Sunflower: Sclerotinia stem rot and Alternaria blight

Sclerotinia stem rot

• Sclerotinia has an extremely wide host range infecting about 370

species of plants. Sunflower crop is more commonly damaged by stalk
rot. Sclerotinia is also a pathogen of common home garden vegetables
and flowers.
 Symptoms
• The symptoms appear on the stalk as a brownish to grey water socked
lesion, most commonly at or near the leaf node.
• canker develops around the stalk, and the decayed tissues have a wet pulpy
appearance.
• The stalk falls at the point of decay and tissue above canker die. The dense
mycelium and sclerotia develop in and outside the stalk when the weather is
wet.
• Finally affected tissues become bleached and have a shredded appearance.
• Stalk decay may move both to upper and lower portion of the stalk upto the
base and head. Sometimes the fungus decays the petiole, reaches to stem
and causes rot.
 Pathogen
• The causal organism is Sclerotinia sclerotiorum (Lib.) de bary. The
pathogen belongs to family Aganomycetaceae, order Aganomycetales and
sub-division Deuteromycotina.
• The pathogen produces hard, black coloured sclerotia which are of different
shapes and size.
• The sclerotia survive in the soil for several years. They germinate and
produce either a white mycelium or a mushroom –like structure called as
apothecia.
• The apothecia are tan to brown measuring about 1/8 to ¼ inch in diameter.
They produce ascospores which can infect the plants. The ascospores are
spread by wind from one sunflower field to another. During dry periods the
ascospores can survive for two to three weeks only.
 Disease Cycle

• During high soil moisture for at least

two weeks the sclerotia germinate to
form apothecia. The apothecia
produce ascospores continuously for
a week or more depending on
moisture. The ascospores are carried
to sunflower plants by wind.
Apothecia are produced abundantly in
crop of dense canopies and which are
frequently irrigated. Ascospores
germinate on a film of water on
senescing plant tissue in the soil
before infecting the plant. They may
also infect the host through wound
caused by insect etc. The pathogen
can infect the seed and remains on the
seed coat in the form of mycelium.
However, the spread of the fungus
through seed is not important. The
leaf infection can lead to stalk rot.
 Control
• The control measures of Sclerotinia stalk rot of sunflower are not to
plant on infested soil and to prevent the build up of sclerotia in soils
either by monitoring of crop for disease incidence or through crop
rotation.
• At present, no resistance is apparently available but some hybrids
show difference in susceptibility. Chemical control is not satisfactory.
Alternaria blight
• Alternaria blight is a major disease of sunflower in humid areas of
India and many other countries where sunflower is grown as oil seed
crop. The yield loss may be from 15-90% and oil loss from 20-30 %.
 Symptoms
• The symptoms of the disease appear as dark brown spots on the
leaves. These spots are irregular in shape and size with dark border
and grey centre. The spots on young plants have a yellow halo. The
spots may coalesce and the leaf withers. On stem, the lesions appear as
dark flecks which enlarge to form long and narrow lesions. The stem
lesions are randomly distributed and often coalesce to form large black
areas resulting breakage of the stem
Symptoms
 Pathogen

• The disease is caused by Alternaria

helianthi (Hansf.) Tubaki and
Nishihara. The pathogen belongs to
family Dematiaceae, order
Moniliales and sub-division
Deuteromycotina. The
conidiophores are cylindrical,
scattered, gemiculate and septate.
The conidia are ellipsoid, slightly
curved with transverse and
longitudinal septa and 40-110 x 13-
28µ in size. The conidia are not
produced in chain.
 Disease Cycle
• The pathogen overwinters on
diseased stalk and can be seed
borne but rarely. Seedling blight
caused by Alternaria may develop
when sunflower plants emerge in
humid condition in infested soil.
Plants at maturing stage are
more susceptible than the young
plants. Safflower and cocklebur
serve as alternate host of A.
helianthi. The disease
development is favoured by 25 –
27 C temperature and atleast of
12 hours wet foliage. Moisture
for longer periods can cause
severe disease.
 Control
• Satisfactory control measures include crop rotation and chopping and
burying of infected plants. Fungicidal sprays and seed treatment with
captan significantly reduce the infection. The disease is controlled by
spraying 0.2% Dithane M-45 any other copper fungicide on the 30th,
40th and 50th days.
Mustard: Alternaria blight, white rust, downy
mildew and Sclerotinia stem rot
Symptoms
• The symptoms caused by A. brassicicola appear as dark coloured
circular lesions on the leaf. Concentric rings may also form in the
lesions.
• The spots may be linear on stem, petioles and pods. Similar spots are
also caused by A. brassicae except that these spots are smaller and
lighter in colour.
• When too many spots are formed on leaves, they die prematurely
indirectly affecting the yield.
Pathogen
• Alternaria brassicicola (Schw.) Wiltshire and Alternaria brassicae
(Berk.) Sacc. are the causal pathogens.
• The conidiophores of A. brassicicola are septate, olive green and
branched measuring 5 – 7.5 X 35 – 45µ.
• Conidia are linear; develop in chains of 8 – 10 and measure 11 – 17 X
50 – 75µ on maturity.
• In A. brassicae, the conidiophores arise in fascicles. The conidia borne
singly or in short chains and are dark, obclavate, muriform and
measure 125 – 225 X 16 – 18µ.
Disease cycle
• In temperate regions, these pathogens are seed borne but in tropical
regions seed borne inoculum does not play any role.
• Spores and mycelium in plant debris serve as major means of
perpetuation especially in tropical regions.
• Conidia are abundantly formed in humid weather and disseminated by
wind and cause infection to mustard even from other cruciferous
plants.
• After infection, the fungi become subcuticular in leaves and
subsequently develop conidia which are dispersed and cause infection
to healthy crop plants.
 Control
• Seed treatment is required in temperate regions only but not in
tropics. Foliar sprays with chemicals like Dithane M-45 and other
copper fungicides have been found very effective to control the
disease.
White Rust
• The pathogen causes both local and systemic infection and symptoms may appear
to all plant parts except roots. In case of local infection, white pustules are
irregularly formed on leaves and stems.
• These pustules may merge together to form larger pustules. The host epidermis is
ruptured showing white powder of spores. When fungus becomes systemic it
causes deformities to stem and floral parts.
• Due to hyperplasia and hypertrophy of tissues, the axis of the inflorescence and
flower stalk become thickened, floral parts become swollen and green to violet in
colour.
• The petals look like sepals and stamens become leafy. The carpels may be open
and ovules and pollen grains atrophied causing sterility to ovary.
• The swollen parts carry the oospores of the fungus. In case of early infection
whole plant may remain dwarfed and only small leaves will develop.
• Swelling on stem may be restricted to some portion or may spread to whole stem.
The stem and floral axis may twist showing a zigzag appearance and lateral shoots
may appear on the stem.
Pathogen
• The causal pathogen is Albugo candida (Lev.) Kuntze also known as Cystopus candidus Lev.
The pathogen belongs to family Albuginaceae, order Peronosporales and subdivision Mastigomycotina of Eumycota.
• The pathogen is an obligate parasite. The mycelium develops intercellularly with knob shaped haustoria.
The sporangiophores develop from the mycelium and produce sporangia in basipetal succession in chains.
• A gelatinous pad is formed between the sporangia which swell during the presence of moisture thus helps in disintegration and freeing
the sporangia. The sporangia germinate and produce zoospores in water.
• The zoospores swim in water with the help of flagella and later become round and encysted and go for hibernation. Under favourable
conditions (optimum temperature 10 C and maximum 25 C) the encysted zoospores germinate by producing germtube and infect the
host through stomata and form new mycelium.
• Sexual organs are formed from the mycelium within intercellular spaces of systemically invaded tissues.The oogonium is globose,
terminal or intercalary and is clearly defined into a periplasm and a single central oospere.
• The antheridium also develops near the oogonium and at the point of their contact, the wall become thin and a papilla of the oogonium
protrudes into the anthridium but disappears soon. The fertilization tube from the antheridium enters into the oosphere passing through
the thin wall.
• The nuclei of both antheridium and oosphere undergo two mitotic divisions and form a granular body known as coenocentrum in the
oosphere.
• A single female functional nucleus is attached at a point near it. The fertilization tube penetrates the coenocentrum and finally discharge
a single male nucleus which fuges with the female nucleus and thus fertilization takes place resulting the formation of oospore.
• The oospore is formed by the development of a thick and tuberculate wall around the oosphere. The fuged nucleus of oospores
undergoes several mitotic and one meotic division and thus forms about 30 nuclei. These oospores germinate and produce zoospores for
further infection to the healthy plants.
Disease cycle
• The pathogen perpetuates through oospores lying in the soil or on
plant debris. Weed hosts also serve as a source of primary inoculum.
Secondary spread takes place by means of sporangia and zoospores.
Moist and cool weathers favour the development of the disease.
 Control
• Early sowing is useful to avoid floral malformation.
• Other measures like clean cultivation, destruction of plant residue and
crop rotation are also useful to avoid disease in the crop.
• If required, fungicides such as Dithane M -45 @ 0.2% etc. should be
sprayed. Resistant varieties like Kranti, TM-20, RN-510, MDYR-
2029, NPJ-81, PAB-2001 and PAB2002 etc. should be sown.
 Downy mildew

• The disease is commonly found on mustard and damage plants at early

stages of growth and also to inflorescence at later stages.
• The disease can cause a loss upto 37-47 % with a mixed infection with
white rust in pod yield and upto 17-32 % in seed yield of Brassica
juncea.
Symptoms
• Pulpish brown spots are formed underside the leaf. The upper surface
above the lesions show tan to yellow colouration. The cottony growth
of the fungus appears on the Pulpish brown spots are formed underside
the leaf. The upper surface above the lesions show tan to yellow
colouration. The cottony growth of the fungus appears on the
 Pathogen
• The causal pathogen is Peronospora parasitica (Pers.) ex Fr. and belongs to
family Peronosporaceae, order Peronosporales and sub-division Mastigomycotina.
• The pathogen is an obligate parasite and the mycelium is intercellular with
branched haustoria.
• The numerous branched conidiophores emerge through the stomata on the lower
surface of leaves.
• The conidiophores are dichotomously branched 6-8 times at the tip. A single
conidium is formed on each tip of the branch and is oval, ellipsoidal and hyaline,
and measure 24-27 X 15-20µ.
• The conidia fall of and germinate through a lateral germtube. Sexual organs
develop late in the season.
• The oogonium is spherical and fertilized by a single antheridium. The oospores are
globose measuring 26-43µ in diameter and are enclosed in a crest-like fold and
appear pale yellow in colour and germinate by a germ tube. More conidia develop
at 13 C than 18 C.
Disease cycle
• The pathogen perpetuates in soil through oospores. The seeds may
also carry the infection of oospores as a contamination. Wild hosts
also serve the source of primary inoculum. Secondary spread is
through conidia.
 Control
• Cultural practices like crop rotation avoiding cruciferous plants,
eradication of weed hosts, deep summer ploughing and destruction
of crop residue are important.
• Spraying with fungicides like Dithan Z-78 (0.3%), Blitox-50 (0.3%) etc.
is useful to control the disease.
• In India at Pantnagar mustard varieties YRT-3 and TMV-2 were found
resistant to downy mildew pathogen.
 Sclerotinia stem rot
• Indian mustard (B. juncea) is the major oil seed crop in India. The
losses caused by the disease in seed depend on the time of disease
appearance.
• Maximum losses upto 92.32 % were recorded in seed yield when the
plants were infected at the age of 70 days.
Symptoms
• First symptoms of stem rot appear in the field 65-70 days after
sowing.
• Diseased plants can be identified by sudden drooping of leaves and
finally drying of plants.
• Lodged stems come in contact of soil and develop watery lesions with
snowy white mycelium and black, irregularly shaped sclerotia.
Pathogen
• The causal pathogen is Sclerotinia sclerotiorum (Lib.) de Bary and
belongs to family Aganomycetaceae, order aganomycetales and sub-
division Deuteromycotina.
• The pathogen infects about 400 other plant species.
Disease cycle
• The primary survival structure of the fungus is sclerotium.
A sclerotium is a hard resting structure consisting of a light coloured interior
portion called as medulla and an exterior black protective covering called
the rind.
• The rind contains melanin which is highly resistant to degradation. The
medulla consists of fungal cells rich in glucans and proteins.
• The sclerotia can come to the fresh crop by wind from infected fields,
remains in plant debris, through contamination or irrigation.
• The sclerotia are also carried by seed or contaminated soil. The disease
cycle starts from sclerotia in the soil.
• They germinate by carpogenic germination which results in the production
of a small mushroom-like structure called as apothecium.
• The apothecium produces ascospores which are wind transported to
healthy plants.
• The sclerotia may also germinated directly producing mycelium on certain
hosts.
 Control
• The pathogen is soil borne and the sclerotia can survive in soil for
several years, crop rotation of non-host crops of atleast 4-5 years may
be helpful.
• Use of certified seeds, avoid excessive irrigation, sowing in rows with
wider row spacing and destruction and burning of crop debris are
important to avoid stem rot disease.
• Chemical controls are most effective when combined with cultural
control strategies and are usually not necessary if sound cultural
practices are followed.
• In India, genotypes ZYR-6, PCR-10, cutlass etc. were found resistant.