leave cream to white velvet texture on the
surface of leaf.
❑Etiology:
➢The algae (Cephaleuros virescens (Kunze)) after a period of vegetative growth
develop its reproductive structure.
➢Certain cells become sporangia. They are of 2 types.
➢Those formed directly on the thallus are sessile and thick walled, 40-50micrometer
in diameter with orange pigments.
➢They are formed singly on the vegetative filaments. Some are produced above the
surface on special sporangiophores consisting of thick, rigid, septate hairs with a
length of 50micrometer, swollen into a vesicle at the tip. Each vesicle carries 3-6
sporangia on curved pedicels.
➢When the sporangia are riped, the contents are converted in to zoospores and
liberated through an opening in the wall.
➢The zoospores are orange in color, ovoid and swim actively by means of cilia.
❑Disease cycle/ Perpetuation:
Besides mango, algae attack many types of other plant species. The disease
is more common on closely planted mother plants. Fruiting bodies of algae are
formed in a moist atmosphere. Zoospores formed by sporangium initiate fresh
infections. Pathogen invades cortical cells of host plant and mainly spreads with rain
splashes and winds.
❑Management:
➢Avoidance of close planting.
➢Sprays of Bordeaux mixture (1 %) or copper oxychloride (0.25%) helps in checking
the disease.
8. Pink diseases: Erythricium (Batryobasidium) salmonicolor
❑Symptomps:
➢The disease is noticed as a pinkish powdery coating on the twigs and
branches.
➢Later the fungus invades bark to get established in the internal tissues and
interferes with the transport of nutrients.
➢Often the fungal growth spreads to girdle the stem.
➢Severely infected bark gets shredded and the wood exposed. Leaves turn
yellow and dry. Roots are not infected.
➢The pink colour on the tissues represents profuse conidial production
by the fungus and hence the name ‘pink disease’ is given
❑Etiology:
Pink pustules found on twigs and branches. However, Microscopic
examination of naturally infected branches showed the pustular forms
producing hyaline non-septate, hyphae and masses of irregularly shaped
hyaline, unicellular, ellipsoid spores, 10- 24 µm ×8-12 µm.
❑Disease cycle:
The fungus persists from one season to another through dormant mycelium
inside the bark and the cankerous tissues serve as a potential source of
infection in wet season. The disease is seen after rainy season.
❑Management:
1. The disease can be kept under control by cutting and removing the
affected branches. Cut ends should be protected with Bordeaux paste.
2. The disease can also be controlled by lime sulphur and oil based copper.
9. Loranthus : Loranthus falcatus(Parasitic plant)
It is also known as Mistletoes. It is a partial stem parasite of many perennial
dicot trees having woody nature. The parasite has true functional leaves however it
lacks a true root system and therefore, it is unable to sustain in absence of host
plants. The parasite has to depend on the host for nutrition and water. Nutrients and
water absorbed by roots of the host plant are diverted for the growth of the parasite.
As a result, the growth of the host above the point of penetration show
marked reduction. Simultaneously, parasite develops at a faster rate. Development of
many Loranthus branches completely weakens the host. Vigour of the host plant is
markedly reduced and automatically, there is a reduction in yield and quality of fruits
of the host plant.
➢Life Cycle of the Parasite:
Berry type fruits are produced on Loranthus branches in summer. Birds upon
consuming these berries disseminate the seeds, which remain adhered on tree trunks
at the branching junctions of the host. Seeds on the host surface(tree trunk)
germinate on the onset of monsoon and directly penetrate the host. Initial growth of
the parasite is slow.
Upon penetration into the host, sucking organ ‘haustorium is produced by the
parasite within the host tissue, which penetrates and absorbs nutrients from the
xylem of the host. Establishment of parasitic relationship results into the
development of big knot or gall-like overgrowth and the point of contact of the
parasite and host.
❖Host Range:
There are many cultivated and wild hosts of the parasite.
Cultivated Hosts: Mango, Citrus, Jackfruit, Sapota.
Wild Hosts: Teak, Shiwan, Harda, Beheda.
❖Management:
➢Removal by the scrapping of the parasite from the infected branch before flowering
with the help of Amar Loranthus cutter.
➢Well established Loranthus bushes are cut below the point of penetration and
destroyed.
➢Application of 0.5% Glyphosate at the point from where the Loranthus growth has
been scrapped to avoid further re-emergence of the parasite from the established
haustorium.
10. Stone graft Mortality: Fusarium oxysporium and some abiotic reason
Stone grafting is the efficient and popular technique of rapid
multiplication of quality planting material in mango. Severe mortality of
sprouted grafts takes place if proper care is not taken.
Causal Organism:
During the investigation was initially thought that the disease is
caused by fungus Fusarium oxysporum. However, it was observed that the
wilting continued after fungicidal covering. The detail investigations
revealed that different non biological (abiotic) causes are associated with this
disease. These are:
➢Use of improper potting mixture and poor drainage in polybags.
➢Incompatibility between rootstock and scion.
➢Exposure of graft to intense rain showers
❖Symptoms:
➢Newly sprouted grafts having light green colored leaves show sudden
drooping and loss of turgidity followed by wilting of the graft in the next
two to three days.
➢There is longitudinal shrinkage of the stem followed by drying of leaves.
Normally such type of wilting is observed 15-20 days after sprouting.
➢Rootstock of such wilted plants many times sprouts from the base
indicating the incompatibility of rootstock and scion
❖Management:
➢Selection of good quality seed (stone).
➢Deep the stones in 0.1 percent Carbendazim to control Sclerotium growing
on the stone
➢Grafting should be done at a proper stage when the stem is red-brown in
colour.
➢Select healthy matured scion stick of proper girth (pencil size).
➢It scion is too broad two root stocks should be used to supply adequate
nutrients to the scion.
➢Use well drained soil and FYM in 3:1 proportion as a potting mixture.
➢Provide six punched holes at the base of plastic bag for proper drainage.
➢Drench 0.1% Emisan or 1% Bordeaux mixture solution 50-100 ml in each
bag to avoid development of Sclerotium in soil.
➢Follow regular plant protection measures in the nursery to avoid pest and
disease problem in the initial stage of graft growth.
11 Lime induced chlorosis in mango
The lime induced iron chlorosis in fruit trees is a widespread and up to now
unresolved problem in plant nutrition on calcareous soils in arid and semiarid areas.
On average some 20% to 50% of different kinds of fruit trees suffer from this type of
physiological disorder and show symptoms of iron deficiency such as:
➢The leaves loose green colour and turn white and is called “Bleaching”.
➢The size of the leaf is reduced. In severe cases of iron deficiency, the leaves dry from
tip downwards.
➢The deficiency is common in soils with high calcium content. Hence, the effect is
known as “calcium induced iron chlorosis”
❖This is accompanied by poor yields, low fruit quality and the complete loss of trees.
Management :
➢In order to overcome iron chloroses ironchelates are either applied to the leaves or
to the roots of the trees.
➢Two sprays at fortnight interval with ferrous sulphate 2.5 g per liter.
Lecture 18-19,
By
M.Sc. Agri., NET
Citrus fruit crop Diseases, Symptoms, Etiology, Disease cycle
1. Citrus canker : Xanthomonas campestris pv citri
2. Gummosis : Phytophthora parasitica, P. palmivora,
: P. citrophthora
3. Fruit rot :P. palmivora,
4. Citrus greening : Liberobactor asiaticum
( Phloem limited bacteria)
6. Tristeza : Citrus tristeza virus (CTV)
7. Citrus Exocortis : Citrus exocortis viroid (CEVd)
8. Scab of citrus : Elsinoe fawcetti
9. Mottle leaf of citrus : Zn deficiency
1. Citrus canker : Xanthomonas campestris pv citri
Symptoms:
The disease attacks/affects seedling and all plant parts grows up trees viz.,
on leaves, twigs, branches on fruits and on roots.
A. Seedling disease: In young plants, especially in the nursery, the disease
causes serious damage. Badly cankered leaves are shed and the assimilating
surface of leaves is reduced while the canker spots often girdle the stems to
cause partial or complete death of the plants
B. Tree
➢On leaves: Initially water soaked patches appear which slowly turn brown
and produce corky raised spots which leads to yellow hallow..
➢ On twig and Branch : Same as on leaves but yellow hallow is absent, bark
eruption takes place and, we can see bacteria oozing out during warm rainy
season from cracks. The canker growth often encircle the twig causing the
death of the portion above the infected area leading to die-back of shoots.
➢On fruits : the infection spreads to the fruit on which typical cankerous
spots are formed. Yellow hallow around the canker is absent in fruit.
Brownish corky out growth with cracks and crater like appearance at a later
stage is the common symptom. Fruit size is reduced and marketing quality
deteriorates. Fruit rottening is common when stored.
❑Etiology:
➢It is Gram negative, non spore forming, aerobic bacteria.
➢It is rod shaped, forms chains and capsules and is motile by one polar
flagellum.
❑Disease cycle:
➢Survives in infected leaves for 6 months.
➢Bacteria overwinters in leaf, twig and fruit canker lesions
➢Citrus leaf miners (Phyllocnistis citrella) helps in the dissemination of the
pathogen
➢Spread by rain splashes
➢Dropped off canker affected leaves and twig should be collected and burnt.
➢Disease free nursery stock should be used for planting in new orchards.
➢Prune badly infected twigs before the onset of monsoon
➢Streptomycin sulphate 500-1000 ppm; or Phytomycin 2500 ppm or Copper
oxychloride 0.2% at fortnight intervals.
➢Control leaf miner when young flush is produced.
2. Gummosis :P. parasitica, P. Palmivora, P. citrophthora
3. Fruit rot :P. palmivora
❑ Symptoms:
❖ Gummosis:
➢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.
❖Fruit rot:
This is a severe diseases of mandarin orange in heavy rain fall areas
of South India.
➢Quick shedding of leaves is earliest symptoms.
➢ Fruits at all stages are infected.
➢The affected leaves show water – soaked patches on rind and subsequently
such fruit drop off and rot.
➢Prior to death, the plant usually blossoms heavily and dies before the fruits
mature
➢The surface of dropped fruit gets covered by cottony growth of the fungus.
Foul odour is emitted by the rotting leaves and fruits.
➢The pathogen may cause bark rot, crown rot and girdling of the base of
stem. Repeated attack by the pathogen may reduce vigour of the tree which
may die
❑Etiology:
➢The hyphae are usually intercellular or intra cellular.
➢Sporangia are ellipsoid or ovoid with the widest part near the base,
papillate and with short pedicel.
➢The sporangia measure measure 35-60 µm X 20-70 µm the base of
the sporangium is usually rounded and attached with the
sporangiophore most at right angle. It shows sympoidal growth with
sporangium at the tip and release zoospore, biflagellate and motile.
➢Chlamydospores are 30-40 µm in diameter. Oospore are 30 µm in
size.
❑DISEASE CYCLE OF WILT
➢The fungus survives in the form of dormant mycelium and under
moist conditions. The fungi produces large numbers of motile
zoospores, which are splashed onto the tree trunks.
➢Secondary infections often occur through lesions created by
Phytophthora
Management
➢Injuries to crown roots or base of stem during cultural operations should be
avoided.
➢Proper drainage facilities are be provided.
➢Excess irrigation and continuous contact of trunk with water should be
avoided
➢If lesion has girdled less than ½ the girth, remove the diseased bark with
a knife along with ½” of un-invaded bark.
➢Resistance rootstock like to sour orange & Cleopatra mandarin may be used
➢Bark of trunk should be coated with Bordeaux paste
➢Drenching the soil around plant bases with B.M. 1.0% control the disease.
➢Spraying with B.M. 1% alone or with tin sulphate or difolatan 0.3% or
metalaxyl-mancoze 0.2% for control the disease.
4. Citrus greening : Liberobactor asiaticum (Huanglongbing (HLB) )
❑Symptoms:
This disease affects almost all citrus varieties irrespective of root stock.
➢Stunting of leaf, sparse foliation, twig die back, poor crop of
predominantly greened, worthless fruits.
➢Sometimes only a portion of tree is affected. A diversity of foliar chlorosis.
➢A type of mottling resembling zinc deficiency often predominates.
➢Young leaves appear normal but soon assume on outright position,
become leathery and develop prominent veins and dull olive green colour.
Green circular dots on leaves.
➢Many twigs become upright and produce smaller leaves.
➢Fruits small, lopsided with curved columella. The side exposed to direct
sunlight develops full orange colour but the other side remain dull olive
green.
➢Low in juice and soluble solids, high in acid. Worthless either as fresh fruit
or for processing. Seeds poorly developed, dark coloured, aborted.
➢Infected budwood; psyllid vector-Diaphorina citri
➢Greening Effects on Citrus Production
• Bitter-tasting, lopsided fruit, small in size
•May not colour properly with portions remaining green
❑Etiology:
• Liberobactor asiaticum is Phloem-limited bacterium
•Transmitted by psyllids •Graft transmissible
•Not currently cultured
❑ Disease Cycle:
➢It is transmitted by infected bud-woods and through citrus psylla
even a single psylla is capable spreading of disease.
❑Management
➢The disease can be controlled by removal of affected and
unproductive trees and by replanting disease- free budded plants
raised on improved.
➢Control psyllids with insecticides.
➢Use pathogen free bud wood for propagation.
➢500 ppm tetracycline spray, requires fortnightly application.
❑ Symptom :
➢The plant is affected at all stages viz., branches, leaves & fruits.
➢The disease causes defoliation and tip drying of twigs, called whither tip.
➢Shedding of leaves and dieback of twigs.
➢Acervuli appear as black dots on the dead twigs. Light green spots appear
which later turn brown.
➢The leaves also may show the spot dark brown marginal ring and greyish
white central patch with numerous black acervuli arranged in concentric
ring.
➢The pathogen also infects the stem-end of immature fruits causing fruit
drop.
➢The spots on fruits may vary from small specks to 1 cm in dia. They
reddish brown and become dark brown to black later. Circular and sunken
acervuli develop on these spots.
➢In severe cases branches also show die back symptoms.
❑Etiology:
➢Septate mycelia, asexual fruiting body is the –acervulus and setae are
present
➢Primary source of inoculum: Dormant mycelia
➢Secondary source of inoculum: Conidia produced in Acervulus
❑Disease cycle:
➢Infected plant parts (diseased twig, leaves and fruits) are primary
source of infection.
➢Secondary spread through air-borne conidia
❑Management
➢Avoid excess N application.
➢Irrigation during summer is required.
➢Spray P. fluorescens (FP 7) at 3 weeks interval commencing from
October at 5g/like on flower branches.
➢Spraying twice with Carbendazirn (Bavistin 0.1%) or Benomyl-
@1gm/lt at 15 days interval during flowering controls blossom
infection.
➢Spraying of copper fungicides (0.3%) is recommended for the
control of foliar infection.
➢Postharvest disease of mango caused by anthracnose could be
controlled by dip treatment of fruits in Carbendazim (0.1%) in hot
water at 520C for 15 minutes
6. Tristeza : Citrus tristeza virus (CTV)
❑Symptoms:
➢It affects all kinds of citrus plants but primarily orange, grapefruit and lime
➢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.
❖Typical Symptoms of tristeza
➢Leaf: Chlorosis is the common symptom followed by leaf size reduction,
leaves fall and die back of defoliated twigs.
➢Stem: Bark eruption and pittings on stem (V shaped depression on the
stem and stem twisting occurs.)
➢Fruits: In the affected fruits, thicknesss of the rind is increases and,
mesocarp decreases.
➢Root stocks are susceptible, phloem necrosis is the common symptom,
root discoloration and root decay occurs which leads to sudden leaf
dropping.
❑Etiology:
➢Tristeza is a highly flexuous filamentous virus 2000nm long
and 10-12nmin 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.
❑Disease Cycle:
➢The disease primarily spreads through grafting and budding. Under field
conditions, it is transmitted by the black citrus aphid, Toxoptera citricida. The virus
is not seed borne.
❑Management:
➢Strict quarantine measures to be enforced
➢Use certified bud wood 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.
7.Citrus Exocortis : Citrus exocortis viroid (CEVd)
❖Symptoms:
➢This disease pertains to the bark, bark discoloration and its removal
occurs at the later stage, followed by yellowing of leaf, defoliation and
death of the plant.
➢The plant show cracking and scaling of the bark. Scaling is characterized
by narrow vertical strips of the outer portion of the bark.
➢Symptoms first appears on rootstock near the soil line and gradually
extends up ward to the bud union and down to the roots. Bark becomes
dead and dries. Diseased tree remain are stunted.
❑Etiology
Viroid (free RNA without protein coat with molecular weight of
119000 & 371 nucletides )
❑Disease Cycle:
Disease spreads mechanically through leaf to leaf rubbing, wounds,
use of infected secateures
PSI: Cuscuta reflexa
SSI: Grafting and budding operations.
❑Management
➢Seedlings are developed from nucellar seeds.
➢Irrigation management
➢Nutrient management
➢Avoid excess of N applicationbut more application of potassium is
the best.
8. Scab of citrus/ Verucosis : Elsinoe fawcetti
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.
❑Etiology :
Elsinoe fawcetti produces smaller ascospores (sexual spores) and it
also produce single‐celled, hyaline, elliptical conidia (asexual spores)
with sizes of around 3–4 µm × 4–8µm. Conidia can be propagated
through budding.
❑Disease Cycle :
➢It is believed that the pathogen perpetuates and survives in adverse
season as perithecium.
➢Secondary spread occurs through the conidial which are mostly
produced on the host surface.
➢Conidia are produced at 7 °c& 33°c temperature and at 66-100% RH
conditions on young lesions.
➢Conidia from old lesions are dispersed during rains but only to a
short distance.
❑Management :
➢Collect infected leaves and burn them.
➢Avoid excess N application and use recommended dose of potassium
in the soil
➢Disease can be controlled by spraying with 1% Bordeaux mixture or
difolatan and benomyl.
➢Chemical:Carbendazin spray @1.25gm/lit
9. Mottle leaf of citrus : Zn deficiency
❑Symptoms
➢Leaf symptoms include small, narrow leaves (little leaf) and
whitish-yellow areas between the veins (mottle leaf)tree.
➢Irregular and chlorite leaf spots, mottled leaf, small leaves and
severe dieback of twigs.
➢The area near midrib and lateral veins remain green. Terminal
twigs have narrow small erect leaves. Small, thin skinned fruits
❑Management:
➢Use an annual foliar spray (zinc sulphate) on the spring flush
leaves when they are about two-thirds their full size @SpraysZinc
sulphate (23% Zn) + manganese sulphate150 g/100
Lecture 20-21,
By
M.Sc. Agri., NET
Grape vine Diseases, Symptoms, Etiology, Disease cycle
1. Downy mildew : Plasmopara viticola

2. Powdery mildew : Uncinula necator
3. Anthracnose : Gloeosporium mpelophagum
4. Bacterial Canker : Xanthomonas campestris pv. viticola
5. Grape fan-leaf virus : Grapevine fan-leaf virus (GFLV)
1. Downy mildew : Plasmopara viticola
❑ 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.
➢Dwarfing of tender shoots.
➢ Infected leaves, shoots and tendrils are covered by whitish growth of the
fungus.
➢White growth of fungus on berries which subsequently becomes leathery
and shrivels. Infected berries turn hard, bluish green and then brown.
➢Later infection of berries results in soft rot symptoms. Normally, the fully
grown or maturing berries do not contact fresh infection as stomata turn
non-functional.
❑Etiology:
➢P. viticola is a biotroph.
➢The intercellular mycelium of the fungus is coenocytic, thin-walled,
hyaline, and produce spherical or pear shaped haustoria.
➢Sporangiophores arise from hyphae under high humid conditions. The
branching of the sporangiophores is at right angles to the main axis and at
regular intervals. From the apex of each branch 2-3 sterigmata arise and bear
lemon shaped, papillate sporangia.
➢Sporangial germination may be through zoospores or by germ tube based
➢on humidity and temperature
❑Disease cycle:
➢Sporangia or zoospores by wind, rain etc.
➢Oospores present in the infected leaves, shoots and berries also as dormant
mycelium in infected twigs.
❑Management
➢Collect and burn fallen leaves and twigs
➢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
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
2. Powdery mildew : Uncinula necator (I.S: Oidium tuckeri)
❑ 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.
❑Etiology:
The mycelium is ectophytic and produces bilobate or
multilobate appressoria. The conidiophores are simple, multiseptate
and erect bearing a chain of 3-4 conidia.
❑DISEASE CYCLE OF P.M. GRAPE
❑DISEASE CYCLE
➢Primary infection through dormant mycelium and conidia present in
the infected shoots and buds.
➢ Secondary infection through air-borne conidia.
❑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.
3. Anthracnose/Birds eye disease : Elsinoe ampelina,
I.S : Gloeosporium mpelophagum
❑ 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
❑Etiology:
➢ Anamorph – Gloeorporium ampelophagum, produce hyaline, single celled
conidia.
➢Teleomorph - Elsinoe ampelina, Produces hyaline 4 celled ascospores.
❑Disease Cycle
➢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.
❑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 Carbendazim @ 0.1 %
➢Grow resistant varieties like Banglore blue, Golden muscat, Golden
queen and Isabella.
4. Bacterial Canker : Xanthomonas campestris pv. viticola
❑ Symptoms:
➢Small irregular water soaked spots appear on leaves, that translucent to
light and have a necrotic pinhead sized centre.
➢Numerous spots coalesce to form large patches.
➢Leaves also shows vein infection. Infected leaves after drying remain
attached to the stem.
➢Lesion are brown to black, elongated and cankerous on petioles and
cane. Severely infected leaves defoliated
➢On the stem disease starts as brown black spots around nodes. In
advance stage girdling and cracking of nodes occurs. Finally it leads to
break down of the plant.
➢Berries shows brown to black and cankerous lesions severely affected
ones become small and shriveled.
Etiology:
Bacterium is Gram negative, rod shaped with rounded ends, motile by
single polar flagellum. It Measure from 0.4-1.2 X 2-3µm in size
A. Leaf necrosis caused by Xcv .
B. Typical bacterial canker in a stem and petiole
C. Colonies of Xcv
D. canker in grapevine var. Italia tem incited by the bacteria after inoculation.
❑Disease cycle:
➢The alternative hosts are neem, mango and Phyllanthus maderaspatensis
➢The bacterium survives in the infected twigs and dry leaves up to 65
days.
➢Secondary infection takes place through wind, and rain water splashes
➢Disease spreads to distant places by diseased cuttings.
❑Management:
➢Regular inspection of vineyard and destruction of infected plant
materials.
➢Use of disease free cuttings and late October pruning are
recommended to manage the disease.
➢Spraying with Streptocycline (300ppm), starting from two leaf stage up
to 70 days is also effective.
5. Grape fan-leaf virus : Grapevine fan-leaf virus (GFLV)
❑Symptom :
➢Infected young leaves show variegated mottling.
➢The malformed leaves have open petiolar sinuses. Widening of the
petiolar sinuses and reduction of areas between the veins give the
impression of a half-closed fan.
➢Affected leaves stand upright along the axis of young shoots and
become cup-like.
➢The dark green areas in the mottled leaf bulge upward and leaf surface
become rough.
➢The characteristic symptom of the disease is the underdeveloped leaves.
➢The infected leaves turn light yellow and show cupping.
➢The distance between internodes is reduced and nodes and internodes
become thin and weak. Growth becomes zig-zag at the nodes.
➢Few lateral branches are produced and axillary branches proliferate to
produce small, thin and weak, secondary branches.
➢Infected plants do not produce flowers and fruits even at the age of three
years.
➢Plants become stunted and produce very few and weak rootlets.
❑Etiology:
Virus – virus particles are isometric, SS DNA virus and 25-30 nm
in dia. Thermal inactivation point in 60-65 degree C. Longevity in
vitro is 15-30days at 20 degree C. Dilution end point is between 103
and 104.
❑Transmission:
➢The vectors are Nematodes like Xiphinema index and X. italiae are the
vectors
➢The virus is mechanically transmissible to Cucumis sativus,
Chenopodium amaranticolor, Gomphrena globosa, Nicotiana tabacum cv.
‘White Burley’, Phaseolus vulgaris cv. prince.
➢The disease has been transmitted by grafting or budding of the
diseased scion onto the healthy rootstock of variety Emperor. It is not
transmitted through pollen.
❑Management:
➢Soil application with nematicide controls the nematode vectors and
reduce spread of the disease.
Lecture 22 & 23
By
M.Sc. Agri., NET
Apple fruit crop Diseases, Symptoms, Etiology, Disease cycle and
Their Management
1. Scab : Venturia inaequalis
2. Powdery mildew : Podosphaera leucotricha
3. Fire blight : Erwinia amylovora
4. Crown gall : Agrobacterium tumefaciens
5. Mosaic : Apple mosaic virus (ApMV)
1. Scab : Venturia inaequalis
❖ Symptoms:
➢Scab infections usually noticed on leaves and fruits
➢Affected leaves become twisted or puckered and have black, circular
spots on their upper surface.
➢On the under surface of leaves, the spots are velvety and may
coalesce to cover the whole leaf surface
➢Severely affected leaves may turn yellow and drop
➢Scab can also infect flower stems and cause flowers to drop
➢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.
❑Etiology :
Mycelium is septate. The conidiophores arise from hyphal stands or
form more compact stroma. They are brown continues or rarely septate and
vary length. The conidia are generally unicellular but often they become 2
celled through septation. They are ovate to lanceloate with truncate base.
They measure 12-22 X 6-9 µm. Mature ascocarps are 90-150 µm in dia
spherical dark brown to black with short beak and distinct ostiole around
which single celled setae present.
❑Disease Cycle :
➢The fungus primarily over winters on infected fallen leaves in the orchard
floor.
➢Ascospores are released in the spring at about bud break stage and
disseminated by wind during rainy season.
➢Moisture is required for the spores to germinate.
➢Several secondary cycles of infection, arising from spores produced in
primary lesions, may occur during the growing season.
➢In short:
•P.I: Ascospores formed from pseudothecia
•S.I: Wind borne conidia
❑Management:
➢Clean cultivation, collection and destruction of fallen leaves and pruned
materials in winter to prevent the sexual cycle.
➢Choose resistant varieties like Emira and Red free and new apple hybrides
like Ambstarking Ambroyal, Ambrich and Ambred.
➢Spray Tridemorph 0.1% before flowering.
➢Spray Mancozeb 0.25 % at bearing stage.
➢Spray 5 % urea prior to leaf fall in autumn and 2 % before bud break to
hasten the decomposition of leaves.
Sl Tree stage Fungicide/100lit
No.
1 Silver tip to given tip Captafol 200 gm (or) Captan 300 g or
Mancozeb 400 g
2 Pink bud or 15 days after Captan 250 g or Mancozeb 300 g

1st spray
3 Petal fall Carbendazim 50 g
4 10 days later Captan 200 g.or Mancozeb 300g
5 14 days after fruit set Captofol 150 g

1. Powdery mildew : Podosphaera leucotricha
❖ Symptoms:
➢Powdery mildew of apple produces symptoms on young shoots, leaves,
blossoms, and fruit. In general, symptoms are most noticeable on the
leaves and fruit.
➢The first sign of powdery mildew in spring is a 3- to 4-day delay in the
opening of infected buds.
➢ Leaves and blossoms of these buds soon become covered with a white
to light gray powder, the spores of the powdery mildew fungus.
➢Flowers do not develop normally, are likely to be greenish white, and
produce no fruit.
➢On leaves of new shoot growth symptoms of powdery mildew are
feltlike, white patches on the margins and lower surfaces.
➢Infected leaves curl upward and soon become covered with a powdery
coating of spores. New infections of succulent leaves and growing shoots
reduce the size of the entire shoot. By midsummer, leaves and shoots may
turn brown.
❖Disease symptoms
❑Etiology:
P. leucotricha is obligate parasite continuously produces asexual
spores (conidia) on specialized short stalks called conidiophores. Conidia
are hyaline (clear, without color), measure 20-38 × 12 µm, and contain
distinct fibrosin bodies.
This fungus also produces sexual spores (ascospores) in sac-like asci
enclosed in fruiting bodies (ascocarps). Each ascocarp contains a single ascus
with eight ascospores, each of which is elliptical and measures 22-36 x 12-15
µm. Ascocarps are recognized as distinct black dots on the surface of a
mycelial mat. Ascocarps are densely grouped together, measure 75-96 µm in
diameter and have apical and basal appendages.
❑Disease Cycle:
P. leucotricha overwinters as mycelium in dormant flower and shoot
buds infected the previous year. In spring, the infected buds break
dormancy and the fungus resumes growth, colonizing the developing shoots
and young leaf tissue. From these primary infections, asexual conidia are
produced on conidiophores and the secondary spread occur through wind
borne conidia.
❑Management:
➢Cultural Practices
Primary infections can be controlled by removal of the primary inoculum
sources (i.e., flower and shoot buds infected the previous year)
➢Chemical Control
Secondary infections and fruit infections can be controlled by foliar
fungicide applications.Spray Dinocap 0.05% or Chinomethionate 0.1%
3. Fire blight : Erwinia amylovora
❑ Symptoms:
Fire blight symptoms may appear on the blossoms, shoots, branches, trunk and
rootstock. Blighted blossoms appear wilted, shriveled and brown. Young fruitlets are
also very susceptible and appear water soaked and slightly off-colour soon after
infection. Fruitlets quickly turn brown to black and eventually shrivel up.
A. Blossom and Spur blight:
➢Blossom blight symptoms most often appear within 1-2 weeks after bloom and
usually involve the entire blossom cluster which wilts and dies, turning brown on apple
and quite black on pear.
➢When weather is favourable for pathogen development, globules of bacterial ooze
can be seen on the blossoms. The spur bearing the blossom cluster also dies and the
infection may spread into and kill portions of the supporting limb.
Shoot blight:
B. Shoot Blight
➢Shoot blight starts at the growing tips of shoots and moves rapidly down into older
portions of the twig. Blighted twigs first appear water-soaked, then turn dark brown
or black.
➢As blighted shoots wilt, the twigs bend at the growing point and resemble a
shepherd’s crook or an upside down “J”. Blighted leaves remain attached to the dead
branches throughout the summer. During warm and humid weather infected shoots
will ooze droplets of creamy white bacteria.
C. Stem Cankers
➢As fire blight bacteria move through blighted twigs into the main branches,
the bark sometimes cracks along the margin of the infected area causing a
distinct canker.
➢Bark on younger trees becomes water soaked and the cankers have a dark
brown to purple color. Sapwood beneath a canker has a reddish brown
appearance and may be soft to the touch. Cankers can girdle the main branches
and trunk causing additional dieback.
D. Fruit Blight
➢Both apple and pear fruit may be blighted. Rotted areas turn brown to black
and become covered with droplets of whitish tan colored bacterial ooze. Fruit
remain firm and eventually dry out and shrivel into mummies.
E. Rootstock Symptoms
➢Fire blight symptoms on rootstocks usually develop near the graft union.
Symptoms are similar to those of stem cankers. Fire blight infections in
rootstocks can rapidly kill the tree by girdling the rootstock.
Droplets of amber coloured bacterial ooze
The curved “shepherd’s crook” at the tip of the

Blossom blight diseased twigs
❑Etiology:
The bacterium is rod shaped and 1.0-2.0 X 0.8-1.2 µm in size. It is gram
negative and motile by peritrichous flagella. Bacterium occurs usually
singly but pairs and chains of 3-4 bacteria also exits. Each bacterial enclosed
in a capsule.
❑Disease cycle:
➢The bacteria overwinter in bark tissues along the edges of cankers caused
by infected in previous years.
➢The bacteria multiplies in the spring, the cankers exude a characteristic
ooze and the bacteria are disseminated by rain and insects to vulnerable
tissues especially open blossoms, tender vegetative shoot tips, and young
leaves.
➢The bacteria penetrate the tree through natural openings or wounds.
Secondary infection arises from ooze from fresh infections.
❖Dissemination:
➢Disease is disseminated by bees and other pollinating insects and by rains.
➢Primary source of inoculum: Infected cankers
➢Secondary source of inoculum: Water splash borne bacterial cells.
❑Management:
➢Remove fresh infections as soon as they are noticed.
➢Prune the infected branches at least 30-40 cm below the visible diseased part.
➢Dip tools in a disinfectant after each cut.
➢Pruned branches should be removed and burned immediately.
➢Summer pruning (other than removal of strikes) should be avoided during a
serious outbreak to avoid further spread of the disease.
➢Excess nitrogen application should avoid. Nutrient application should be
balanced, preferably based on soil and leaf analysis.
➢Resistant cultivars: Red Delicious, Liberty, Enterprise and Freedom are some of
the varieties are resistant to the disease.
❖Chemical Control:
➢Sprays of Antibiotic streptomycin, fixed copper compounds (copper oxychloride),
and copper sulfate (Bordeaux) as well as the biopesticides like Blight Ban and
Bloom time.
➢Spray with Streptomycin 500 ppm.
❖Insect control:
➢It is suspected that insects that cause wounds (leafhoppers, plant bugs, pear
psylla) can create places for bacteria to enter the tree and also that some summer
infections (shoot blight) are probably facilitated by insects.
4. Crown gall : Rhizobium rhizogenes (old name Agrobacterium tumefaciens)
❑ Symptoms:
➢Small outgrowths on stem and roots near soil line
➢Galls are spherical, white or flesh coloured (young stage)
➢The galls vary in size 7-10mm in dia.
➢Galls become hard and corky on woody stems,
➢They are generally knobby and knotty and become more cleft as they grow
older.
➢ Affected plants stunted with chlorotic leaves
❑Etiology:
The bacterium is gram negative and rod shaped and 0.7-0.8 X 2.5-3.0 µm in
size. It is and motile by peritrichous flagella. Bacterium occurs usually singly
but pairs and chains of 3-4 bacteria also exits. Each bacterial enclosed in a
capsule.
❑Disease cycle:
The bacteria are very common in soils, since they infect so many plants.
They can enter through wounds! So many types of wounds – pruning
wounds, those introduced by mowing or cultivating, freeze damage, wind
damage, or insect injuries.
❑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.
5. Mosaic: Apple mosaic virus (ApMV)
❑ Symptoms:
➢The symptoms differ in expression on different host plants with different
virus strains.
➢ Leaves of apple trees infected with mosaic disease develop bright pale-
yellow, bright cream colored irregular chlorotic spots, which expand
during spring. Chlorosis can develop along leaf veins, creating a
reticulated appearance or, in other cases, can manifest as large, amorphous
chlorotic areas between leaf veins. Lesions may change to necrotic spots in
the affected leaves after exposure to summer sun heat (Dursunoglu and
Ertunc, 2008) and leaves may drop prematurely.
➢The distribution of symptomatic leaves may be erratic throughout
individual trees or limited to a single limb.
➢The number and severity of symptomatic leaves directly correlate with
temperature, with more severe symptoms in years with moderate spring
temperatures.
❑Etiology:
The virus particle is isometric and 25 and 29 nm in diameter.
Bromoviridae, subgroup 3 in the genus Ilarvirus Ilarvirus [9,10].
The genome is tripartite having single stranded positive-sense RNA (RNA1,
RNA2 and RNA3) and an encapsidated subgenomic RNA4. The RNA1 and
RNA2 each encode single replication-associated proteins; RNA3 encodes a
movement protein (MP) and coat protein (CP), whereas RNA4 is a
subgenomic RNA that functions as mRNA for CP [9]
❑Transmission:
The ApMV is generally graft-transmissible as it persists in
vegetative propagation material (scion) from infected trees, which
constitutes the main source of inoculum for the virus. It is not
transmitted through sap, seed or aphids but probably transmitted by
pollen to pollinated plant
Management:
➢Preventive measures to avoid planting of infected material are of
the greatest importance.
➢Transmission can occur in the orchard through root grafts; roguing
infected trees will limit the spread.
Peach fruit crop Diseases, Symptoms, Etiology, Disease
cycle and Their Management
1. Leaf curl : Taphrina deformans
Strawberry fruit crop Diseases, Symptoms, Etiology, Disease

cycle and Their Management
1. Leaf spot : Mycospharella fragariae.
1. Leaf curl : Taphrina deformans
❑ Symptoms:
➢Symptoms of leaf curl appear in the spring.
➢It attacks the leaves, causing curling and blister formation.
➢The leaves start turning yellowish or reddish and fall off prematurely.
➢The infected portion develops a pink or reddish bronze colour.
➢Growth of the tree is affected with a reduction of yield.
Typical symptoms of peach leaf curl.

Note the malformation of infected tissues.
❑Etiology:
➢Mycelia are intercellular and do not produce ascocarp.
➢Asci are produced individually and measure 25- 40 x 8 - 11 µm.
➢Each ascus bears eight ascospores with a diameter of 3 to 7 µm.
❑Disease cycle:
The pathogen spreads through wind and rain and attacks the leaves
as they break bud and fruit begins to develop during cool, wet weather. A
single layer of spore-producing tissue develops on the infected plant part,
giving the blistered area a white or translucent appearance when fresh.
Spores are released from this tissue from late spring to midsummer and
remain on twigs and bud scales until following spring season.
PSI: Dormant mycelia in affected stem.
SSI: Air borne conidia.
❑Management:
➢Remove and burning of infected shoots.
➢Spray the plants with Bordeaux mixture 1% or 0.1% Carbendazim.
➢Spray Mancozeb 0.25 % at 20 days before harvesting.
1. Strawberry Leaf spot : Mycospharella fragariae.
❑ Symptoms:
➢Leaf spot is most frequently evident on the blades of the leaflets, but may
appear on the petioles, fruit and fruit stems.
➢The lesions may be seen first on the upper surface as small, deep-purple,
somewhat indefinite areas.
➢As the spot enlarges, the central area becomes brown, which soon turns to
a definite white spot in older leaves or light brown in young tender leaves.
➢An indefinite, dark purple zone surrounds the central light area, giving the
hole a bird’s-eys effect.
➢When infections are bunched on the leaf, the purplish area may become
confluent and extend around a number of white spots, and if infection
occurs near the edge of leaflet, purpling often extends to the border.
➢On the under surface part of the leaf, symptoms are much the same as on
the upper, but coloring is less intense.
➢Here the prominent veins which are touched by any of the spots take on a
reddish-purple color that extends some distance beyond the infected spots.
Etiology:
M. fragariae reproduces by forming perithecia that are black, partially
embedded, globose (100 to 150 µm) and minutely ostiolate. Within each
perithecium, asci (30 to 40 x 10 to 15 µm) that are cylindrical to clavate, have short
stalks, and contain 8 spores, are formed in small clusters. Ascospores (12 to 14 x 3 to
4 µm) are hyaline and two-celled with a median septum with each cell generally
containing two oil drops.
The anamorph of M. fragariae, Ramularia brunnea is actually more
commonly found on strawberries during the growing season, especially in southern
latitudes. This anamorphic state produces conidia that are elliptical to cylindrical
(20 to 40 x 3 to 5 µm) hyaline, and zero- to four-septate. The conidia are often
formed in short chains and are borne on short, hyaline, unbranched, and frequently
curved conidiophores.
❑Disease cycle:
The disease cycle starts when the pathogen overwinters as
mycelium or fruiting structures in leaf debris and spores are spread
by rain splash infecting new leaves as they emerge in the spring
when conditions are favourable. Disease development is most
successful in cool daytime temperatures and cold nighttime
temperatures, high relative humidity, and wet conditions.
❑Management
➢Curing of planting material
➢Caprtonbal @ 13kg/ha as soil application
➢Copper Oxy chloride (0.3%) or Carbendazim (0.1%) sprays.
Lecture 24
By
M.Sc. Agri., NET
Potato crop Diseases, Symptoms, Etiology, Disease cycle and
Their Management.
1. Early blight : Alternaria solani
2. Late blight : Phytopthora infestans
3. Black scurf : Rhizoctonia solani
4. Leaf roll : Potato leaf roll virus
5. Mosaic :
a. Mild mosaic/Interveinal mosaic : (Potato virus X) PV X
b. Severe mosaic :Potato virus Y (PV Y)
c. Rugose mosaic of potato : Potato virus X &Y
1. Early blight : Alternaria solani
❑ Symptoms:
➢This is a common disease of potato occurring on the foliage at any stage of
the growth and causes characteristic leaf spots and blight.
➢Normally the disease symptoms become apparent during tuber bulking
stage and develop leading to the harvest.
➢The early blight is first observed on the plants as small, black lesions
mostly on the older foliage.
➢Spots enlarge, and by the time they are one-fourth inch in diameter or
larger, concentric rings in a bull's eye pattern can be seen in the center of
the diseased area.
➢Tissue surrounding the spots may turn yellow. If high temperature and
humidity occur at this time, much of the foliage is killed.
➢Lesions on the stems are similar to those on leaves, sometimes girdling the
plant if they occur near the soil line.
❑Etiology:
➢The mycelium is septate, branched, light brown colour, spread
inter and intracelluar in the host tissue.
➢The conodiophore are short, light brown, septate arise from disease
tissue and emerge through stomata.
➢The conidia are borne in chain at tip of conidiophores. Conidia are
obclavate, muriform with 5-10 transverse septa.
❑Disease Cycle/perpetuation of Early blight of disease:
➢Primary Infection: Mycelium or conidia in infected plant debris
➢Secondary Infection: Conidia dispersed by wind, water or rain
splashes
❑Management of early blight disease
➢Use of disease free seed
➢ Practicing crop rotation helps to minimize the disease incidence.
➢Removal and burning of diseased crop debris
➢Nursery spraying after 2 weeks after sowing with COC 50WP
➢Mancozeb@0.25% or chlorothalonil@0.2% or Zineb@ 0.25% spray at
weekly intervals.
➢ Spray Mancozeb + urea solution i.e. at the rate of 2 g Mancozeb 75
WP + 10 g urea per litre of water at 15 days interval when symptoms
start.
2. Late blight : Phytopthora infestans
❑ Symptoms:
A. Symptoms on leaf
➢The first symptoms of late blight in the field are small, light to dark
green, circular to irregular-shaped water-soaked spots. These lesions
usually appear first on the lower leaves. Lesions often begin to develop
near the leaf tips or edges, where dew is retained the longest.
➢During cool, moist weather, these lesions expand rapidly into large,
dark brown or black lesions, often appearing greasy. Leaf lesions also
frequently are surrounded by a yellow chlorotic halo
➢The lesions are not limited by leaf veins, and as new infections occur
and existing infections coalesce, entire leaves can become blighted and
killed within just a few days. The lesions also may be present on petioles
and stems of the plant.
➢The lesions are not limited by leaf veins, and as new infections occur
and existing infections coalesce, entire leaves can become blighted and
killed within just a few days. The lesions also may be present on petioles
and stems of the plant.
B. Symptoms on tubers:
➢Late blight infection of tubers is characterized by irregularly shaped,
slightly depressed areas that can vary considerably from brown to
purplish of variable size on the skin.
➢A tan to reddish-brown, dry, granular rot is found under the skin in the
discolored areas and extending into the tuber usually less than ½ inch
❑Etiology:
➢Mycelium is coenocytic, hyaline, branched and both inter and intracelluar
➢The conidiophores are aerial and arise from the internal mycelium
through stomata
➢ and lenticel on the tubes. They are slender hyaline, branched and
indeterminate.
➢The sporangia are thin walled, hyaline, oval or pear shaped with a definite
papilla at the apex germinating by zoospore. Oospore are thick walled and
yellowish.
❑Disease cycle:
The infected tubers and the infected soil may serve as a source of
primary infection.
The diseased tubers are mainly responsible for persistence of the disease
from crop to crop.
The air borne infection is caused by the sporangia.
❑Management:
➢Protective spraying with mancozeb or zineb 0.2 % should be done to
prevent infection of tubers.
➢Tuber contamination is minimized if injuries are avoided at harvest
time and storing of visibly infected tubers before storage.
➢The resistant varities recommended for cultivation are Kufri Naveen,
Kufri Jeevan, Kufri Alenkar, Kufri Khasi Garo and Kufri Moti.
➢Destruction of the foliage few days before harvest is beneficial and this
is accomplished by spraying with suitable herbicide
1. Black scurf : Rhizoctonia solani
❑ Symptoms
➢Symptoms can be observed on above and below ground plant parts.
➢Symptoms observed above ground early in the season include necrosis
at the tips of the sprouts (which may eventually cause the emerging
plant to die) and sunken lesions on stolons, roots, and stems.
➢ Later in the season, sclerotia are produced in the tubers creating a sign
called black scurf which is simply, sclerotized mycelium.
➢ Stems with cankers can become girdled, resulting in stunted plants.
➢ Leaves of infected plants develop a purplish and chlorotic coloration.
In severe infections, green tubers develop above the ground.
➢Affected tubers are deformed and can produce sclerotia on the surface.
Sunken leisons on stem Tuber russet
❑Etiology:
➢Rhizoctonia solani is a basidiomycete fungus that does not produce any asexual
spores (called conidia) and only occasionally will the fungus produce sexual spores
(basidiospores). In nature, R. solani reproduces asexually and exists primarily as
vegetative mycelium and/or sclerotia
➢Young mycelium of R Solani is silvery and become yellow to brown at maturity 8-
12 µm in dia.
➢Having frequent septation and branched.
➢Sclerotia are dark brown to black.
➢They are roughly spherical or somewhat flattened or irregular, shape of micro
scleortia is oval to irregular
❑Disease Cycle
➢P.I: Oospores (Pythium) or Sclerotia (Rhizoctonia) in soil
➢S.I: Seedlings raised in infected soil carry the disease to field
❑Management:
➢Disease free seed tubers alone should be planted.
➢If there is a slight infection of black scurf that can be controlled by
treating seed tubers with mercuric chloride solution for 1.5 hr with
acidulated mercuric chloride solution for 5 min.
➢Treating the soil with pentachloroni trobenzene at the rate of 70 kg/ ha
lowers the incidence of the disease, but it is too expensive and
cumbersome.
➢Well sprouted tubers may be planted shallow to control disease.
➢The disease severity is reduced in the land is left fallow for 2 years.
4. Leaf roll : Potato leaf roll virus
❑ Symptoms:
➢The symptoms appear early and young leaves show an upward roll.
➢ Leaves become dry, leathery and thick. They turn brittle and give
their distinctive rattle when shaken.
➢Plants may also be severely stunted, erect and light green.
➢Tubers are reduced in size and number. With some varieties, a net
necrosis develops inside the tuber.
❑Transmission
➢ Infected tubers (Sap inoculation)
➢ Spread by aphids, Myzus persicae and Aphis gossypii
❑Management:
➢Disease free seed tubers for planting.
➢Use of disease free certified seed.
➢Rouging of diseased plants and burying them deep in soil.
➢Aphid control.(Phorate 10 G ,10Kg/ha or monochrotophos).
5. Mosaic :
a. Mild mosaic/Interveinal mosaic : (Potato virus X) PV X
❑ Symptoms:
➢Often referred as latent potato mosaic
➢ Light yellow mottling with slight crinkling on potato plants
➢ Interveinal necrosis of top foliage
➢ Stunting of diseases plants
➢ Leaves may appear slightly rugose where strains of PV Y combines
b) Severe mosaic – Potato virus Y (PV Y)
Also called potato leaf drop streak
❑Symptoms
➢ Chlorotic streaks on leaves which become necrotic
➢ Necrosis of leaf veins and leaf drop streak
➢ Interveinal necrosis and stem/petiole necrosis
➢ Plant remain stunted in growth
➢ Rugosity and twisting of the leaves occurs in combination with PV X
and PV A
C. Rogose and Common Mosaic : Potato virus X &Y
❑Symptoms
➢Black streaks appear in leaf veins and on stems.
➢Early-season infection shows shriveled leaves that hang from the stem
by a thread of dead tissue.
➢Later in season, the plants become bare with a few leaves on top. Late-
season infection does not show any symptoms.
➢Plants from infected seed tubers have mottled and wrinkled leaves that
are distorted ("rough") and reduced.
➢Stems are brittle and dwarfing is common. Harvested tuber size is
greatly reduced.
➢The primary pathogen is Potato Virus Y (PVY) which may act alone or
in conjunction with PVX. There are many strains of PVY with differing
characteristics and behaviour. PVY is spread by both seed and aphids.
❑Transmission
a.) Mild mosaic/Interveinal mosaic
➢Spreads mechanically through rubbing of leaves, contact of infected plants
(Sap inoculation), seed, cutting knives, farm implements.
➢ Root clubbing of healthy and diseased plants in field
b) Severe mosaic – Potato virus Y (PV Y)
➢ Infected tubers (Sap inoculation)
➢ Spread by aphids, Myzus persicae and Aphis gossypii
❑Management:
➢Disease free seed tubers for planting.
➢Resistant varieties (like chippewa & Irish cobs).
➢Use of disease free certified seed.
➢Rouging of diseased plants and burying them deep in soil.
➢Insect control in case of Mild and Rugose mosaic.(Phorate 10 G ,10Kg/ha)
➢Avoid working of labour and animals from diseased to health crop in case
of latent mosaic virus.
➢Early harvesting of the crop.
2. . Powdery mildew : Erysiphe phoygoni
❑ Symptoms:
➢It is characterised by a white powdery growth on the leaves, stems and
pods.
➢ First symptoms appear on the leaves in the form of white floury patches
on both sides of leaves.
➢ The disease then spreads to other green parts of the plant such as tendrils,
pods, stems etc.
➢ The patches on the leaves originate in the form of minute discoloured
specks from which powdery mass radiates on all sides.
➢In the advanced stages of the disease large areas of the host get coveted
with white floury patches.
➢ Infected plants impart dirty appearance.
➢In extreme severe infections the infected leaves are shed leaving stem
devoid of the leaves..
➢ Affected seeds become brown.
➢ Water stress accelerates mildew development. Warm days and cool nights
favour disease development.
➢The fungus is seed-borne. It causes considerable damage and may result
up to 20-30 % losses in pod number
❑Etiology:
The fungus is an obligate parasite having septate, hyaline, profusely
branched superficial mycelium sending finger shaped haustoria to the host
cells.
oblong to cylindrical shape, not including fibrosin bodies, 32–44 x 12–15 µm
in size.
❑DISEASE CYCLE OF POWDERY MILDEW
➢ Primary source of infection-Infected debris
➢ Secondary source of infection-wind blown conidia
➢Fungus survives in summer leftover debris.
➢Seed is not considered as main source of inoculum.
➢Avoid late planting.
➢ After harvest, collect the plants left in the field and burn them.
➢ Grow resistant varieties like JP-83, PM-2, JP-4, and JRS-14.
➢ By formulation of wettable Sulphur such as Sulfex and Thiovit at 3 kg/ha.
➢ 0.03 % Calixin followed by Karathane (0.2%) and Bavistin (100 ppm)
Symptoms:
➢Pea rust is characterized by the appearance of two types of symptoms in
India. Early symptoms develop on abaxial side of older leaves and form
round to oval aecidia.
➢Initially aecidia form creamy white to light yellow to bright orange colored
pustules on the leaf and stem.
➢These pustules further developed and spread to other parts of the plants.
An aecidia is a cluster of several small cups like structure on the plant.
Aeciospores released from the aecial cups are deposited as yellow powder.
➢Small aecidial pustules are mostly confined to the leaf. However it can be
seen on stem also.
➢Uredial pustules developed on both the surface of leaf but mostly confined
to the stem.
➢They appear as powdery light brown pustules. The ruptured epidermis on
infected portion of host exposes black to brown powdery mass.
➢Telial symptoms appear after aecial/uredial infection late in the same
season or on the part of plant leading to senescence.
➢Grain size is significantly reduced in badly infected genotype and colour of
the grain becomes dull.
❑Etiology:
➢Pycniospores:
➢Aeciospores
Designates aecia (aecidia) with aecisopores. Aeciospores were round
to angular or elliptical with fine warts, yellowish in colour and 14-22 m in
dia.
➢Uredospores
Uredospores are light brown, spiny, elliptical, single called,
pedicillate, 20-30 x 18-26 mm and possess 3-4 germ pores.
➢Teliospores
pedicillate, thick walled with flattened apex and 25-38 x 18-27 mm in
diameter. They were light brown with papillate apex.
➢Basidiospores:
Basidia with basidiospores. The teleutospore germinates and forms a
4-celled basidium on which four, single celled hyaline basidiospores were
formed.
❑Disease cycle:
infected crop
➢Cultural practices viz., planting time, planting geometry, intercropping
and row spacing.
➢Use of foliar fungicides as Hexaferb and Dithane M-45 give best control.
effective.
❑Symptom
➢Symptom of the disease is more pronounced in 3 to 5 week old plants. In
young seedlings, cotyledons droop and wither.
➢Yellowing of lower leaves and stunting of plants.
➢The xylem vessels develop brown discoloration and get distorted.
➢Leaflet margins curl downward and inward.
➢The stem may be slightly swollen and brittle near the soil.
➢Internal woody stem tissue often is discolored, turning lemon brown to
orange brown.
➢Externally, the root system appears healthy; however, secondary root rots are
likely to occur on plants wilted for long periods.
➢Eventually, wilted plants may die.
❑Etiology:
➢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 conidiophore, are thin walled, 3 to
5septate, fusoid and pointed at both ends.
➢Chlamydospores are roughwalled or smooth, terminal or intercalary, may
be formed singly or in chains.
❑Disease cycle
implements.
➢Avoid early sowing in badly infested areas.
➢Seed treatment with T. viride @4g/kg or P. fluorescens @ 10g/ kg of
seed or Carbendazim or Thiram 2g/kg of seed.
➢Spot drenching with Carbendazim 1g/lit or P. fluorescens / T.
viride 2.5 kg/ha with 50 kg FYM.
Lecture 25-26
By
M.Sc. Agri., NET
Cucurbits Diseases, Symptoms, Etiology,
Disease cycle and Their Management.
1. Downy mildew : Pseudoperonospora cubensis

2. Powdery mildew : Erysiphe cichoracearum,
Sphaerotheca fuligena
3. wilt : Fusarium oxysporum f.sp. niveum
4. Angular leaf spot : Pseudomonas syringae pv. lachrymans
5. Mosaic :Cucumber mosaic virus
6. TOSPO virus : Tomato spotted wilt virus (TSWV)
1. Downy mildew : Pseudoperonospora cubensis
Host Members of Cucurbitaceae, the gourd family, including cucumber
(Cucumis sativus), squash (Cucurbita spp.), melon (Cucumis melo) and
watermelon (Citrullus lanatus).
❑ Symptoms:
❖Cucumber, squash and pumpkin
➢Downy mildew symptoms first appear as small yellow spots or water-
soaked lesions on the topside of older leaves.
➢ The centre of the lesion eventually turns tan or brown and dies.
➢ The yellow spots sometimes take on a "greasy" appearance and do not
have a distinct border.
➢During prolonged wet periods, the disease may move onto the upper crop
canopy.
➢This is the earliest symptom produced by the disease, but will disappear as
moisture dissipates.
➢Early lesions are light green in appearance and become chlorotic and
finally necrotic as host plant cells die.
➢ Severe infection results in leaves that are completely dead and curled up.
This symptom has been described as “wildfire” as the leaves appear to be
burned.
➢A greater proportion of mishapen fruit (especially in cucumber)
❖Watermelon and cantaloupe.
➢Symptoms on watermelon and cantaloupe are typically irregular shaped
lesions on the foliage that turn brown rapidly.
➢Infected leaves may experience an upward leaf curl
➢ In cantaloupe crops, the lesions appear irregular shaped, whereas the
lesions are smaller and rounder on infected watermelon leaves.
➢As the disease progresses, the lesions expand and multiply, causing the
field to take on a brown and "crispy" appearance.
❑Etiology:
P. cubensis is an obligate parasite . The mycelium is coenocytic
and intracellular with small finger like haustoria. 1-5 sporangiophores
arise through stomata. Spore bearing tip are subacute. Sporangia are
grayish to olivaceous purple. Ovoid to ellipsoidal, thin walled with
distal papilla & 21-39 µm X 14-23µm. Zoospore are 10-30µm in dia.
Oospore are not common.
❑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
➢Avoid excess overhead irrigation.
➢Wider spacing and planting sites with good drainage.
➢Seed treatment with Apron at 2 g/kg.
➢Spray metalaxyl@0.2% or chlorothalonil@0.2%
➢ Spray zineb@0.3% at 10 days interval
2. Powdery mildew : Erysiphe cichoracearum or Sphaerotheca fuligena
❑ Symptoms :
➢Powdery mildew forms obvious patches of whitish mycelium
(resembling talc) on upper and lower leaf surfaces, petioles, and
stems.
➢First noted on the older leaves, powdery mildew appears as pale
yellow spots on stems, petioles, and leaves.
➢These spots enlarge as the white, fluffy mycelium grows over plant
surfaces and produces spores, which give the lesions a powdery
appearance.
➢Affected leaves become dull, chlorotic, and may show some degree
of wilting in the afternoon heat; eventually they become brown and
papery.
➢The diseased areas turn brown and dry. This leads to premature
defoliation and death
➢Fruits remain undeveloped and are deformed
❑Etiology:
E. Cichoracearum the conidia measure 63.8 X 31.9 µm. The
clestothecia are globose 80-100 µm in dia., containnig 10-15 asci,
which are 58-90 µm in size.each ascus contains two ascospores and
are oval or sub cylindrical.
S. fulinginea occasionaly brownish when old. Conidia are in
chains with fibrisin bodies, ellipsoid to barrel-shaped and 25-37 X
14-25 µm. Conidial germ tubes mostly forked perithecia are round,
66-98 µm in dia. Asci are broadly elliptic and are 50-80 X 30-60 µm.
In each ascus 8 ellipsoid ascospores are found.
❑Disease cycle:
➢P.I: Collateral hosts or through Cleistothecia
➢S.I: Wind borne conidia
❑Management
➢Plant resistant varieties where available.
➢Choose planting sites with good air movement and free of shade.
➢Spray Calixin 0.1% or Karathane @0.2%
3. Wilt : Fusarium oxysporum f.sp. niveum
❑ Symptoms:
➢ Symptoms can occur at any stage of growth
➢On young seedlings, a hypocotyl rot and damping-off may occur. In
older plants, there is marginal yellowing progressing to a general
yellowing of the older leaves, and wilting of one or more runners.
➢In some cases, sudden collapse occurs without any yellowing of the
foliage.
➢On stems near the crown of the plant, a linear, necrotic lesion may
develop, extending up the plant and usually on one side of the vine.
One runner on a plant may wilt and collapse, with the rest of the
runners remaining healthy.
➢In a wet weather , a white or pinkish fungus growth develops on the
surface of dead stems.
➢Vascular discoloration should be evident and is very diagnostic.
Mature plants often wilt severely (collapse) late in the season because
of the fruit load stress.
❑Etiology :
The fungus produces three types of spores, small colourless,
oval to narrowly elliptical, non-septate microconidia, lagre sickle
shaped, septate macro-conidia and thick walled Chlamydospores.
❑DISEASE CYCLE OF WILT
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 wind
and irrigation water.
❑MANAGEMENT
➢Treat the seeds with Carboxin or Carbendazim at 2 g/kg.
➢Apply increased doses of potash with a balanced dose of
nitrogenous and phosphatic fertilizers.
➢Apply heavy doses of farm yard manure or other organic
manures. Follow mixed cropping with non-host plants.
➢Use resistant varieties.
➢ Maintaining a pH of 6.5 to 7.0.
4. Angular leaf spot: Pseudomonas syringae pv. lachrymans
❑ Symptoms:
➢Small, round water-soaked spots appear on leaf tissue, and expand until
they are confined by veins, giving them the characteristic angular look.
➢Under moist conditions a milky white exudates containing bacterial cells
may ooze out of the lesion on the lower leaf surface.
➢These wet-looking spots will dry out and turn yellow-brown or the dead
tissue may fall out leaving a “shot-hole” appearance.
➢Yellowing of the leaf between lesions may occur where disease severity is
high.
➢Similarly, water-soaked spots may appear on stems and petioles, drying
out to form a whitish crust.
➢Spots can also appear on fruit, where they are tiny and water-soaked but
dry to form whitish, chalky, spots.
➢These spots cause internal decay of fruit, and fruit that is infected early
may be deformed. Affected plants will grow poorly, produce less fruit, and
affected fruit is unmarketable.
❑Etiology :
➢The bacterium is gram negative, aerobic and rod shaped motile with 1-5
polar flagella & 0.8-1.2 µm in length.
➢It forms capsule and green fluorescent pigment in culture.
❑Disease cycle:
The Pseudomonas bacterium is a seed borne pathogen. In addition, the
pathogen can overwinter in infested crop residues. The secodary spread
through irrigation water.
❑Management
➢Plant certified, pathogen-free seed produced in arid western locations.
Resistant cucumber varieties are available.
➢Do not grow cucurbits in the same field more than once every three or four
years and avoid excessive nitrogen fertilization.
➢Limit the use of overhead irrigation and avoid cultivating, harvesting, or
otherwise handling plants when they are wet.
➢Where ever feasible, cleanly plow under or collect and burn crop debris
immediately after harvest.
➢Apply a recommended bactericide at first sign of disease.
(Streptocycline/Streptomycine). Spray 400ppm Streptomycin sulphate.
➢Tank-mix the recommended bactericide with effective fungicides to protect
the plants against fungal diseases.
5. Cucumber Mosaic: Cucumber mosaic virus
❑Symptoms
➢Symptoms of CMV in cucurbits generally manifest as severe stunting,
prominent yellow foliar mosaic, plant and leaf malformation, and stunting
due to drastic reduction of leaf size and stem internodes.
➢When the virus becomes systemic, leaves prominently curl downward,
develop a mosaic pattern, and remain small.
➢Flowers develop abnormalities and have greenish petals.
➢Foliar and flower symptom intensity varies with species and cultivar:
symptoms are most severe in summer squash, some pumpkins, and many
melons and less severe in cucumber, winter squash, and watermelon.
➢Infected fruit are often distorted and discolored, remain small, and, when
severely infected, produce a negligible amount of seeds.
❑Survival and spread
➢ Survive on weeds, ornamentals or other crops
➢ Transmitted by aphids (Aphis craccivora, Myzus persicae) and spotted and
striped cucumber beetles
➢Collateral hosts: Banana, clover, corn, passion fruit, safflower, spinach,
sugarbeet, wild cucumber, Commelina communis, C. diffusa, C. nudiflora,
Solanum elaegnifolium, Phytolacca sp., periwinkle, Gladiolus sp., Impatiens sp.
and Phlox
❑Management
➢Rogue out infected plants
➢Eliminate perennial weed hosts
➢Vector control by spraying monochrotophos or phosphamidon,
1.5 ml per liter of water
3. TOSPO virus : Tomato spotted wilt virus (TSWV)
❑ Symptoms:
➢Cucurbits infected with tospovirus exhibit a variety of symptoms.
Leaves can show bronzing to severe systemic chlorotic spotting.
Other symptoms include leaf deformation, mosaic, die-back and
overall plant stunting.
➢ Fruit symptoms can range from chlorotic ring spots on young
fruit to necrotic lesions on older fruit.
➢Fruit cracking may also be observe
❑Etiology:
➢Tospo virus spp. possess a tripartite single-stranded RNA genome with a
negative or ambisense expression strategy.
➢ Genomic RNAs are encapsidated by nucleocapsid proteins (N) and
enveloped by a lipoprotein membrane
❑Transmission:
Western flower thrips (Frankliniella occidentalis), Tobacco thrips (F. fusca),
Melon thrips (Thrips palmi).
❑Management
➢In protected culture and transplant nurseries, utilize mesh screening
(minimum 72 mesh /192 microns) and phytosanitary measures to minimize
tospovirus infection by excluding thrips.
➢Avoid planting near or downwind of ornamentals or older crops, which
can serve as reservoirs for thrips and tospovirus.
➢ Control weeds and cucurbit volunteers.
➢Implement a comprehensive insecticide program beginning prior to
sowing or transplanting to manage thrips early larval stages and limit
secondary tospovirus spread.
Lecture 27 & 28
By
M.Sc. Agri., NET
Onion crop Diseases, Symptoms, Etiology, Disease cycle and
Their Management.
1. Purple blotch :Alternaria porri

2. Stemphylium blight : Stemphylium vesicarium
3. Downy mildew : Peronospora destructor
4. Smut :Urocystis cepulae
5. Smudge :Colletotrichum circinans (Berk.)
6. Erwinia rot :Erwinia carotovora subsp. carotovora
1. Purple blotch :Alternaria porri
❑ Symptoms:
➢This disease occurs mainly at the top of the leaves, the infection starts with
whitish minute dots on the leaves with irregular chlorotic areas on tip
portion of the leaves.
➢Circular to oblong concentric black velvety rings appear in the chlorotic
area.
➢Sometimes yellow halo is seen around lesions
➢Spots coalesce and leaves die from tip backwards
➢Diseased leaves break at point of infection & hang down
➢Infection also seen on outer scales of bulb, seed stalk and neck
➢Severely infected crop dries up
➢Bulbs become dry and papery.
❑Etiology:
Alternaria porri mycelium is branched, coloured and septate.
Conidiophores arise singly or in groups. They are straight or
flexuous, sometimes geniculate. Conidia are solitary, straight or
curved and obclavate. The body of the conidium may be ellipsoid,
tapering to the beak.
❑Disease Cycle :
➢Primary inoculum :
The primary cycle, when infection starts from infected Plant
debris and seed bulb
➢Secondary spread :Air-borne conidia
❑Management:
➢Disease free bulb should be selected for planting
➢Seeds should be treated with Thiram @ 4 g/kg seed.
➢The field should be well drained.
➢Three foliar sprayings with Copper oxychloride 0.25 % or
Chlorothalonil 0.2 % or Zineb 0.2 % or Mancozeb 0.2 %.
❑ Symptoms:
➢Small yellow to orange flecks or streaks develop in the middle of the leaf
which soon develop into elongated, spindle shaped to ovate elongate
diffused spots surrounded by characteristic pinkish margin.
➢The spots progress from the tip to the base of the leaves. The spots coalesce
into extended patches, blighting the leaves and gradually the entire foliage.
➢stemphylium vesicarium may enter purple blotch lesions, causing a black
fungal growth. Since this fungus is usually found co-infecting with Alternaria
porri, symptoms are identical or at least very similar to purple blotch.
However, Stemphylium leaf blight lesions appear to be a darker, more olive-
brown to black color than do purple blotch lesions.
➢Lesions are often more numerous on the sides of onion leaves facing the
prevailing wind.
❑Etiology:
➢ Ascospores are yellowish brown and ellipsoidal, with the upper half
narrowly tapered (Fig 1.3). Matured ascospores have 5 - 7 complete
transverse septa and zero to several incomplete longitudinal septa. The
average size of a mature ascospore is about 18 × 38 µm.
➢Conidia are olive-brown, oval to ovoid, and are borne on conidiophores
that are pale to brown with dark edges and bands. The conidia have 1 - 5
transverse septa and are constricted at 1 - 3 transverse septa. The conidia
also have 1 - 2 complete longitudinal septa.
❑Disease cycle:
The disease cycle of SLB is characterised by sexual and asexual In
the sexual phase, pseudothecia develop on both diseased and symptomless
tissues of host and non-host plants. On onion, however, pseudothecia
development is restricted to the inflorescence. The development of
pseudothecia in temperate regions occurs in the winter at temperatures
between 5 - 15 °C and high relative humidity. At these low temperatures,
ascospores maturation takes 1 - 6 months. The pseudothecia are black and
bear several cylindrical asci. Pseudothecia release ascospores in the spring,
coinciding with rainfall events.
❑Management:
➢Use of host resistance would be the most efficient way to manage
SLB on Allium crops.
➢Biological control agents such as Bacillus subtilis, Saccharomyces
cerevisiae, Pseudomonas fluorescens and Trichoderma species
reduced the severity of disease.
➢Three foliar sprayings with Copper oxychloride 0.25 % or
Chlorothalonil 0.2 % or Zineb 0.2 % or Mancozeb 0.2 %.
3. Downy mildew: Peronospora destructor
Symptoms:
➢Downy mildew is characterized by pale–green, yellowish to brownish
areas of irregular size and shape (oval to cylindrical) on infected leaves or
seed stalks. These areas may consist of alternating yellow and green layers of
tissue.
➢The causal organism of DM produces fruiting bodies and spores called
sporangia on the surface of the leaves and seed stalks.
➢The masses of spores are at first transparent to greyish, and then rapidly
become violet in color.
➢Leaves become girdled in the region where mildew develops and the
leaves collapse.
➢This results in dead leaf tips that usually can be seen within defined
regions in a field. The dead leaf tissue is rapidly colonized by purple blotch,
which is dark in color and obscures DM. DM seldom kills onion plants, but
bulb growth may be reduced.
➢ Bulb tissue, especially the neck, may become spongy and the bulb may
lack keeping quality.
➢Bulbs can also be infected and often sprout prematurely or shrivel in store.
❑Etiology:
The sporangiophores are non septate, long and swollen at the base. Sporangia
are pyriform to fusiform, attached to the sterigmata by their pointed end. These
sporangia germinate by one or two germ tubes. The coenocytic mycelium is
intercellular with filamentous haustoria. Oogonia are formed in the intercellular
spaces.
❑Disease cycle:
➢Primary Spread
The fungus overwinters in volunteer onion, culls, and wild Allium species.
When favorable environmental conditions occur, the overwintering fungal
mycelium in systemically infected plants produces spores.
➢Secondary Spread
The mycelium of DM in leaves of infected onion plants in commercial bulb
production fields produces a new crop of spores called conidia in cycles of
approximately 11–15 days
❖Cultural Control
➢Minimize canopy leaf wetness:
•Avoid sprinkler irrigation, especially when the canopy begins to fill.
•If avoiding sprinkler irrigation is not feasible, adjust the irrigation
schedule to maximize leaf drying and prevent extended leaf wetness
between irrigation events.
•Plant in fields where there is good air movement.
•Select fields that are well drained.
•Align rows with the prevailing winds.
•Change planting date to avoid having a full canopy during conditions
favorable for downy mildew.
➢Use a 3-year rotation away from Allium crops in fields where the disease
has occurred.
➢Use disease-free bulbs, sets, and seed.
➢Remove and destroy material of any Allium plants, including residue from
the previous crop, volunteer plants, and culls from storage.
➢Avoid entering fields when leaves are wet.
❖Chemical:
Spray metalaxyl@0.25% or COC@ 0.3% or Mancozeb@ 0.2% at 10 days
interval
4. Smut : Urocystis cepulae
❑Symptom
➢Fungus attacks cotyledons of young plants soon after their emergence
causing dark, elongated eruptive spots
➢On older leaves, the lesions may extend from base to the tip and appear
as blisters
➢Lesions develop into thickened areas of several mm in size
➢Lesions burst open releasing masses of black smut spores
➢Severely affected plants killed within 3-4 weeks of emergence
➢Surviving plants are stunted with stout, brittle, distorted leaves bearing
lesions throughout their length
➢Numerous blisters appear on leaves and bulb scales of mature plants
which rupture to expose masses of black powdery spores
❑Etiology:
The sori of urocystis cepulae contain dark coloured and powdery
spore masses. The spores are found in permentant balls. Each ball consists of
an enveloping cortex of tined, sterile, bladder like cells with one or two
central dark coloured thick walled chlamydospores. The spores germinate by
means of short promycelium while still in the ball.
❑Disease cycle
➢P.I: Spore balls in infected soil
➢S.I: Wind blown soil and surface drianage water, onion bulbs and onion
transplants
❑Management
➢Seed Treatment with thiram@3 g/Kg seed
➢Crop rotation and use of disease free seedlings
➢Cultivar, Hardy white bunching is resistant
➢Spray with captan or ferbam @0.2% along with a sticker
5. Smudge :Colletotrichum circinans (Berk.)
Symptoms:
➢Chiefly a disease of scales of bulb. Red scaled onions are usually
resistant to the smudge due to the presence of proto-catacheuic acid and
catechol
➢Damping off in seed bed under wet and warm conditions
➢Disease appears at all stages and also during storage and transportation
➢Sub-cuticular, dark green to almost black smudge appear on the bulb,
neck or green leaves that are clinging to bulb after digging
➢Circular lesions with concentric rings of dark stromata and mycelium
appear on leaves
➢Small, sunken and yellow lesions on inner scales
➢Pinkish mass of fungal growth on lesions under humid conditions
❑Etiology:
➢Acervuli with dark, almost black, acicular setae having a bulbous base
and 1 to 3 septae, measured up to 290 by 8 µm.
➢Conidia were hyaline, unicellular, 16-25 x 3-5 µm, slightly falcate,
guttulated.
➢Apressoria are subglobose, ellipsoid, clavate or irregular, 1- or 2-celled,
measuring 6.5-13.5 x 5.5-8 µm.
❑Disease cycle
➢P.I: Soil and on infected onions as stromata
➢S.I: Wind borne conidia
➢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
6. Erwinia rot :Erwinia carotovora subsp. carotovora
(Dickeya chrysanthem)
Symptoms:
➢Bacterial soft rot is mainly a problem on mature bulbs.
➢Bacterial soft rot usually starts at the neck of the bulb, and progresses
downward along one or more scales.
➢ At first the tissue is water-soaked. Later it disintegrates into a soft, slimy
mass.
➢The decay does not spread readily from scale to scale. One or two scales
may be completely rotted while the remainder are sound.
➢ Eventually, the diseased bulbs can be detected by gently squeezing them,
whereupon a watery fluid is exuded.
➢ An offensive sulfurous odor is usually associated with the liquid squeezed
from the neck of diseased bulbs.
❑Etiology: It is a gram-negative bacillus that belongs to the family
Pectobacteriaceae. Members of this family are facultative anaerobes. It is a motile,
nonsporing, straight rod-shaped cell with rounded ends. Cells range in size from 0.8 to
3.2 μm by 0.5 to 0.8 μm and are surrounded by numerous flagella (peritrichous).
❑Disease cycle
Soft rot bacteria commonly exist in the soil and plant refuse. They enter onions
through wounds and aging tissue under moist conditions. Onion maggots are
particularly effective at spreading the disease. The bacteria may persist in the intestinal
tract of the onion maggot larvae and adult flies and thus can be carried from one place
to another. During harvest, the practice of cutting the onion tops creates openings for
the bacteria. Also, bruising or other damage from mechanical activity leaves bulbs
susceptible to infection, particularly if they are stored in warm, humid conditions.
❑Control
➢The first step in controlling soft rot is to control other diseases and avoid injury to
the plants. This includes controlling insects such as the onion maggot that wound
plants and transmit the bacteria.
➢Cure bulbs thoroughly so that the outer scales and neck tissues are completely dry
➢If wounds are protected within hours after they occur with sprays containing copper-
based materials, the wounds will likely heal rapidly and infection will be reduced.
Garlic crop Diseases, Symptoms, Etiology, Disease cycle and Their
Management.
1. Neck and bulb rot : Botrytis allii, Botrytis porri

3. Black mould : Aspergillus niger, Aspergillus alliaceous
1. Neck and bulb rot : Botrytis allii, Botrytis porri
❑ Symptoms:
➢Neck rot is found upon the bulbs at the time of harvest
➢Affected scale tissue become soft
➢Dense layer of grey mould appear at the neck
➢Infection progresses most rapidly down the scales which have been
originally infected
➢Dark sclerotia appears on the older decayed tissue.
Black sclerotia on bulb
❑Etiology:
The conidia of B. allii have a maximum length of 15 μm and mean size of 10.2 ×
5.7 μm. The scales inside the bulb become progressively translucent and watery and
mycelium develops between them. A mass of grey conidiophores and conidia
develop on the mycelium and blackish sclerotia form at the site of the initial infection
❑Disease cycle:
Pathogen survives in soil and garlic bulb as a primary source of
inoculum in the form of sclerotia (resting spore) for many years.
❑Management:
➢Promoting rapid drying at harvest and good aeration in storage is best for
managing Botrytis on bulbs
➢Additionally, cooler storage temperatures may help control the disease
❑Symptoms :
➢Infection occurs on radial leaves of transplanted seedlings at 3- 4 leaf stage
during late March and early April.
➢The symptoms appear as small yellowish to orange flecks or streaks in the
middle of the leaves, which soon develop into elongated spindle shaped
spots surrounded by pinkish margin.
➢The disease on the inflorescence stalk causes severe damage to the seed
crop.
❑Etiology:
➢ Ascospores are yellowish brown and ellipsoidal, with the upper half narrowly
tapered (Fig 1.3). Matured ascospores have 5 - 7 complete transverse septa and
zero to several incomplete longitudinal septa. The average size of a mature
ascospore is about 18 × 38 µm.
➢Conidia are olive-brown, oval to ovoid, and are borne on conidiophores that
are pale to brown with dark edges and bands. The conidia have 1 - 5 transverse
septa and are constricted at 1 - 3 transverse septa. The conidia also have 1 - 2
complete longitudinal septa.
❑Survival and spread
The fungus survives in plant debris or soil
❑Management:
➢Use of host resistance would be the most efficient way to manage SLB on
Allium crops.
➢Biological control agents such as Bacillus subtilis, Saccharomyces cerevisiae,
Pseudomonas fluorescens and Trichoderma species reduced the severity of
disease.
➢Three foliar sprayings with Copper oxychloride 0.25 % or Chlorothalonil 0.2 %
or Zineb 0.2 % or Mancozeb 0.2 %.
3. Black mould : Aspergillus niger, Aspergillus alliaceous
Symptoms:
➢Whole tissue become black powdery mass
➢Individual bulbs shrivel and become light in weight
➢Under high humid condition the inner tissues become moderately
soft
➢Infected bulbs lose their pungency and smell
➢Rotten garlic cloves show black, brown, pink or white coloured
rotting.
❑Etiology:
➢Mycelium - branched, septate thick walled foot cells differentiate and give
rise to a single conidiophore
Conidiophore - globose on which brown sterigmata are formed
➢Vesicle, sterigmata, conidia make up the black head - characteristic of the
fungus
Management:
➢Store and transport bulbs at temperatures below 15 degree C and at low
humidity to slow growth of the fungus.
➢Reduce bruising and injury during harvest, handling, and transport to
minimize the opening of invasion sites for the fungus.
➢Harvest onions promptly and do not delay drying. Do not use heated air
for drying.
➢Maintain stable temperatures during transport, as well as when bulbs are
going into and coming out of storage.
Lecture 31 & 32
By
M.Sc. Agri., NET
Marigold crop Diseases, Symptoms, Etiology, Disease cycle and
Their Management
1. Botrytis blight : Botrytis cinerea
2. Alternaria blight : Alternaria tagetica
1. Botrytis blight : Botrytis cinerea
❖ Symptoms :
➢Disease symptoms appeared as dead blotches on leaves, flowers, and
stems.
➢Rotting of stems may cause plants to collapse, flower buds may fail to open
and diseased flowers that open become decayed and drop prematurely.
➢Flowers turn a papery brown and become covered with gray, fuzzy masses.
➢Tan to brown spots with a target-like appearance can also develop on the
leaves.
➢These patches are often associated with flowers which have dropped onto
the leaf surface.
➢Flower parts become necrotic and die. A gray mass of spores develops on
necrotic tissue during wet conditions.
❑Etiology :
The conidia of Botrytis spp. have a maximum length of 15 μm and
mean size of 10.2 × 5.7 μm. The scales inside the bulb become progressively
translucent and watery and mycelium develops between them. A mass of
grey conidiophores and conidia develop on the mycelium and
blackish sclerotia form at the site of the initial infection.
❑Disease cycle:
Pathogen survives in soil and plant debris as a primary source of
inoculum in the form of sclerotia (resting spore) for many years.
❑Management:
➢Remove all dead and dying plant parts (particularly blossoms) on and
around plants.
➢Avoid overhead irrigation or apply such that plants are not wet for
extended periods of time.
➢Space plants for good air circulation.
➢Control can also be achieved with the use of fungicide sprays applied as
soon as symptoms are visible (iprodione, chlorothalonil, and thiophanate-
methyl).
2. Alternaria blight : Alternaria tagetica, Alternaria zinnae
❖ Symptoms:
➢In alternaria leaf spot, brown necrotic spots formed on leaves, which
increases in size during later stage of infection and the entire foliage
gets damaged by the infection and results in poor vegetative growth.
➢The infection can lead to premature defoliation and finally death of
the plant.
➢Alternaria zinnae cause inflorescence blight of marigold in which
elongated lesions are formed on inflorescence.
➢Light tan to dark brown, large irregular blotches appears on the
leaves with zonation.
❑Etiology:
Alternaria tagetica conidia are olivaceous brown, musiform with 6-10
transeverse septa, obclavate, beaked, smooth and 32-192 µm X 12-28 µm.
Alternaria zinnae conidiophores are brown, erect to slightly bent, septate,
simple, mostly solitary and 37.8-84 µm X 4.2-8.4 µm. Conidia are light to
dark brown with 7-10 cross septa and 2-7 longitudinal septa, betaken beak
simple, long, hyaline septate and 105-231µm X 13.3-25.5 µm.
❑Disease cycle:
➢The disease is externally and internally seed born.
➢The pathogen survives through spores (conidia) or mycelium in diseased
plant debris or weed.
❑Management
➢Crop rotation helps reduce disease carryover but does not eliminate
airborne spores from another field.
➢Use seed with high germination (over 90%).
➢Seed treatment with Thiram + Captan (1:1) 0.3% and four sprays of Zineb
(0.25%) were found quite effective to control Alternaria disease.
Rose crop Diseases, Symptoms, Etiology, Disease cycle and
Their Management
1. Dieback : Diplodia rosarum
2. Powdery mildew : Sphaerotheca pannosa
3. Black leaf spot : Diplocarbon rosaea
1. Dieback : Diplodia rosarum
❑ Symptoms:
➢Drying of twigs from tip down wards.
➢Blackening of the twigs.
➢The disease spreads to root and causes complete killing of the plants.
Drying from tip Blackening of twigs

❑Etiology:
The fungus produces round, black pycnidia which bear spores. The
pycnidiospores are dark coloured and two celled. Perithecia are immersed in
the host tissue and are surrounded by a pseudostroma. Ascospores are
ellipsoidal or fusoid, hyaline, two celled with the septum in or near the
middle.
❑Disease cycle:
➢Primary infection:The fungus persist in dead twig and the stalks of the
withered blooms.
❑Management
➢Pruning should be done so that lesions on the young shoots will be
eliminated.
➢Apply chaubatia pastic in the pruned area.
➢Spray with COC 0.2% (or) Difolatan 0.2% (or) Chlorothalonil 0.2% (or)
Mancozeb 0.2%
2. Powdery mildew : Sphaerotheca pannosa
❑Symptoms:
➢The symptom appears as grayish-white powdery substance on the surfaces
of young leaves, shoots and buds.
➢Infected leaves may be distorted, and some leaf drop may occur.
➢Flower buds may fail to open, and those that do may produce poor-quality
flowers.
➢It can occur almost anytime during the growing season when temperatures
are mild (21- 26 °C) and the relative humidity is high at night and low
during the day.
➢It is most severe in shady areas and during cooler periods.
Powdery mildew on leaves on stalks on buds

❑Etiology:
Mycelium is white , septate, ectophytic and sends globose haustoria
into the epidermal cells of the host. Conidiophores are short and erect.
Conidia are one celled, oblong, minutely verrucose with many large fat
globules and 22.5 – 29.0 x 12.9 to 14.5 micron meter. Cleistothecia are formed
towards the end of the season on the leaves, petals, stems and thorns.
Cleistothecia are with simple myceloid appendages. Each ascus contains
eight ascospores.
❑Disease cycle:
➢The fungus over winters as mycelium in dormant buds and shoots which
are not entirely killed. Either conidia or ascospores serve as primary
inoculum.
➢The secondary spread is through wind borne conidia
❑Management
➢Collection and burning of fallen leaves.
➢Spray with Wettable sulphur 0.3% (or) Dinocap 0.07% (or) Carbendazim
0.1% 2-3 sprays at 15 days interval is effective.
➢Sulphur dust at 25 kg/ha.
➢Use of sulphur at higher temperature conditions will be phytotoxic .
3. Black leaf spot : Diplocarbon rosaea
❑ Symptoms:
➢ Black lesions with feathery margins surrounded by yellow tissue are
found on the leaves.
➢Infected leaves drop prematurely. Purple/red bumpy areas on first year
canes may be evident.
➢Plants may be weakened due to defoliation and reduced flower
production may be observed.
❑Etiology:
The vegetative body of the fungus consists of two parts viz., the
subcuticular mycelium and the internal mycelium. The fungus produces
acervuli on the central part of the tar spots as blister like projections. Asci
are discoid, sub epidermal, erumpent and 84 to 224 µm in dia. Stroma is
thin. Conidiophores are hyaline short and cylindrical. Conidia are hyaline,
two celled, fusiform or allantoid to obclavate, upper end round, base
narrow, guttulate, 18 – 25 x 5 – 6 µm.
❑Disease cycle:
➢The fungal spores are spread by splashing rain or water. Germination of
the spores and infection occur when free water remains on the leaf surface
for a period of 6 hours or longer. Leaf spots develop within 5 to 10 days.
❑Management:
❖Cultural:
➢Roses should be planted where the sun can quickly dry the night's dew.
➢ Space roses far enough apart for good air circulation
➢Avoid overhead watering and keep foliage as dry as possible.
➢Remove infected canes and burn diseased leaves.
❖Chemical:
➢Spraying with Mancozeb (or) Chlorothalonil 0.2% (or) Benomyl 0.1% or a
copper dust

Path 365

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Path 365

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Course title: Diseases of Field and Horticultural

Crops and their Management -II

Course : PATH 365 Credit: 3(2+1) Semester-VI

Disease Causal organism

Teliospores of Puccinia graminis

❑Disease cycle in India:

❑Disease Cycle of red rot of sugarcane:

Reddish discolouration Yellowing of leaves Shrinkage of cane

Profuse tillering Whitining of leaf Grassy shoot Reduced inter nodal

Stunted growth Orange pin head dots

1. Sclerotinia stem rot : Sclerotium rolfsii

Course : PATH 365 Credit: 3(2+1) Semester-VI

Diseases Causal organism

Embedded Sclerotia in Pod & Stem

Course : PATH 365 Credit: 3(2+1) Semester-VI

1. Wilt : Fusarium oxysporum f.sp.ciceri

Vascular wilt and yellowing field

Seed discolouration caused by botrytis infection

Symptoms of leaf infection

Ascochyta blighted patches occur within a crop

Course : PATH 365 Credit: 3(2+1) Semester-VI

Uredia and telia on flax boll

Course : PATH 365 Credit: 3(2+1) Semester-VI

Course : PATH 365 Credit: 3(2+1) Semester-VI

iii)Vein blight or vein necrosis or black vein:

Course : PATH 365 Credit: 3(2+1) Semester-VI

Lecture 15, 16 & 17

Disease Causal organism

Course : PATH 365 Credit: 3(2+1) Semester-VI

Course : PATH 365 Credit: 3(2+1) Semester-VI

1. Downy mildew : Plasmopara viticola

Course : PATH 365 Credit: 3(2+1) Semester-VI

2 Pink bud or 15 days after Captan 250 g or Mancozeb 300 g

4 10 days later Captan 200 g.or Mancozeb 300g

5 14 days after fruit set Captofol 150 g

The curved “shepherd’s crook” at the tip of the

Strawberry fruit crop Diseases, Symptoms, Etiology, Disease

Typical symptoms of peach leaf curl.

Course : PATH 365 Credit: 3(2+1) Semester-VI

Course : PATH 365 Credit: 3(2+1) Semester-VI

1. Downy mildew : Pseudoperonospora cubensis

Course : PATH 365 Credit: 3(2+1) Semester-VI

1. Purple blotch :Alternaria porri

1. Neck and bulb rot : Botrytis allii, Botrytis porri

Black sclerotia on bulb

Course : PATH 365 Credit: 3(2+1) Semester-VI

Drying from tip Blackening of twigs

Powdery mildew on leaves on stalks on buds

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