Diseases of
Lentil, Pea and Cotton
Lentil diseases
Sr. No. Diseases
1. Rust
2. Wilt
Rust
• The rust pathogen attacks all aerial parts of
the lentil plant.
• Yellowish-white spermagonia and aecial
cups develop on the lower surface of a leaf,
surface of leaflets and pods.
• The aecia are borne singly or arranged in a
circular manner as small groups on leaflets.
• They eventually turn light brown before brown
uredinia, circular to oval in shape (diam.
∼1 mm), develop on both surfaces of the
leaves, stems and pods.
• Pustules are powdery and may coalesce with
each other. Later in the season telia are formed
from the same mycelium, mainly on stems and
branches of the plant.
• Telia are firm in texture, raised and black in
color. Under heavy infection, pustules on leaves
and stems cause leaf drop and premature plant
death.
Infection
Causal Organism - Uromyces viciae-fabae
is an Autoecoius and Macrocyclic rust
(Macrocyclic rusts are those which produce all the five spore stages.) These
rusts are also known as long-cycled rusts. These spore stages may be
produced in the same host as in case of autoecious rusts or on two different
unrelated hosts as in heteroecious rusts.)
• Kingdom - Fungi
• Sub-division - Basidiomycotina
• Class - Basidiomycetes
• Order - Uredinales
• Family - Pucciniaceae
• Genus - Uromyces
Identifying characters
• Spermagonia mostly on lower leaf surface, amphigenous (growing on
both sides of leaves) in small groups associated with aecia.
• Aecia mostly on abaxial (lower) leaf surface in small groups,
predominantly along veins surrounding the spermagonia or sometimes
scattered, peridium cupulate, whitish, 0.3–0.4 mm diam.; aeciospores
18–26 × 15–21 μm, broadly ellipsoid, wall hyaline (colorless), finely
verrucose and 1–1.5 μm thick.
• Uredinia amphigenous, yellowish brown (cinnamon), 0.5 mm diam.;
urediniospores 22–32 × 17–25 μm, broadly ellipsoid, wall light golden
brown, 1–2.5 μm thick, uniformly echinulate, pores three to five,
equatorial or occasionally scattered.
• Telia sometimes on adaxial surface or sometimes amphigenous and on
stems, exposed, blackish brown, compact and 1–2 mm diam;
teliospores ellipsoidal, obvoidal or cylinderical, rounder or subacute
above, 24–40 × 17–26 μm; wall chestnut-brown, smooth, 1–3 μm thick
at the sides, 5–12 μm thick at the apex, pedicels brownish at least
apically, up to 100 μm long.
Disease cycle
• All five spore states (spermagonial, aecial,
uredinial, telial and basidial) occur, and there
are no alternate hosts. Although U. viciae-
fabae is autoecious, it has collateral hosts.
• Infected plant debris mixed with lentil seeds
or residues in crop fields are believed to act
as the primary source of inoculum. However,
collateral hosts of U. viciae-fabae may also
serve as sources of inocula.
Favourable environment
• Urediniospores germinate well in the
temperature range from 5 to 26 °C, with
optimum germination at 20 °C.
• Infection of leaves by urediniospores
progressively increases as leaf wetness
period increases and the lower the
temperature, the slower the infection
process
Management
Burning rust infected lentil plant debris to reduce potential inoculum helps in
minimizing rust occurrence the following season.
Delayed sowing of lentil effectively reduced rust disease,
The disease incidence was less in lentil sown as a mixed crop with wheat than
as an individual crop.
A substantial reduction in rust severity could be achieved through the use of row
spacing wider than 15 cm.
Early maturing cultivar shortens the number of generation times available for the
development of lentil rust epidemics, and allows it to escape serious damage.
Select seed from disease free area.
Seed treatment with Carbendazim/ SAAF super 2g/kg of seed.
Spray Triademefon (5 g/10 lt), Oxy carboxin (1.5 g/lt) or Zineb (3g/lt). Repeat
after 12-15 days.
Grow resistant varieties
Wilt
• Fusarium wilt of lentil is an important disease
reported in every-continent where lentil is
grown except Australia
• The disease may cause complete crop
failure under favorable conditions for disease
development, and can be the major limiting
factor for lentil cultivation in certain areas.
• The common name lentil wilt has been used
to describe many general wilting and dying
symptoms.
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 of individual branches.
• Seeds from plants affected in mid-pod-fill to late pod-fill are
often shrivelled.
Causal organism : Fusarium oxysporum
fsp. lentis
• Kingdom - Fungi
• Sub-division - Deuteromycotina
• Class - Deuteromycetes
• Order - Moniliales
• Family - Tuberculariaceae
• Genus - Fusarium
Identifying characters
Mycelium : Extensive, hyaline,
often with some tinge of pink-purple Macro conidia
or yellow, septate, inter and
intracellular. Mycelium in
Conidiophores : Simple, xylem vessel
slender, short, aseptate or septate
formed in the sporodochia.
Conidia : Two types-
Macro-conidia - Boat shaped or
crescent, hyaline, long, pointed at
the tip, knotched at the base,
septate (3-5 septa),
Micro-conidia - Small, elliptical or
curved, unicellular or with one
septa, gathering in short chains or
in spore balls, hyaline,
Chlamydospores : Spherical, thick
walled, terminal or intercalary.
Micro conidia
Disease Cycle
Fungus survives in the soil and infected
plant debris as microconidia,
macroconidia and chlamydospores.
Infect the fresh plants in coming season.
Favourable environment
• 20-250C and
• acidic soil favours the development of
pathogen.
Management
1. Deep summer ploughing by MB plough.
2. Crop rotation for at least for three years.
3. Seed treatment with SAAF super @2.0 g or Captan 3.0 g/kg of
seed.
4. Apply Trichoderma FYM (1 q FYM + 1 kg. Trichoderma
formulation mix and keep for 20 days) in a acre for three
consecutive years reduces the wilt incidence.
5. Grow resistant varieties
Diseases of Pea
Powdery mildew
Downy mildew
Rust
Anthracnose
Wilt
Bacterial blight
Pea top necrosis
Powdery mildew
White powdery specks
appeared on lower leaves.
Later it spread on upper
leaves and on both surfaces
of infected leaves
Leaf area covered by white
powder which is aggregation
of mycelium, conidiophores
and conidia of pathogen.
Causal organism – Erysiphe polygoni/pisi
• Kingdom - Fungi
• Sub-division - Ascomycotina
• Class - Ascomycetes
• Order - Erysiphales
• Family - Erysiphaceae
• Genus - Erysiphe
• species - polygoni/pisi
(Gr. Erys = red + siphon = tube)
Identifying characters
Mycelium: External mycelium hyaline, rarely
light brown septate without hyphopodia (one
or two cells, more or less lobed serves as
on organ of attachment), branched with
intracellular haustoria either globular type or
digitate (finger) type.
Conidiophores : Long, hyaline, erect, septate,
arise singly, bears conidia in chain at the tip.
Conidia : Elliptical, barrel shaped (some times
cylindrical) with rounded edges, hyaline,
unicellular and formed in basipetal
succession, size 25-35 x 13-16µ.
Ascocarp : Cleistothecia sharp, black, size 85-
126µ, spherical, minute bodies with
characteristic myceloid appendages (10-30
no.).
Disease cycle
Pathogen survive on infected plant debris in the form of
cleistothecium. In next season, cleistothecial wall ruptures,
ascospores from ascus come out and infect lower leaves.
Conidia produced on lower leaves infection spread by air
and caused secondary infection and this cycle continue up
to crop maturity.
Pathogen also survive on the annual and perennial host
plants in conidial state and recurrently infects the crop
plants whenever available.
Favourable environment
Temp.- 20-240C
Dry weather
Rain damage the conidiophores
Management
Destroy infected crop debris to reduce primary inoculum.
Grow disease free seed preferably certified seed.
Early varieties and early sowing reduce the disease
severity.
Apply sulphur dust 200 mesh 25-30 kg/ha.
Spray Sulfex (3 gm)/ Bavistin (1 gm)/Calixin or
Karathane (1 ml)/lt. Repeat after 12-15 days.
Grow resistant varieties- Rachna, Pant P-5, DMR 11,
HUP 2, JP 885, KFP 103, Ambika, Subhra, Aparna, Azad
P-4, Pusa Panna.
Rust
Erupted pustules appeared on the all green
parts as yellow, rounded or elliptical shaped.
Uredinium small, rounded to oval, powdery,
light brown on both surfaces and green parts.
Telium dark brown or black on the same
pustules where uredinum formed.
Aecium rounded or longitudinal, in groups on
lower surface of the leaves.
Uredospores Teliospores
Pustules
Basidiospores
Aeciospores
Causal Organism - Uromyces fabae/pisi
Autoecious and Macrocyclic rust
• Kingdom - Fungi
• Sub-division - Basidiomycotina
• Class - Basidiomycetes
• Order - Uredinales
• Family - Pucciniaceae
• Genus - Uromyces
• species - fabae/pisi
Identifying characters
Mycelium : Septate at irregular intervals,
intercellular and have knobed haustoria.
Uredospores : Globose, loosly echinulate,
yellowish brown, stalked, size 20-30 µ.
Teleutospores : Round or ovate or
irregular with brown warty wall, roundish
un-thickened apex with papilla, stalked,
unicellular, size 25-38 x 18-27 µ.
Aeciospores : Round to angular or
elliptical, yellow in colour, with fine
warts, formed in cup shaped aecia,
size 14-22 µ in dia.
Disease Cycle
• Seed borne, pathogen survives on broad
bean, lentil and lathyrus plants round the
year serves as primary source of
inoculum.
• Infect new crop plants in coming cropping
season.
Favourable environment
• Temp. - 12-220C
• wet weather.
Management
Deep summer ploughing.
Destroy crop debris and volunteer groundnut
plants.
Select seed from disease free area.
Seed treatment with Carbendazim/ SAAF super
2g/kg of seed.
Spray Triademefon (5 g/10 lt), Oxy carboxin (1.5
g/lt) or Zineb (3g/lt). Repeat after 12-15 days.
Grow resistant varieties – Hans, DMR 11, Type
163.
Downy mildew
• 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.
Causal organism- Peronospora viciae
• Kingdom - Fungi
• Sub-division - Diplomastigomycotina
• Class - Oomycetes
• Order - Peronosporales
• Family - Peronosporaceae
• Genus - Peronospora
Identifying characters
• Mycelium : Hyaline, coenocytic, profusely branched and
inter-cellular.
• Sporangiophores : Determinate, emerge in clusters
from the stomata of under surface of the leaves, long,
slender, unbranched for two third or more of their length,
then dichotomously branched two to seven times. The
ultimate branches called sterigmata, are at obtuse or
acute angles with each other, bear conidia singly at the
pointed tip of sterigmata.
• Sporangia : Spherical, oval or elliptical, single celled,
greenish yellow, borne singly at the pointed tip of
sterigmata.
• Oospore : Spherical, greenish yellow, thick outer wall
marked by large raised reticulations
Disease cycle
• The pathogen survives as oospores on
the affected plant tissues in soil and on
weed hosts.
Favourable conditions
• Atmospheric temperature in the range of
10-20 °C
• relative humidity >90% favours disease
development
Management
Clean cultivation in and around the field.
Select disease free seeds preferably certified seeds.
Destroy infected plant parts before maturity so that oospores will not be formed and
hence primary inoculum will be very less for infection in next season.
Deep summer ploughing reduce the population of oospores in soil resulted in very less
for infection in next season.
Crop rotation for 3-4 years.
Select upland and well drained fields for cultivation.
Early sowing crop escapes from infection.
Rouge out infected plants after 15-20 days after sowing reduces the secondary infection
in the field.
Seed treatment with Metalaxyl (Ridomil) @2.0 g/kg of seed.
Spray Mencozeb (Dithane M 45) @3.0g/lt. or Metalaxyl (Ridomil) or Metalaxyl MZ (Ridomil
MZ) @2.0 g/lt. First spray after 2-3 weeks of sowing and second before flowering.
Grow resistant varieties
Diseases of Cotton
• Angular leaf spot/ Bacterial blight/
Black arm
• Wilt
• Root rot
• Anthracnose
• Powdery mildew
• Leaf spot
• Damping off
Angular leaf spot/ Bacterial blight/
Vein blight/Black arm
It was first reported from USA in 1891.
In India, it is first reported from Tamil
nadu in 1918.
It is prevalent in Maharashtra, MP, UP,
AP and Tamil nadu.
On an average 16-27% loss in yield
recorded. Infection on bolls renders
them un-useful for lint purpose.
1. On cotyledon
Small, round brown water soaked spots on
lower surface of the cotyledon of newly
emerge plants.
Later these spots increase in size, black
and destroy entire cotyledon and
ultimately infected plants die.
2. On leaves
Small, dark green water soaked spots firstly
on lower surface of leaves and later on upper
surface also.
These spots increase in size upto 5 mm,
brown-black, angular in shape, surrounded
by veins of leaves.
After sometimes, these angular spot
coalesce with each other and infected leaves
become blighted, die prematurely and shred
off.
3. On branches
Sunken, dark brown to black, long
lesions on stem, branches and petiole
which girdle these parts and become
black gives rise the Black Arm
appearance.
In severe infection, deep cracks on stem
appears and bacterial ooze out as gum.
4. On bolls
Small, rounded, water soaked, brown to
black sunken spots spread on bolls.
These affect the fibers deeply and seed
rotten.
Fully developed bolls when infected,
opens prematurely.
Causal Organism - Xanthomonas campestris
pv. malvacearum
Kingdom – Prokaryotae
Division – Gracillicutes
Class – Proteobacteria
Family – Pseudomonadaceae
Identifying characters
Bacterial cells rod
shaped, size 1.3-2.7 x
0.3-0.5µ, monotrichous
polar flagellum, Gram –
ve, aerobic, non spore
and capsule forming.
Disease cycle
Bacteria survive in the seed, infected
plant parts and some grasses serves as
primary inoculum.
Secondary infection by means of water,
air and others.
Bacteria enter in the plant surface
through stomata and injuries made by
insects.
Favourable environment
Temp.- 30-350C
RH - 75%
Management
1. Clean cultivation.
2. Destroy infected crop debris.
3. Late sowing, timely irrigation and use of potash reduce the
disease.
4. Delinting of seed with conc. Sulphuric acid for 10-15 min kills the
bacteria present on the surface followed by overnight seed dip in
1000 ppm Streptomycin solution for bacteria present internally.
5. Seed treatment by hot water (560C for 10 min.)
6. Seed inoculation with Pseudomonas fluorescens, P. putida and P.
alcaligenes suppressed the bacterium due to HCN and
siderophore production.
7. Spraying of Streptomycin 500 ppm + Copper oxychloride (3 g/ lt).
Repeat after 15 days.
8. Gossypium arborium and G. haerbacium varieties may be grown.
9. Resistant varieties – BJA 592, P 14, T 128, HG 9, Khandwa 2 and
Badnawer 1.
Anthracnose
• This cotton disease has worldwide
distribution. In India it was first reported
from Bihar in 1918 by Butler and since
then it had been reported from almost
every cotton growing area.
• During certain years, the disease occurs in
severe form causing considerable
reduction in yield.
Symptoms
• The fungus attacks the seedlings, bracts and bolls.
On cotyledons small reddish spots are formed.
• At collar region elongate reddish brown lesions are
formed. Bolls of all stages are attacked.
• Initially small water soaked, circular, sunken,
reddish brown spots appear and their centres
become black as they grow.
• The pinkish-brown spots appear mainly on the
underside of leaves.
• In case of severe infection, area under necrotic
region increases and often results in defoliation.
Causal organism : Colletotrichum gossypii
• Kingdom - Fungi
• Sub-division - Deuteromycotina
• Class - Deuteromycetes
• Order - Melanconiales
• Family - Melanconiaceae
• Genus - Colletotrichum
• Species - gossypii
Identifying characters
Mycelium : Septate, inter and intra
cellular, branched, hyaline.
Acervuli : Cushion shaped, provided with
short conidiophore and sterile setae,
spherical, 70-300 µ dia.
Setae : Straight, unbranched,
tapered towards the apex, brown to
black at base and light brown on the
tip, smooth, thick walled and septate
(3-4 septa).
Conidiophores : Hyaline to brown,
septate, branched at the base,
smooth, short, packed in acervuli, size
20x8 µ.
Conidia : Falcate (sickle shaped), posses
large oil globule in centre, hyaline, thin
walled, unicellular, size 20-80 x 5-7 µ
borne singly on tip of short
conidiophores, oil globule at the
centre.
Disease cycle
• The pathogen is primarily seed-borne
and secondary spread is by air and soil-
borne conidia.
• In moist weather the fungus spreads
rapidly in the field, causing seedling blight,
stem lesions and boll rot.
• When the bolls are harvested the infected
seeds from diseased bolls contaminate the
seeds from healthy bolls.
Favourable environment
• The progress of the disease is much more
in moist than in dry weather.
• If there are rains during the first three
weeks after emergence of the plants,
seedling blight is very common.
• Dense canopy with warm (29-33ºC) humid
weather favours the disease development.
Management
• Choose resistant plant varieties when possible.
• To avoid spreading the disease, keep out of gardens/field tools when
plants are wet and make sure to disinfect all garden tools (one part bleach
to 4 parts water) after use.
• Do not compost infected leaves, fruit or stems and thoroughly
clean up garden areas in the fall, after harvest, to reduce over wintering
sites for the fungal spores.
• Copper oxychloride (3g/lt.) applied weekly, starting when foliage begins to
develop in the early spring and continuing throughout the growing season.
Spray early in the day, and avoid applications during hot weather.
• Seeds may also be treated prior to planting.
• Neem oil spray is an organic, multi-purpose fungicide/insecticide/miticide
that kills eggs, larvae and adult stages of insects as well as prevents
fungal attack on plants.
• Apply early, at the first sign of spring budding, every 7-14 days as a
preventative measure or on a 7-day schedule until existing problems are
eliminated.
Vascular wilt
• Wilt is one of major disease of cotton, found wherever this crop
is grown. It is believed to have originated in Mexico or Central
America.
• In India the disease was reported first reported from Madhya
Pradesh in 1908
• It is widely prevalent in Maharashtra, Tamil Nadu, Karnataka
and other states.
• It occurs more in the heavy, black cotton soils than in sandy
loam soils.
• Gossypium arboreum and G. herbaceum types of cotton are
more susceptible for the pathogen.
• The fungus also infects the other hosts like brinjal, chilli,
tobacco and bhindi.
Symptoms
• All growth stages of cotton plants are susceptible to fusarium wilt.
• Seedlings often die and older plants are subject to sudden,
severe wilting and often plant death before reaching maturity.
• In less severe infections plants may survive but become stunted
and have reduced yield.
• Cotton seedlings infected with fusarium wilt display darkened leaf
veins followed by leaf yellowing and drop.
• High levels of the fungus in the soil may result in seedling death.
• Leaf yellowing in older plants generally starts in the lower leaves
and spreads up the plant.
• Yellowing begins at the edge of the leaf, spreading inwards, and
affected leaves eventually wilt and die.
• Death of the whole plant can occur, starting from the top of the
plant.
• When the stem or root of an infected plant is cut lengthways,
brown discolouration of internal tissue can be seen.
Mechanism/identification
The drying is mainly due to choking of xylem
vessels by mycelia strands of the causal fungus
which hinders the normal flow of water and
nutrients to various plant parts up taken by the
roots.
In field, the stem of infected plant when tear
longitudinally shows blackening of pith region.
Microscopically, transverse section of infected
stem shows presence of mycelial strands in the
xylem vessels.
• Further, the pathogen excrete certain toxic
substance like ‘Fusaric acid’ in the
vascular system of the plants which is
translocated throughout the plant and this
toxin is primarily responsible for wilting.
• The pathogen is known to produce certain
‘pectinolytic, cellulolytic and proteolytic
enzymes’ which cause disintegration of
cell wall. And produces gummy substance
in the vascular vessels. This substance is
also partly responsible for plugging the
vessels.
Causal organism : Fusarium oxysporum f.sp.
vasinfectum
• Kingdom - Fungi
• Sub-division - Deuteromycotina
• Class - Deuteromycetes
• Order - Moniliales
• Family - Tuberculariaceae
• Genus - Fusarium
• Pathogen have dense mycelium with
sporodochium. mycelium is branched, septate and
hyaline which later on develops in to a fruiting body
called sporodochium.
• Macro conidia are formed on small conidiophores
on sporodochium. Macro conidia are sickle shaped,
septate having 3-4 cells, borne on sporodochium.
Macro conidia measure 32-48 x 3.5-4.5 mµ.
• Micro conidia are single celled, ovoid to elliptical,
hyaline and measure 6.4-10.6 x 2.3-3.2mµ.
• Pathogen also produces thick walled structure
chlamydospores which are formed from hyphal cell
terminal or intercalary at the end of the crop season
or during adverse condition.
Disease cycle
• The pathogen perpetuates as chlamydospores on infected
plant debris in the soil.
• Pathogen also survives saprophytically by colonizing dead
host tissues, multiplying and producing conidia.
• Primary infection takes place in field during planting or at
vegetative stage of the plant.
• Infection always occurs through injured root hairs, root lets.
• Spread Fusarium wilt is spread over long distances in
contaminated soil.
• Contaminated soil can be carried on the roots of host plants,
boots and clothing, vehicles, machinery and equipment.
• Fusarium can also be carried in contaminated plant
material, or on seeds.
• Pathogen also survives on pigeon pea, coffee, castor,
alfalfa, solanum etc.
Environmental conditions
• Optimum temperature for disease
development ranges between 25- 280C
while slowed down at higher temperature
(35 -370C).
• Soil moisture of 50-60% is more favorable
for disease development.
• Diffuse light, short day length and
deficiency of nitrogen favour disease
development.
• Heavy soil with a pH of 7.6-8.0.
Management
1. Selection of disease free field for cultivation.
2. Use well drained and leveled fields and do not select low lying areas for cultivation
of crop.
3. Irrigation fields after crop harvest followed by deep summer ploughing exposing
inoculum to hot summer days.
4. Application of well decomposed FYM or compost @5 t/acre favours the antagonistic
fungal and bacterial organisms.
5. Flooding the fields for few days when there is no crop.
6. Grow paddy under submerged condition. Uproot and burn diseased crop debries.
7. Seed treatment by using Conc, H2SO4 @ 1li/10kg. of seed followed by captan 4gm or
carbedazim/ thiophanate methyl/ carboxin @ 2gm/kg of seed 24 hrs. prior to sowing.
8. Crop rotation for 3-4 years raising non host crops like colocasia, mustard, cucurbits,
maize, turmeric ginger cowpea etc. to reduce pathogen’s population.
9. Use of FYM or vermi compost based bio control agent i.e. Trichoderma harzainum, T.
viride as soil amendment @25 kg /ha. Use of oil cakes like neem cakes, Mahua
cakes.
10. To induce resistance in young plants, MoP 7.5 kg. and urea 5.0 kg. mixed in 400 lt of
water for 1 acre, sprayed in morning hours when the plants are 2-3 months old.
11. Grow resistant varieties- Varalakshmi, Vijay, Pratap, Jayadhar, Verum, LD 254 and
327, JLA 101 etc.