Important Diseases of Wheat (Triticum aestivum L)

Rusts of Wheat Caused by Fungus Puccinia

1. Black or Stem Rust:- Puccina graminis f.sp. Tritici

2. Brown or Leaf Rust:- Puccina recondita

3. Yellow or Strip Rust:- Puccina striiformis f.sp. Tritici

4. Loose Smut :- Ustiago nuda tritici (Ustilago tritici)

5. Karnal Bunt - Neovassia indica

6. Powdery Mildew - Erysiphe graminis var. tritici

7. Alternaria Blight - Alternaria triticina / Bipolaris sorokiniana

8. Yellow Ear Rot:- Clavibacter tritici & Anguina tritici

9. Ear Cockle:- Anguina tritici

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 Symptoms and Signs
On wheat and other grass hosts:
After 7 to 15 days infection
Elongated to irregular shaped pustules (uredinia) of brick-
red urediniospores break through the epidermis and
develop on the upper leaf surfaces, leaf sheaths, glumes
and awns.

29
 Black or Stem Rust:- Puccina graminis f.sp. Tritici
Distribution:- Black rust of wheat world wide distributed where ever wheat is
grown.
Symptoms:-
1. The black or stem rust comes in later stage of crop.
2. 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.
3. Uredial pustules/sori are oval to spindle shaped and dark reddish brown (rust) in
color.
4. Uredial pustules/sori emerge by rupturing 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.
5. As the infection advances teliospores are produced in the same pustule (at the
end of crop season) . The colour of the teluto pustule changes from rust colour
to black as teliospore production progresses.
6. If a large number of pustules are produced, stems become weakened and lodge.
7. In diseased affected plants the transpiration is increased.
Microscopically, these red spores are
covered with fine spines

30
Berberis vulgaris: dicot
Stage 0:Spermagonium
Stage I: Aecium

Wheat(Triticum aestivum L.): Monocot

Stage II: Uredium
Stage III: Telium
Stage IV: Basidium

25
Rusts can produce up to five spores types during their life
cycle
0-Pycniospores (Spermatia)-Haploid gametes in
heterothallic rusts.
I-Aeciospores-non-repeating dikaryotic vegetative spores
II-Urediniospores-repeating dikaryotic vegetative spores.
These spores are referred to as the repeating stage because
they can cause auto-infection (re-infect the same host
from which the spores were borne). These spores are
red/orange and are a characteristic sign of rust fungus
infection.
III-Teliospores-Diploid spores that produce basidia and
are the survival stage of life cycle. These are sexual spores.
IV-Basidiospores-stem from basidia. Haploid spores
which infect the alternate host.
50
Causal organism:- Puccina graminis f.sp. Tritici
• Puccina graminis f.sp. Tritici is a obligate parasite always require living host for
growth and development, like other rust pathogens, it is polymorphic species producing a
succession of different type spores.
• It is hetericious fungus, only the uredospores and teliospores are produced on wheat/cerial
hosts.
• Basidiospores are produced on inactive substrate where teliospores are present.
• The pathogen attacks other host (Barbery) to complete its life cycle.
• Other spores are Pycniospores (produced in pycnia) 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.
Aeciospores (produced in aecia), produced on the lower leaf surface, are yellow.
• They are bell-shaped and extend as far as 5 mm from the leaf surface.
Puccinia Uredo-
sporangium-
Wheat

18
Stage III: Telia bearing teliospores
(n+n>2n)

19
Germinated Teluto spore and formation of
Basidium & Basidio spores
Basidio spore
Sterigmata (+) Or (-)

Epibasidium

Hypobasidium Basidium

21
Infection of Puccinia on Barberry
leaf Lower and Upper sides

22
Stage I: Aecia bearing
aeciospores (n+n)

23
Disease Cycle
Pre disposing (Environmental)Factor
Warm ‐humid weather conditions with intermittent rains.
Hot days 25‐30ºC and mild nights (15‐20ºC)
Leaf wetness from rain or dew

Management:-
➢Cultural practices
➢Grow early maturing resistant wheat varieties.
➢Appropriate spacing and fertilizer (N) application
Chemical control
➢Prophylactic sprays of Mancozeb (Dithane Z‐78) @ 0.25%
➢Tilt (Propioconazole) 25 EC @ 0.1% at 15 days intervals
 Brown or Leaf Rust:
Puccinia recondita f. sp. tritici.
The disease is restricted to wheat and certain grasses, it is earlier rust appear in India (Pusa Bihar when
crop is 5-6 week old)
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.
➢ Heavy infection which extends to the flag leaf results in a shorter period of grain fill and small
kernels.
➢ The pustule gathered in clusters or irregularly scattered but never in rows.
➢ The pustules are bigger in size than yellow rust.
➢ Severe conditions the fungus interferes with leaf function (transpiration rate increased which
results late maturation of ears and poor grain filling).
 Symptoms and Signs
Scattered oval to circular small
brown pustules (rusty-red uredospores)
containing a powdery mass of orange to
red-orange spores develop on the upper
leaf surfaces, leaf sheaths, glumes and
awns.

38
Causal Organism:- Puccinia recondita
• Uredospores rounded (spherical) brown in colour 16-28 micron in size, minutely echinulate and
single uredospore have 7-10 germ pore.
• Infection of uredospore by germtube enter through stomata.
• The apprisorium formed germtube over the stometa which in contact with gaurd cells.
• Within substomatal cavity the invading hypha expends into a vesicle from which branching hypha
develop to invade the leaf tissues.
• The telutospores of the mycelium similar to P. Striformis the are 2-3 celled, smooth and brown in
colour. The number of chamber in the sorus is more than yellow rust.
• The pycnidial and aecial stage of this fungus formed on species of Thalictrum (Thalictum
polygomum) and about 11 other species are reported to susceptible to this rust fungi.
• The alternate host of the fungus do not occur in the plain region in India.

Pre-disposing (Environmental) factors:-

▪ Warm ‐humid weather conditions with intermittent rains.
▪ Hot days 25‐30ºC and mild nights (15‐20ºC)
▪ Leaf wetness from rain or dew
Management:-
• Mixed cropping with suitable crops.
• Avoid excess dose of nitrogenous fertilizers.
• Spray Zineb at 2.5 kg/ha or Propioconazole @ 0.1 %, Dithen M45 @ 105-2.00Kg/ha
• Grow resistant varieties like PBW 343, PBW 550, PBW 17,Vijaya , Rohini BL-1473, Gautam
Black pustules form as the plant approaches
maturity(Telia). Microscopically, teliospores are
two celled and thick walled.
Life Cycle of Puccina recondita
 Yellow or Strip Rust:- Puccina striiformis f.sp. Tritici
Distribution:-
In India:-Hills, foothills, Plains of north wstern India, Southern hill zone.
In World:- Euro, Australia (Commonly known as yellow rust).The yellow rust is most destructive
than black stem rust, due to destruction of crop foliage the affected plants produce severely shrivelled
grains, which results drastic reduction in production.
Symptoms:-
▪The disease generally appear in earlier than black rust and before grain development.
▪ Mainly occur on leaves than the leaf sheaths and stem.
▪Bright yellow pustules (Uredia) appear on leaves at early stage of crop and pustules are
arranged in linear rows as stripes.
▪The stripes are yellow to orange yellow. In severe conditions this serial arrangement change
into large patches.
▪Uredospores do not break epidermis quickly as in other rusts. But in last epidermis breaking
the yellow spore mass of uredospores are exposed in air.
▪After some time telia appear on under surface of leaves which are also arranged in long
stripes and are dull black in colour.
▪Plants attacked by yellow rust generally show a poorly developed root system because rust
fungus interfear in translocation of food material from leaves to roots.
 Symptoms and Signs
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.

44
Mature pustules will break epidermis
and release yellow-orange masses of
urediniospores

45
Causal Organism:- Puccina striiformis f.sp. Tritici
The uredospores of yellow rust are nearly spherical, binucleate and unicelluler, their size is
very variable being 23-35 X 20-25 micron, spore wall is colourless and may possess 6-16
germpore. After germination of spore, germtube form the appresorium over the stomata of leaf
surface. Appresorium form a tube which enter through stomatal opening and form a large thick
walled cylindrical substomatal vesicle which placed just bellow the stomatal slit. From here an
infection hypha arise, the mycelium expend rapidly, some short hypha form club shaped haustoria,
which obtain food from adjoining cells. These hyphae collect beneath the epidermish and form the
uredosori. The teliospores are dark brown in colour, often flattened on the tip. Sterile paraphyses
are also present at the end of sorus. The teliospore are capable for the emidiate germination at the
time of maturity.
Pre-disposing (Environmental) Factors:- Uredosori Teliospores
• Cool ‐humid weather conditions with
• intermittent rains.
• Cooler climates (10‐16ºC )
• Leaf wetness from rain or dew
• Heavy dew or intermittent rains can
• accelerate the spread of the disease
Uredospores Uredopstules
Stages of rusts in wheat

49
Life cycle of Puccinia striiformis
Pre-disposing (Environmental) Factors:
•Cool ‐humid weather conditions with intermittent rains

•Cooler climates (10‐16ºC )

•Leaf wetness from rain or dew

•Heavy dew or intermittent rains can accelerate the spread of the disease.

Management of disease
➢Mix cropping and crop rotation.

➢Avoid excess dose of nitrogenous fertilizers.

➢Dusting of sulphur @ 35- 40 kg/ha.

➢Spay the crop with Mancozeb @ 2g/l.

Grow resistant varieties and early intervention are the key principles of controlling wheat rust
diseases.
 Disease Cycle of rusts in India
Rust Recurrence in India
-Mehta from 1920 to 1950 studied the
perpetuation of rusts in more detail and proved
that the
• Barberis species found in India do not play any
role in the perpetuation of stem rust in India.
• Similarly it has been proved that Thallictrum
species occurring in the hills are also not playing
any role in the perpetuation of stem rust.

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•Rusts over summer in cooler
climates of hills on self-sown wheat
plants, ratoon tillers and also on
summer crop grown in Nilgiri and
Palini hills in south India. The fixed
path between Nilgiri and Palini hills
to Narmada and Tapti river belt is
known as Puccinia path.
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•Initially, Mehta had shown the movement of leaf rust
both from north and south Indian hills. Later, Joshi
and his team supported this view and further
demonstrated that leaf rust ( P. recondita ) spreads
both from southern and northern hills. It is introduced
from Nilgiri and Palini hills and is established in the
plains of Karnataka and Tamil Nadu in South India.
The rust population from southern foci moves
northwards towards Maharashtra and Madhya
Pradesh. The spread of leaf rust over the Indo-
Gangetic plains is predominantly from the warmer
north-eastern region and is influenced by the number
of rainfall during winter month.
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•Stripe rust (P. striiformis) is a major problem only in
cooler parts of the country especially north and
north-western region. Its infection in south, central
and eastern parts remains isolated and seldom
become a serious threat to wheat. In north India, the
inoculum moves from northern hills and get
established in the plains of Punjab, Haryana and
western Uttar Pradesh. In the foot hills and northern
Indian plains stripe rust spread much faster by
uredospores than leaf rust due to favourable cool
temperature but the spread after February is checked
due to rise in temperature and this time the telial
stage is developed which does not play any role in
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the spread of the disease.
 Loose Smut Of Wheat:- Ustilago nuda f.sp. Tritici
This disease is very common and widespread. It causes great
damage in the wheat growing tracts of India, particularly in the
Punjab, Uttar Pradesh and certain districts of Madhya Pradesh.
Symptoms:-
• It is very difficult to detect infected plants in the field until
heading. At this time, infected heads emerge earlier than
normal heads.
• The entire inflorescence is commonly affected and appears as
a mass of olive-black spores, initially covered by a thin gray
membrane. Once the membrane ruptures, the head appears
powdery. Diseased
• Spores are dislodged, leaving only the rachis intact. In some
cases remnants of glumes and awns may be present on the
exposed rachis. Smutted heads are shorter than healthy heads
due to a reduction in the length of the rachis and peduncle.
• All or a portion of the heads on an infected plant may exhibit
these symptoms. While infected heads are shorter, the rest of
the plant is slightly taller than healthy plants.
• Prior to heading affected plants have dark green erect leaves.
Chlorotic streaks may also be visible on the leaves.

Healthy
 Causal Organism:- Ustilago tritici Infected Embryo

• The causal organism of this disease is Ustilago tritici (Pers.) Rostr. and the host
is Triticum vulgare.
• The mycelium of the fungus lies dormant in the grain therefor the fungus is
internaly seed borne .
• It has a dikaryotic mycelium. The hyphae ramify the intercellular in spaces of
the host tissue. They absorb nutrition from the host cells by diffusion.
• The mycelium grows keeping pace with the growth of the host plant. It is
chiefly confined to the stem.
• At the time of flowering and when the inflorescence is still enclosed by the boot
leaf, the mycelial hyphae enter into the ovaries of flowers.
• Within the ovary each hypha grows vigorously and branches repeatedly to form
a dense mass of hyphae The latter destroy the host tissue in the ovaries and
surrounding floral parts.
• The cells of these hyphae are binucleate. The hyphae undergo additional
septation to form short binucleate cells. Healthy Embryo
• These cells swell and round off to form binucleate smut spores.
• The smut spores are called the teliospores and are produced in enormous
numbers
• They are spherical to oval and measure 5.9 µ in diameter.
• They have a finely echinulate thick spore wall which is olivaceous brown but
slightly lighter on one side.
Teliospores
Classification:
Phylum: Basidiomycota
Class: Ustilaginomycetes
Sub-class: Ustilaginomycetidae
Order: Ustilaginales
Family: Ustilaginacae
Causal organism: Ustilago tritici (Persoon)
Rostrup (1890)
(Obs. syn. Ustilago nuda var. tritici Schaffnit)
(Syn. Ustilago segetum var. tritici (Pers.) Brunaud
(1878))
(Mathur and Cunfer 1993, and Wikipedia)
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Disease Cycle of Loose Smut ( Ustilago tritici)
Pre-disposing (Environmental) Factors:-

• Wind

• Moderate rains

• Cool temperatures (16-22 degrees Celsius)

 Management of Loose Smut of Wheat
• Disease control:
The disease is internally seed borne and as such spray of
fungicides is not effective in controlling the disease.
• Seed treatment
• Use of resistant varieties:
The most successful method is the use of resistant varieties.
• Crop rotation:
Crop rotation at suitable intervals is also effective in disease
control.

65
Seed treatment
(a) Hot water treatment:
The seeds are first soaked in water for five hours at 20˚C , the
water is drained off and then they are treated with hot water
at 49˚C for about a minute and finally with hot water at 52˚C
for 11 minutes. Immediately after the hot water treatment ,
the seeds are cooled off by dipping in cold water and dried.
The dormant mycelium inside the seed dies off by this
treatment.
(b) Use of systemic fungicides:
Several fungicides like carboxin, vitavax and benlate @ 2.0
g/Kg seed and Propioconazole @ 0.1% are used for seed
treatment to reduce the pathogen infectivity. A combination
of vitavax with thiram is very effective for disease control.
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 Karnal Bunt of Wheat:- Neovossia indica
Distribution:-
The disease first reported from Karnal, Hryana by Mitra 1931. This disease
generally found in Panjab and western district of UP, Uttarakhand. In now days
this disease present in Delahi, Hryana, Rajasthan, Punjab, western part of UP
and Uttarakhand.
Symptoms:-
➢ Symptoms of Karnal bunt are often difficult to distinguish in the field due to the
fact that incidence of infected kernels on a given head is low. There may be
some spreading of the glumes due to sorus production but it is not as extensive
as that observed with common bunt.

➢ Symptoms are most readily detected on seed after harvest.

 Karnal Bunt of Wheat:- Neovossia indica
➢ The black sorus, containing dusty spores is evident on
part of the seed, commonly occurring along the
groove.
➢ Heavily infected seed is fragile and the pericarp
ruptures easily.
➢ The foul, fishy odour associated with common bunt is
also found with karnal bunt.
Healthy ear Diseased ear
➢ The odour is caused by the production of
trimethylamine by the fungus.
➢ Seed that is not extensively infected may germinate
and produce healthy plants. Healthy seeds

➢ While diseased seeds usually retain a partial seed

coat, the embryo and part of the endosperm have been
converted to masses of small black spores.
Infected Seeds
Causal Organism:- Neovocia indica
•The pathogen is heterothallic and undergoes sexual reproduction after teliospore germination.
•Primary and secondary sporidia or hyphae as compatible mating types must fuse to form a
dikaryon which enhances the chances of variation due to heterozygosity that plays a significant
role in the production of new variants.
• The pathogen infects the ovaries in the growing wheat heads and converts all or part of the wheat
seed into a black powder consisting of millions of teliospores.
•The major impact of Karnal bunt of wheat is on quality and not on reduction in yield. Infected
seeds are the most important carrier of pathogens for trans-regional and long-distance dispersal of
the spores.
Pre-disposing (Environmental) factors:-
•Progression of disease is favoured by moderate temperatures(16-24 degrees Celsius).
• high relative humidity or free moisture.
• cloudiness, and rainfall during anthesis.
• Disease Cycle:-
• The fungal spores are transferred by means of air, equipment, tools
or by man moving from milling places.
• The spores remain viable for several years in soil ,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.
• On germination, each teliospore produces promycelium which
bears 110–185 primary sporidia at its tip.
• 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 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 .
Disease Cycle of Karnal Bunt (Neovotia indica)
Management:-
▪Karnal bunt is difficult to control due to its intermittent nature. Therefore, quarantine
restriction is applied by approximately 70 countries on wheat trade where Karnal bunt
is known to occur .
▪Use of resistant varieties eg. PBW 502, N-75-3 and N-75-5
▪Seed treatment with Carboxin + thiram (Vitavax 200 or RTU-Vitavax-Thiram)
▪Foliar application of fungicides between late boot and flowering.
▪Propioconazole, Agrozim and Bavistin (carbendazim) and Bayleton (triadimefon).
▪ Foliar spray by fungicide, propiconazole (Tilt 25EC20.1%) should be given at the
time of anthesis as the disease is air borne.
▪Integration of propiconazole with bioagent fungus (Trichoderma viride) gives almost
complete control.
▪The number of viable teliospores in the soil can be reduced by increasing the time
between wheat crops.
▪ Rotation with non-host crops may reduce viable spores sufficiently to control the
disease
Powdery Mildew of Wheat: - Erysiphe graminis var. tritici
Distribution:-
Powdery mildew, is one of the most common and damaging
foliar diseases in wheat. Powdery mildew exists almost
everywhere wheat is grown. As an obligate parasite, the
fungus grows only on living tissue.
Symptoms
Powdery mildew can easily be diagnosed by the white,
powdery patches that form on the upper surface of
leaves and stem.
Greyish white powdery growth appears on the leaf,
sheath, stem and floral parts.
Powdery growth later become black lesion and cause
drying of leaves and other parts. Severe infections
can result in wheat plant stunting.
Heads on the later tillers may show more heavy
infection because they reside lower in the wheat
canopy, where humidity remains high.
The leaf tissue on the opposite side of growth turns
yellow and then changes to tan or brown.
Causal Organism:- Erysiphe graminis var. Tritici
Fungus produces septate, superficial, hyaline mycelium on leaf surface with short conidiophores.
The conidia are elliptical, hyaline, single celled, thin walled and produced in chains.
Dark globose cleistothecia containing 9-30 asci develop with oblong, hyaline and thinwalled ascospores.

Pre-disposing (Environmental) Factors:-

▪ Use of high dose of nitrogen fertilization and high stand densities.
▪ Cool, moist weather conditions with high relative humidity
97 to 100 percent – enhance germination of the fungal infection.
• Optimum temperatures for development of powdery mildew
are 59 to 70 degrees F, typically making it the first leaf disease
of the season.

Conidia and conidiophores

Disease Cycle :-
Typically, the lifecycle of powdery mildew begins in the fall, Management:-
soon after winter wheat planting.
Fungus remains in high hills during summers in infected plant ▪ Crop rotation with non
debris as dormant mycelium and asci. host crop can help deter
Primary spread is by the asciospores and secondary spread
through airborne conidia. diseases.
Spring infections occur when spores are dispersed by wind ▪ Good weed control from
and rain.
As the major cause of powdery mildew, conidiospores are preplant, at planting and
produced in large numbers from initial infections. throughout the growing
Windborne spores land on plant surfaces and germinate,
resulting in new infections on healthy plants or secondary season also helps protect
infections on plants already infected. against disease
New spores can reproduce in seven to 10 days.
The fungus can spread throughout the growing season, ▪ Spray Wettable Sulphur
especially on susceptible varieties infected in early spring 0.2% or Carbendazim @
and when weather conditions are favourable.
500 g/ha.
 Alternaria leaf blight of wheat:-
Alternaria triticina
Distribution
The occurrence of a blight disease caused by an Alternaria
species on wheat [Triticum spp.] was first recorded by
Kukarni (1924) from Maharasthra, now a days disease are
known to occure in Bihar, Uttar Pradesh, Andhra Pradesh .
In addition, the fungus has been reported from North
Africa, Mexico, Bangladesh, Italy, the Middle East ,
Nigeria, Lebanon, France ,Greece, Macedonia, Turkey,
China and Argentina.
Symptoms
Lower most leaves are always the first to show the sign of infection,
which gradually spreads to the upper leaves.
The disease first makes it appearance as small, oval, discolored
lesions, irregularly scattered on the leaves.
The spots became irregular in shape as these enlarge and take up dark
brown to grey color.
As the disease progresses, several spots come closer and cover large
leaf areas, eventually resulting I death of the entire leaf.
A bright yellow marginal zone is sometimes seen around the spots.
In case of severe attack, leaf sheaths, awns and glumes are also
infected.
Black powdery spores of the fungus cover the lesions at this stage
under moist conditions.
These spores are disseminated by wind and cause disease on healthy
leaves and plants.
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 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.
Mycelium 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 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. 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.
• Favourable conditions:-High humidity or irrigation, as well
as warmer temperatures (20 to 25ºC) favor infection and disease
development.

• Management:-
• Pre soaking of seeds in water for 4 hrs. Followed by 4hrs. Water
treatment at 520C for 10 minutes.

• 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.
 Seed gall nematode of wheat/Ear cockle/Tundu disease of wheat
Distribution:-
• First reported in England in 1743 by Needham.
• First reported in Nepal in 1966 and caused
considerable loss in Rupendehi and Nawalparasi.
• The nematode very often present in association with
the bacterium (Clavibacter tritici) causing tindu
disease of wheat.
• Corinetoxin produced with association are toxic to man
and even death of cattle and sheep when such infected
seeds are feed.
• Known to prasent in entire major wheat growing areas
of the world, more common in europ, Asia, Africa and
India.
Causal Agent:- Anguina tritici
• Pathogen is large nematode about 3.2mm long and 120
micron in diameter.
• Host: specific to wheat.
• Nematode lay eggs and produces all its juvenile stages
and adults in seed galls.
 Symptoms of disease
• The nematode affects all growing stages.
Infected crop
• Infected seedlings are more or less severely
stunted and show Characteristics rolling and
twisting of 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.
• Plant show spreading nature and tents towards
more tillering.
• 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 its
kernel turned into nematode galls.
• Galls are shiny at first but turn brown or balck
as the head matures.
• Mature galls are hard, dark, rounded and shorter
than normal wheat kernels. Healthy
 Galled seeds Healthy seeds

Stem
Thickening

Thousands of J2 liberating from wheat gall

 Life Cycle and epidemiology
➢The nematode lay eggs and all the juveniles and adult stages are produced in seed galls. They can survive up
to 28 years in galls under dry conditions.
➢Each gall contains 10000 to 30000 or even more larvae.
➢The galls fallen on the ground or sown with the seed soften during warm, moist weather and release second
stage juveniles.
➢They swim upward in presence of film of water and feed ecto-parasitically on the tightly compact leaves near
the growing point, causing the leaves and stem malformed.
➢As inflorescence being to form, the juveniles enter to floral primordia and produce third and fourth stage
juveniles within 3-5 days of invasion.
➢The infected floral primordia become seed galls each containing about 80 or more adult males and females.
➢Each female lay up to 2000 eggs within freshly formed galls over several weeks so that each gall contains
10000 to 30000 eggs.
➢The adults die soon after the eggs are laid. The eggs hatch producing first stage larvae within the egg and first
molt soon producing second stage juveniles by the time of crop harvest.
 Interaction of nematode with bacterium
➢In tundu disease of wheat the nematode act as vector.
➢Initial symptoms of disease are same as ear cockle.
➢Low temperature and high humidity favours this disease.
➢Yellow slime ooze from leaves, stem and ear heads.
➢Upon maturity, turns brown.
➢No grain formation.
➢Ear heads may not emerge from boot leaf.

Management:-
❖Use only healthy seed from healthy crop.
❖Cleaning of contaminated seeds by sieving or floating in 10% salt solution.
❖Follow 2-3 years crop rotation with non host crop like barley and oat.
❖Hot water treatment of seed, first soaking seed in normal water for 4-5 hours and treating at 54 oC
❖ for 10 minuts.
❖Soil application of nematicides such as Nemaphos, Aldicarp @ 10 kg a.i/ha.
 Red Rot OF SUGARCANE

Red rot of sugarcane was first recorded from java in 1883 and in
Indian subcontinent by Barber and later by Butler in 1906.
 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 after 16
- 21 days after infection and drying of entire
cane takes another 10 days time.
• When the affected cane is split opened, the
pith 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
alcoholic odour.
 Pathogen: Colletotrichum falcatum
(Sexual stage: Physalospora tucumanensis
or Glomerella tucumanensis)

• Septate mycelium which is intercellular and intra

cellular.

• Asexual fruiting body acervuli with setae are formed.

• Sickle shaped conidia with large oil globule in the

center borne on short small conidiophores.

Conidia
Disease cycle of red rot of sugarcane .
 Disease cycle
• The fungus is sett-borne (Seed-borne).
• The fungus also persists in the soil on the diseased clumps and stubbles as chlamydospores
and dormant mycelium.
• The primary infection is mainly from infected setts.
• Secondary spread in the field may be through irrigation water and cultivation tools.
• The rain splash, air currents and dew drops also help in the spread of conidia from the
diseased to healthy plants in the field.
• The fungus also survives on collateral hosts like Sorghum vulgare, S. halepense and
Saccharum spontaneum.

Favourable Conditions:
Mono-culturing of sugarcane, successive ratoon cropping, water logged conditions and injuries
caused by insects.
 Management

• Removal and destruction of infected plant debris, stubbles and trash.

• Deep tillage to incorporate the left over debris.
• Adopt crop rotation by including rice and green manure crops.
• Select the setts from the disease free fields or disease free area.
• Avoid ratooning of the diseased crop.
• Avoid flow of irrigation water from diseased to healthy plants.
• Soak the setts in 0.1% Carbendazim solution for 20 minutes before planting.
• Hot water treatment of setts at 52 ° C for 30 min or 50 ° C for 2 hours followed by steeping in
0.1% carbendazim solution.
• Setts can be treated with aerated steam at 52° C for 4 to 5 hours and by moist hot air at 54 °
C for 2 hours.
• Grow resistant varieties.
 Sugarcane Smut

• It is considered as an important disease and is common throughout the world.

• In India, it is widely prevalent in almost all the sugarcane growing tracts.
 Symptoms
• Production of long, whip like, black, sooty shoot
from floral shoot which may be often several feet
in length and very much curved.
• A thin silvery membrane covers the whip, which
have 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.
 Pathogen

• The causal fungus of the disease is Ustilago scitaminea

(Sporisorium scitaminium
• Mycelium is septate and intercellular.
• The teliospores are echinulate, light brown and
spherical, measuring 6.5 – 8.5 µ in diameter, globose to
subglobose and reddish brown in colour.
• 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. Teliospores
Disease Cycle
 Disease cycle

• Teliospores may survive in the soil for long periods, upto 10 years.
• The spores and sporidia are also present in the infected plant debris in the soil.
• The smut spores and dormant mycelium also present in or on the infected setts.
• The primary spread of the disease is through diseased seed-pieces (setts).
• In addition, sporidia and spores present in the soil also spread through rain and irrigation
water and cause soil-borne infection.
• The secondary spread in the field is mainly through the smut spores developed in the whips,
aided by air currents.
• The fungus also survives on collateral hosts like Saccharum spontaneum, S. robustum,
Sorghum vulgare, Imperata arundinacea and Cyperus dilatatus.

Favourable Conditions :
• Mono-culturing of sugarcane, continuous ratooning and dry weather during tillering stage
favours the disease.
 Management

• Plant healthy setts taken from disease free area.

• Remove and destroy the smutted clump (Collect the whips in a thick cloth bag/polythene
bag and immerse in boiling water for 1 hr to kill the spores).
• Discourage ratooning of the diseased crops having more than 10 per cent infection.
• Follow crop rotation with green manure crops or dry fallowing.
• Grow redgram as a companion crop between 2 rows of sugarcane.
• Treat the setts in hot water at 50° C for 2 hours.
• Grow resistant varieties .
 Sugarcane wilt

 This is an important disease of sugarcane and is common in Srikakulam,

Vishakapatnam and Nizamabad districts of our state.
 The disease occurs singly or in combination with red rot.
 The disease is more in wilt sick soils and in alkaline soils. Moisture stress
aggravates the disease.
 Symptoms
• The symptoms become manifested when the
crop is about 4-5 months old.
• The earliest symptoms are stunting and
retardation in growth of few plants or clumps.
• Later, sudden yellowing and withering of the
crown leaves appear followed by rapid drying
of the cane. The affected canes become light
and hollow.
• When cane is split open longitudinally, pith
dries and become hollow like a boat filled with
greyish white mycelium and conidia.

(A) Crop symptoms, (B) Symptoms on Canes (C) Symptoms

on teared Canes.
 Pathogen

• The pathogen associated with the disease is

Cephalosporium sacchari
• The mycelium is septate and much branched.
• The conidiophores which arise from the hyphae are
aseptate, tapering towards the apex, simple or
verticillately branched.
• Conidia are hyaline, ovoid or oblong ellipsoid and
single celled.

Conidia, conidiophores, hyphae of

Cephalosporium sacchari.
 Disease cycle

• The fungus is primarily sett borne and also survives in the soil as saprophyte for 2-3 years.
• The disease is primarily transmitted through infected seed setts.
• The secondary spread is aided by wind, rain and irrigation water.

• Favourable Conditions
• High day temperature (30-350 C), low humidity (50-60 per cent), low soil moisture,
alkaline soils and excess doses of nitrogenous fertilizers.
 Management
• Select the seed material from the disease-free plots.
• Avoid the practice of ratooning in diseased fields.
• Burn the trash and stubbles in the field.
• Grow coriander or mustard as a companion crop in the early stages of crop.
• Avoid alkaline soils for growing the crop.
• Treat the setts in hot water at 50° C for 2 hours followed by dipping in 0.05% Carbendazim
for 15 minutes.
• Dip the setts in 40ppm Boron or Manganese for 10 minutes.
• Grow resistant varieties.
 Grassy Shoot

 In India the grassy shoot has become an important disease in TN, AP, Karnataka, Bihar and
UP, next to red rot and smut.
 It is more severe in ratoon crops and reduces juice quality, plant height and cane yield
drastically.
 Symptoms
• Initial symptom appears in the young crop of
3 – 4 months age as thin papery white young
leaves at the top of the cane.
• Later, white or yellow tillers appear in large
number below these leaves (profuse
tillering).
• Production of large number of lanky (thin)
tillers and affected plant presents a bushy
appearance.
• This disease appears in isolated clumps.
• The cane becomes stunted with reduced
internodal length with axillary bud sprouting.

(A) Grassy shoot symptoms on crop and (B)single plant.

 Pathogen
• Pathogen associated with the disease is Phytoplasma.
• Phytoplasma is found in the sieve tubes of phloem vessels and move from cell to cell
through pores in the sieve plates.
• Two types of bodies are noticed, spherical bodies of 300-400 nm diameter and
filamentous bodies of 30-53 mm diameter.

Disease cycle
• The pathogen is transmitted through planting material and within the crop by aphids,
viz., Aphis maidis, Rhopalosiphum maidis, Longiunguis sacchari, Melanaphis sacchari and
M. indosacchari.
• In addition, leaf hopper, Proutista moesta also involves in the transmission.
• Sorghum serves as a natural collateral host.
 Management

• Plant disease free setts.

• Remove and burn the infected clumps periodically.
• Avoid ratooning in problem areas.
• Hot Water Treatment (HWT) of setts at 52° C for 30min or Aerated Steam Therapy
(AST) at 50 ° C for 1 hr followed by steeping in fungicidal solution of
carbendazim@0.05% for 15 minutes.
• Control vector by spraying Malathion or Dimethoate@2ml/lt
 Pokkah Boeng

• Pokkah boeng, a Javanese term, which describe a disease as affecting to sugarcane tops, was
first recorded in Java by Walker and Went in 1886 and later reported by Edgerton (1955) and
Martin et.al (1961).
• Pokkah Boeng is the most serious and devastating disease not only in central Uttar Pradesh but
also in the whole of the Southern and Northern sugarcane growing zone of India.
• In India, it is reported from Punjab, Haryana, Uttar Pradesh, Gujarat, Madhya Pradesh,
Andhra Pradesh, Karnataka and TamilNadu States on most of the commercial varieties.
 Symptoms
• Chlorotic Phase: The earliest symptom of Pokkah boeng
is a chlorotic condition towards the base of the young
leaves and occasionally on the other parts of the leaf
blades.
• Frequently, a pronounced wrinkling, twisting and
shortening of the leaves accompanied the malformation
or distortion of the young leaves. The base of the
affected leaves is seen often narrower than that of the
normal leaves..
• Acute Phase or Top-Rot Phase: The most advanced and
serious stage of Pokkah boeng is a top rot phase. The
young spindles are killed and the entire top dies.
• Leaf infection sometimes continued to downward and
penetrates in the stalk by way of a growing point. In
advanced stage of infection, the entire base of the
spindle and even growing point showed a malformation
of leaves, pronounced wrinkling, twisting and rotting of
spindle leaves. Red specks and stripes also developed.
• Knife-cut Phase (associate with top rot phase): The
symptoms of knife-cut stage are observed in association
with the acute phase of the disease characterized by
one or two or even more transverse cuts in the rind of
the stalk /stem in such a uniform manner as if, the
tissues are removed with a sharp knife, This is an
exaggerated stage of a typical ladder lesion of a
Pokkahboeng disease.
 Pathogen

• Fusarium moniliformae is the causal fungus and its

perfect stage is Gibberella fujikuroi
• Hyphae are septate and hyaline.
• Conidiophores are medium length, simple or
branched.
• Macroconidia are slightly sickle-shaped to nearly
straight, 5-7 septate, measuring 31-58 x 2.7-3.6 µm.
• Microconidia abundant, 0 – 1 septate, oval to
clavate, measure 7-10 x 2.5-3.2 µm, and occur in
both false heads and chains.
• Chlamydospores are absent.

(A) mycelium and conidia (B) Light microphotograph of

mycelium and conidia of Fusarium moniliformae
 Disease cycle
• This is an air-borne disease and primarily transmitted through the air-currents.

• .
secondary transmission is through the infected setts, irrigation water, splashed rains and soil

Favourable conditions

• 20-30°C temperature and the average relative humidity higher than 70 to

80% with a cloudy weather, drizzling rains favors the growth of pathogen.
 Management
• Canes showing ‘top rot’ or ‘knife cut’ should be rogued out.
• Spraying of 0.1% Bavistin (1 gm/ lit. of water) or 0.2% Blitox-50 (2gm/ lit. of water) or
Copper oxychloride or 0.3% Dithane M-45 (3 gm/ lit. of water) are the most effective
fungicides for reducing the pokkah boeng disease. Two to three sprayings with an interval
of 15 days interval reduces the multiplication of a pathogen and losses in yield and quality
of cane.
• A paired row or wider spacing planting of sugarcane is necessary to facilitate the plant
protection operations.
 Anthracnose of Cotton

Cotton balls rotting

• The disease is found in most of the cotton growing areas of the world.
 Symptoms
• In seedling stage, small, circular and
reddish spots appear on the cotyledons
and primary leaves.
• The lesions when appear on the collar
region, the stem may be girdled, causing
seedlings to wilt and die.
• The pathogen attacks the stem, causing it
to split and shred the bark.
• Spots on the bolls appear as water
soaked, circular, slightly sunken and
reddish brown which later turn black in
colour.
• The lint become yellow to brown, rot and
transformed into brittle fibres.
• Seeds are also infected and shrevelled
discolored and brown in colour.
• Affected bolls are smaller in size.
Anthracnose symptoms (A) on leaf and (B) on bolls of Cotton
 Pathogen: Colletotrichum capsici
Colletotrichum gossypii.

• The perfect stage of the fungus is Glomerella

gossypii.
• The mycelium of fungus is septate.
• The fungus produces acervuli in which the
Acervuli, Conidia, Setae
setae and conidiophores are present.
• The conidiophores are slightly curved, short,
and club shaped.
• Conidia are hyaline, single celled and sickle
shaped or falcate, borne single on the
conidiophores. .
• Setae are numerous black colored and thick
walled.

Line drawing Conidia and Chlamydospores

 Disease Cycle:
• Primary inoculum: The pathogens are seed borne (survives as dormant
mycelium) and survive as conidia on the surface of seed for about a year.
• The pathogen also perpetuate on the rotten bolls and other plant debris in the
soil.
• Two common weeds namely Aristolochia bractiata and Hibiscus diversifolius are
also susceptible to C. capsici and can also be a source of primary inoculum.
• Secondary spread takes place by air and soil borne conidia. The disease spread
rapidly during wet weather.
• Favourable Conditions: Prolonged rainfall at the time of boll formation
and close planting predispose the disease.
 Management

• Treat the delinted seeds with Carbendazim or Carboxin@2g/kg or Thiram or Captan at

4g/kg.
• Remove and burn the infected plant debris and bolls in the soil.
• Rogue out the reservoir weed hosts and removal of collateral hosts
• Spray the crop at boll formation stage with Mancozeb@0.25% or Copper
oxychloride@0.3% or Ziram@0.25% or Carbendazim@0.1%.
 Vascular wilt of Cotton

• The disease is common in cotton fields in heavy soil with a soil temperature between 20-30
°C during crop season.
• Due to unfavorable soil temperature the disease is not found in loamy and sandy loam soils.
 Symptoms
• In very early stages of the plant growth, vein
clearing on cotyledons and first leaves is
visible.
• Wilting of the seedlings and adult plants even
though there is plenty of moisture in soil.
• Partial wilting is also common where few or
all branches of one side wilt and wither away.
• The diseased plants are often small with
smaller leaves and bolls.
• A discolored ring can be seen in transverse
sections of infected stem and roots.
• Vascular tissues are filled up with a gummy
substance which contains the fungal hyphae.
• In transverse section, discolored 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 Symptoms of Vascular Wilt (A) on cotton crop (B)
and open prematurely. on vascular system
Pathogen : Fusarium
oxysporum f.sp. vasinfectum

• The mycelium is inter or intracellular and

plug the xylem partially or wholly.
• The mycelium of the fungus is white to
greyish white or bluish purple and septate.
• The conidiophores are verticillately Macroconidia and Clamydospores
branched and developed in sporodochia.
• The fungus produces three types of spores.
Macroconidia are 1 to 5 septate, hyaline,
thin walled, falcate with tapering ends.
The microconidia are hyaline, thin walled,
spherical or elliptical, single or two celled.
Chlamydospores are dark coloured and
thick walled.
• The fungus also produces a vivotoxin,
Fusaric acid which is partially responsible
for wilting of the plants. Line drawing of Conidiophore and Microconidia,
Macroconidia and Clamydospores.
Disease cycle
 Disease cycle

• The fungus can survive in soil as saprophyte for many years and chlamydospores act as
resting spores.
• It is also seed borne, the pathogen is both externally and internally seed-borne.
• The primary infection is mainly from dormant hyphae and chlamydospores in the soil.
• After infection the fungus reaches to xylem and multiplies fast. The vessels are plugged
causing wilting of plants due to non-availability of nutrients.
• The secondary spread is through conidia which are disseminated by irrigation water.

Favourable Conditions :
• Soil temperature of 20-30° C, hot and dry periods followed by rains, heavy black soils with
an alkaline reaction,
• Increased doses of nitrogen and phosphatic fertilizers, soil amendment with manganese.
• Wounds caused by nematode (Meloidogyne incognita) and grubs of Ashweevil (Myllocerus
pustulatus).
 Management

• Treat the acid-delinted seeds with Carboxin or Chlorothalonil at 4 g/kg or

Carbendazim@2g/kg seed.
• Remove and burn the infected plant debris in the soil after deep summer ploughing.
• Apply increased doses of potash with a balanced dose of nitrogenous and phosphatic
fertilizers.
• Multiply Trichoderma viride (2kg) in 50 kg of Farm yard manure for 15 days and then
apply to the soil.
• Apply heavy doses of farm yard manure or other organic manures at 10 t/ha. Follow mixed
cropping with non-host plants to lower the soil temperature below 200 C by providing
shade.
• Soil amendment with zinc.
• Grow disease resistant varieties.
Black arm, Bacterial Blight, Angular
Leaf Spot of Cotton

• This is the most serious disorder of cotton crop and is found in most of the cotton growing
countries. The disease is widely distributed in India.
• This disease was first observed in Tamil Nadu in 1918. It is an important disease in
Maharashtra, Karnataka, A.P., Tamil Nadu and Madhya Pradesh.
 Symptoms
The bacterium attacks all stages from seed to harvest. Usually five
common phases of symptoms are noticed.
i) Seedling blight: Small, water-soaked, circular or irregular lesions
develop on the cotyledons. Later, the infection spreads to stem
through petiole and cause withering and death of seedlings.
ii) Angular leaf spot: Small, dark green, water soaked areas develop on
lower surface of leaves, enlarge gradually and become angular
when restricted by veins and veinlets and spots are visible on both
the surface of leaves. As the lesions become older, they turn to
reddish brown colour and infection spreads to veins and veinlets.
iii) Vein blight or vein necrosis or black vein: The infection of veins causes
blackening of the veins and veinlets, gives a typical ‘blighting’
appearance. On the lower surface of the leaf, bacterial oozes are
formed as crusts or scales. The affected leaves become crinkled and
twisted inward and show withering. The infection also spreads from
veins to petiole and cause blighting leading to defoliation.
iv) Black arm: On the stem and fruiting branches, dark brown to black
lesions are formed, which may girdle the stem and branches to
cause premature drooping off of the leaves, cracking of stem and
gummosis, resulting in breaking of the stem which hang typically as
dry black twig to give a characteristic “black arm” symptom.
v) Square rot / Boll rot: On the bolls, water soaked lesions appear and
turn into dark black and sunken irregular spots. The infection slowly (A)Water soaked lesions on leaves. (B &C)
spreads to entire boll and shedding occurs. The infections on mature Lesions on Boll (D) Veinal blight Symptoms on
bolls lead to premature bursting of bolls. The bacterium spreads boll
inside the boll and lint gets stained yellow because of bacterial ooze
and looses its appearance and market value. The pathogen also
infects the seed and causes reduction in size and viability of the
seeds.
Pathogen: Xanthomonas campestrisp.v.malvacearum now
known as Xanthomonas malvacearum.

• The bacterium is rod shaped and 1.3-2.7 x 0.3-0.6 micron in size.

• It is non-endospore forming, encapsulated and motile by single
polar flagellum.
• It is gram negative and aerobic.
Disease cycle
 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.
• It multiplies soon after the seed is sown and infects the seedling through the micropyle.
• Volunteer plants that arise from the bolls falling off prematurely also provide a source of
primary infection.
• The bacterium also attacks other hosts like Thurbaria thespesioides, Eriodendron
anfructuosum and Jatropha curcas.
• The primary infection starts mainly from the seed-borne bacterium.
• The secondary spread of the bacteria may be through wind, wind blown rain splash,
irrigation water, insects and other implements.
• The bacterium enters through natural openings or insect caused wounds.
Favourable Conditions:
• Optimum soil temperature of 28° C, high atmospheric temperature of 30-40 ° C, relative
humidity of 85 per cent, early sowing, delayed thinning, poor tillage, late irrigation and
potassium deficiency in soil.
• Rain followed by bright sunshine during the months of October and November are highly
favourable.
 Management

• Remove and destroy the infected plant debris.

• Rogue out the volunteer cotton plants and weed hosts.
• Follow crop rotation with non-host crops.
• Early thinning, good tillage, early irrigation, early earthing up and addition of potash to
the soil reduces disease incidence.
• Grow resistant varieties
• Delint the cotton seeds with concentrated sulphuric acid at 125ml/kg of seed.
• Treat the delinted seeds with Carboxin at 2 g/kg seed or soak the seeds in 1000 ppm
Streptomycin sulphate overnight or treat the seed with hot water at 52-56° C for 10-15
minutes.
• Spray with Streptomycin sulphate (Agrimycin 100), 500 ppm along with Copper
oxychloride at 0.3%.
 Sclerotinia Stem Rot of Sunflower
CO: Sclerotinia sclerotiorum

• 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.
• A 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
 Management
• not to plant on infested soil.

• (Soil solarization, deep ploughing)

• to prevent the build up of sclerotia in soils either by monitoring

of crop for disease incidence.

• through crop rotation.

• At present, no resistance is apparently available but some

hybrids show difference in susceptibility.

• Chemical control is not satisfactory.

 Alternaria leaf blight of Mustard

Distribution:- It is most devastating disease of oil yielding

brassicas.

Alternaria alternata and A. raphani are widespread in the Northern

hemisphere while A.brassicae and A.brassicicola are
cosmopolitan.

Alternaria usually causes spotting of leaves, damping-off of

seedlings, root and foot rot.

Infected seeds loose seedling vigor and power of germination

which causes damping off.
Symptoms:-

• light brown lesions which later on turns black due to the

abundance of spores which turns to be the source of infection for
other plant parts.

• These lesions rapidly multiply and spread to other plant parts like
stems and siliques etc.

• The black or brown spot contains visible circular, concentric rings.

• The circular spots often merge to form large patches causing the
leaf blight.

• In severe attacks plant shows damping off of seedling, wilting and

rotting at foot and root like symptoms also.

• Host-selective toxins released by the pathogen facilitate necrosis

which increases the severity of disease by decomposing the host
cells using degrading enzymes.
Causal Organism:- Aiternaria alternata, A.raphani, A.brassicae and
A.brassicicola.
Conidia of Alternaria are typically, ovoid to obclavate, often beaked, pale brown to
brown, multi-celled, muriform and form in chain.
Disease Cycle:-
Survival of the pathogen on diseased seed or affected plant debris in tropical or sub-tropical
India, unlike the situation in temperate conditions.
In India, oilseed Brassicas are sown from late August to November, depending on the crop,
prevailing temperature and availability of soil moisture for seed germination. Harvest occurs
from February to May.
Off-season crops are grown in non-traditional areas from May to September and this, coupled
with harbouring of the fungal pathogen by vegetable Brassica crops and alternative hosts
(Anagallis arvensis, Convolvulus arvensis), could be reason for carryover of the A. brassicae
from one crop-season to another.
Thus, air-borne spores of A. brassicae form the primary source of inoculum of this polycyclic
disease.
Disease Cycle of Alternaria Leaf Spot of Mustard
• Favourable Conditions:-
• Moist (more than 70% relative humidity) coupled with warm weather (12-25°C ) and
intermittent rains favours disease development.
• Management:-
• Use healthy and certified seed, maintaining a balanced nutrition, destruction of infected
weed and left over debris, proper field sanitation, eluding irrigation at flowering and pod
formation stages and crop rotation with non-cruciferous crops.

• Surface sterilization of seeds using sodium hypochlorite reduces growth of the Alternaria.

• Treating seeds with hot water also control seed- borne Alternaria infection.

• All the fungicides significantly affect the reduction in disease severity and increase in seed
yield.

• A number of fungicides have been reported to be effective against the spread of against
Alternaria under different field conditions e.g. Dithane M-45 (0.2%), Dithane Z-78 (0.2%),
Iprodione (Rovral) (0.2%), Blitox 50 (0.3%), Baycor (0.2%) and Mancozeb (64%).
 Downy mildew of Mustard

CO: Hyaloperonospora parasitica

Peronospora parasitica.
It is a common and destructive disease of brassica
vegetables.
cottony growth of the fungus on the lower side and on above
chlorotic regions are seen.
Symptoms:-
chlorotic, yellow, irregular areas or lesions on the upper
surface corresponding to a fluffy, white mass of spores
on the underside of leaves.
As the disease develop further, the individual lesions merge
to form large irregular, extremely thin blotches which
become dry and black-gray in color causing premature
falling of leaves.
The development of infection causes early leaf senescence,
defoliation and reduced yield.
The pathogen is often associated to white rust and most
likely responsible for its primary infections.
Spores produced on the bottom of the infected leaf extend
the infection to secondary level.
• CausalOrganism:-
Hyaloperonospora parasitica formerly
known as Peronospora parasitica
• It is an obligate parasite.
• It is strictly intercellular with large finger
shaped branched haustoria, which fill the
cell cavity.
• Numerous erect branched conidiophores
emerge through the stomata on the under
surface of the leaf.
• Favourable Conditions:-
• High humidity, fog, drizzling rains, and heavy dew favor disease development and
spread.
• Optimum conditions for disease development are night temperatures of 10-20°C
for 4 or more successive nights, and day temperature about 75°F or lower.
• Disease Cycle:-
• It is an obligate parasite.
• The pathogen is both soil and seed-borne.
• It can survive in the soil for a long period.
• The main sources of infection are wind, crop debris or soil.
• Oospores act as primary source of inoculum, however conidia cause secondary
infection on host.
• The sexual spores of the fungus are oospores.
• It penerates in the soil through oospores.
• Seeds with contaminated thrash may also carry the disease.
• Wild host plants also serve as source of primary inoculum.
• Conidia are 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.

• Spring-planted, summer-harvested crops have fewer

problems than fall-harvested.

• Spray crop with Indofil M-45 @ 400gm in 150 Ltr of water

per acre for four times with interval of 15 days
White Blister or White rust of Mustard
Distribution:-

White rust is one of the major constraints responsible for low productivity of

cruciferous species.

The pathogen affects both domesticated and wild species of crucifers.

It is an obligate parasite.

It is wide spread in almost all parts of the world.

The fungus produces thick , curd like growth on lower side .

The mycelial growth is dense in comparison to DM.

Off white growth.

Symptoms:-
• The infection can be either local or
systemic.
• All parts of the plant except the root may
show the symptoms.
• In the case of local infection, isolated
pustules develop on the leaves and stems.
• The pustules are raised, shiny white areas,
measuring 1 to 2 mm.
• They appear together as large patches.
When the young stems and inflorescence are infected
the fungus becomes systemic in the tissues and
deformities like hypertrophy occur.
Blisters are also formed on the inflorescence and floral
parts.
The floral parts show swellings and distortions.
The axis of the inflorescence and the floral parts may
be enormously thickened.
In cases where the systemic infection has taken place
early, the entire plant may remain dwarfed and only
small leaves may appear.
The stem often becomes twisted giving a zig zag
appearance.
This is known as STAG HEAD condition, occur due
to disease complex of DM and White rust.
DM becomes systemic in nature.
Causal Organism:- Albugo candida is also known as Cystopus candidus.
The mycellium is intercellular.
The mycellium produces knobed shaped haustaria in the host cells.
A large number of haustaria are seen in a single cell. They loose their viability after some
time. They germinate readily when immersed in water. The germination of the sporangium is
maximum at 25° C.
Favourable Conditions:-
Infection is generally favored by cool [13-18°C ], wet weather in the form of
prolonged dews or fog. Sporangia are produced in the pustules and are spread by wind, rain
or insects to neighboring plants.
Disease Cycle:-
The fungus overwinters as resting spores in decaying infected
plant tissues (mainly stagheads) or as a seed contaminant.
These spores may remain dormant in soil or on seed for a number
of years.
In the spring, some of the spores germinate and infect the
cotyledons and leaves of young susceptible plants.
These infections develop and white pustules are formed on the
underside of leaves or on stems.
The pustules release chalk-like, airborne spores that can spread the
disease to other parts of the plant or to nearby plants to cause
secondary infections on leaves, stems or flower buds. Stagheads
develop from infected flower buds.
At harvest, stagheads may be broken during threshing resulting in
contamination of the seed with resting spores.
Management:-
•The disease can be controlled by crop rotation and clean
cultivation including use of clean seeds and destruction of weeds.
•Swelling of affected part is observed. Because of infection flower
become sterile.
•If infestation observed in field, to control spray with Metalaxyl
8%+Mancozeb 64% @ 2gm/Ltr of water or spray with Copper
oxychloride @ 25gm/Ltr of water.
•If necessary repeat the spray with interval of 10-15days.
 Downy Mildew of Pea
Distribution:- The downy mildew of pea is widely distributed in UK,
Australia, Sweden, New Zealand and India
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 lesions of the upper surface. The downy coating is
whitish when young, but colour gradually turns greyish-violet with age.
• This growth is composed of branches sporangiophores, arising from
mycelium of the fungus which has entered within the leaf tissues. The
infected areas gradually develop into enlarged blotches and often
irregular spots.
• With the spread of infection, blotches also appear on the pods. When
young blotch on the pods are pale green, more or less elliptical to
irregular, but gradually the blotches turn dark to bright-brown. Seeds
lying corresponding to the infected tissues of the pods abort and become
very much reduced in size.
Causal Organism:- Peronospora pisi
Mycelium of the fungus aseptate, branched hyaline hyphae, confined to
the intercellular spaces of the host tissues. The hyphae produce branched,
finger-shaped haustoria which penetrate into the adjoining cells of the
intercellular spaces. The sporangiophores are dichotomousiy 2 to 10
times branched at acute angle, arise directly from the internal hyphae and
emerge in clusters from the stomata of the under surface of the leaf.
Favourable Conditions:-
The disease can develop quickly when conditions are cold (5 - 15°C) and humid over 90 per cent for 4 - 5
days, often when seedlings are in the early vegetative stage. Rain is the major means of spore dispersal
and infection.
Disease Cycle:-
The primary cycle, when infection starts in the leaflets and stipules from the inoculums produced by the
germination of oospores of previous year. 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 the sporangia
germination.
Management:-
Since the causal organism survive season to season in the form of oospores in the plant debris and
following crop rotation of two or three years are very active control measures.
Spraying and dusting of pea crop with fungicides are effective in limiting the spread of disease.
Deep ploughing to bury crop residue.
Use resistant or tolerant cultivar.
Use of Metalaxyl for seed treatment.
Disease Cycle of Downy Mildew of Pea
 Powdery Mildew of Peas
Distribution:-
Disease is distributed in Europe including Great Britain, in USA, Canada, India,
New Zealand, Japan. In Russia, Byelorussia, Ukraine the Powdery Mildew is
distributed on peas everywhere.
Symptoms:-
• 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.
• Severe pod infection can cause a grey-brown discolouration of the seeds and
seed size also reduced.
• Infected plants show increased respiration, transpiration and such plants
decrease photosynthesis.
Causal Organism:- Erysiphe communis Grev. f. pisi
Although E. pisi and E. cichoracearum have also been reported on peas, but E.
polygoni is more destructive. The fungus is an obligate parasite having septate,
hyaline, profusely branched superficial mycelium sending finger shaped
haustoria to the host cells. Conidia are unicellular, colorless, elliptic.
Cleistothecia are yellowish or dark-brown, Asci within Cleistothecia
areellipsoid, narrowed downward, with 4-6 ascospores and ascospores are
unicellular, colorless
Favourable Conditions:-
Under favourable conditions, the disease may completely colonise a
plant in 5-6 days. Once a few plants become infected, the disease rapidly
spreads to adjacent areas. Warm (15-25°C), humid (over 70% RH)
conditions for 4-5 days late in the growing season, during flowering and
pod filling, favour disease development. However, heavy rainfall is not
favourable for the disease as it will actually wash spores off plants.
Night time dews are sufficient for the disease to develop.
Disease Cycle:-
• The primary infection takes place through ascospores released in soil as
a result of disintegration of the wall of cleistothecium. Under favourable
conditions, the ascospores come in contact with the lower most leaves of
the host, germinate by germ tube and cause primary ‘infection’.
• From the lower most leaf, the infection spreads to other leaves. Later the
symptoms in the form of white powdery mass appear. These patches
contain conidia and conidiophores. The primary infection may also come
from the conidia produced on other hosts as the causal organism E.
polygoni has a large host range.
• The secondary infection of the host takes place by conidia which are
produced in large numbers and are disseminated by wind. Upon reaching
the host the conidia germinate and cause infection.
• During the growing season, more than one secondary infection may
occur.
• The cleistothecia-the perennating structures are produced on fallen
infected debris in soil. These remain buried in the soil waiting for the
favourable conditions. These contain asci and ascospores which serves
as primary inoculum of the disease infection.
 Management:-
• Field sanitation, rotation of
crop and destruction of
diseased plant debris may
effectively control the
disease.
• Sulphur dusting @ 25-30
Kg/hectare gives effective
results. Only one dusting is
sufficient.
• Spraying with Karathane
(0.2%), Elosal (0.5%) and
Morocide (0.1%) have been
found effective in
controlling the disease.
• Early maturing and resistant
varieties like P185, 388,
61113, 1683, 6588, Freazer-
656, T-10, T-163 and IC775
should be cultivated.

Disease Cycle of powdery mildew of pea

 Rust of Pea
Distribution:-
Pea rust has been reported from different part of Europe, Africa;
Canada; Australia. In India it is reported from Eastern India, Central
India, Southern parts of India and Himalayan region of Himachal
Pradesh. Pea rust completely destroyed the crop in sub-mountainous
region of North- India.
Symptoms:-
• Symptoms generally appear in the month of February or even later in
the form of numerous orange-coloured pustules having aecia in round
or elongated clusters usually on the lower side of the leaves. Later on,
the symptoms manifest on all other aerial parts like stems, petioles,
tendrils and even the pods.
• The orange-coloured pustule gradually turn brown (due to
development of uredo-stage) during late in the growing season, and
finally become almost black in colour (due to development of teleuto-
or telio-stage) when the crop moves towards maturity. It is important
to note that the uredopustules develop usually on both surfaces of
leaves as well as on other parts, and the teleutopustules also develop
on leaves but they appear most commonly on stems and petioles.
Causal Organism:- Uromyces pisi and U. fabae
The casual organism of pea rust in most parts of India is Uromyces
fabae (Pers.) de Bary. It is a biotrophic, macrocyclic, autocious rust. It
belongs to the Division: Basidiomycotina, Class: Basidiomycetes,
Subclass: Teliomycetidae, Order: Uredinales, Family: Pucciniaceae
Favourable Conditions:-
Persistence of low temperature and moist condition for few weeks in and around the infected field is
thought to be favourable for severe disease incidence. The aeciospores remain viable and infective for
eight, six, four, three, and two weeks at temperatures of 3-8°C, 10-12°C, 17-18°C, 25°C, and 30°C,
respectively. Similarly, the uredospores germinate usually at the optimum temperature of 16-22.5°C.
Disease Cycle:-
•The pathogen perennates via teleutospores present on diseased plant debris or mixed with the seed as
external contaminant.
•The primary infection on the newly growing crop is considered to be caused by the germination of
teleutospores in the month of January.
•The aeciospores play a major role in the dissemination of the pathogen during the crop season resulting in
secondary infection.
Management:-
•Destroy all diseased plant debris after harvest.
•Follow suitable crop rotation with non leguminous crops.
•Mix cropping.
•Sulphur 80% WP at the rate of 1.252 kg in 300-400 l water per acre or Sulphur 85% DP at the rate of 6-8
kg per acre or tridimefon 25% wp at the rate of 0.1% in 300 l water per acre. Second spray after 25 days
of interval.
Disease
Cycle of
Diseases of Lentil
 1. Rust of Lentil
• Symptoms: The disease symptoms are necrosis
and deformity of stem and affected plants often
die.
• Yellowish powdery pustules are developed on
leaves, stem and petioles and even on pods.
• These yellow spots have aecia in round and
elongated clusters.
• Uredopustules develop on both side of leaves,
petiole and stem as powdery light brown pustules.
Dark brown or black teliospores also develop in the same
sorus at later stages.
Later the aecidia and pycnidia develop.
It is autoceous rust.
• Pathogen:
• The causal pathogen is Uromyces fabae (Pers.) de
Bary.
• The pathogen belongs to Basidiomycotina.
• Aeciospores developed in aecia are round to elliptical,
yellowish in colour and measure 14-22 micron.
• Uredospores are round to ovate, light brown and
measure 20-30 x 18-26µ in size.
• Teliospores are subglobose to ovate, brown in colour
and measure 25-38 x 18-27µ.
• This rust is not common in India.
• The disease generally starts from low-lying
patches in the paddock and radiates
towards the border.
• Rust is an autoecious fungus, completing
its life cycle on lentil.
• High humidity, cloudy or drizzly weather
with temperatures 20 to 22°C favour
disease development.
• The disease generally occurs during the
flowering /early podding stage.
• Disease Cycle:
• The dissemination of lentil rust pathogen takes place by
aeciospores which form secondary aecia after infection of
leaves.
• The secondary aecia are formed at a temperature of 17-22°C
but at 25°C the infection causes development of uredia.
• The aeciospores and probably the uredospores do not
survive during off season.
• The teliospores can withstand the summer heat and hence
the lentil rust perpetuates in its telial stage in the left over
diseased plants trash or on seed as external contaminant
and infects the new crop in the next season.
• Aeciospores from lentil have also been found to infect pea
and Vicia faba and Lathyrus.
• However, another species of U. pisi (Pers) Wint. is a
heteroceous rust and commonly occur on cultivated pea.
• The aecial stage of this pathogen develops on
Euphorbia cyparissias L.
• Control:
• Destruction of diseased plant trash after harvest
• crop rotation
• seed treatment with fungicides are the effective control
measures.
• Use of foliar fungicides as Hexaferb and Dithane M-45
give best control.
• Mancozeb (0.2% a.i.), Bayleton (0.05% a.i) and Calixin
(0.2% a.i.)
• Foliar spray of benomyl, carboxin, metalaxyl, oxycarboxin,
thiram, triademafon either alone or in combination of
Dithane M-45 are also effective.
• Lentil varieties Pant L-639, Pant L-406, Pant L-6, pant L-7
and Pant L-8 are resistant.
 Wilt of Lentil
• The disease is common in India on lentil
crop.
• In India lentil wilt was first reported from
undivided Bengal in 1934.
• The pathogen causes serious disease
and is widespread in India.
• It is a soil borne, root pathogen colonizing
the xylem vessels and blocking them
completely to cause wilting
• Symtoms: The disease appears in the field in
patches at both seedling and adult stages.
• Seedling wilt is characterized by sudden drooping,
followed by drying of leaves and seedling death.
• The roots appear healthy, with reduced proliferation
and nodulation and usually no internal discoloration
of the vascular system.
• Adult wilt symptoms appear from flowering to late
pod-filling stage and are characterized by sudden
drooping of top leaflets of the affected plant, leaflet
closure without premature shedding, dull green
foliage followed by wilting of the whole plant or
individual branches.
• Seeds from plants affected in mid-pod-fill to late
pod-fill are often shriveled.
• Pathogen:
• Fusarium oxysporum fsp lentis.
• It belongs to family Tuberculariaceae,
order Moniliales and sub-division
Deuteromycotina.
• The pathogen is present both inter and
intracellularly in vascular bundles of the
host and produces macro and
microconidia over there.
• Disease Cycle: The pathogen is a facultative parasite and
lives saprophytically on organic matter in the soil.
• When the crop is harvested, the roots remain in soil and
pathogen survives on these roots for several years.
• The pathogen may produce chlamydospores which may
face adverse soil conditions and become active and
infect plants when next crop is sown.
• The fungus is soil borne, which can survive in the soil and
plant debris in the absence of its host for a period of 3-4
years.
• The disease is favoured by low soil temperature, 30 per
cent soil water holding capacity and increasing plant
maturity.
• Yield losses depend on the stage at which the plant wilts;
it can be 100 per cent when wilt occurs at pre pod stage,
about 67 per cent when it occurs at the pre harvest stage.
• Management:
• Soil amendment with organic matter enhances
antagonism with other soil microflora.
• Ploughing of the field during summer.
• Following crop rotation with cereal crops which are
not affected by wilt pathogen.
• Seed treatment with benornyl (0.3%) or thiram +
benomyl (1:1, 0.3%)
• Using antagonistic microflora like Bacillus subtilis,
Trichoderma harzianum, T. viride @ 4 g/kg seed etc.
• Resistant varieties, Pant L-4, Pant L-6, Pant L-8 and
Noori.
• Macrocyclic all five stages of the life cycle
• macrocyclic heterceious – Pgt.,
• macro autoceious – Pea rust, lentil rust.
• rust fungi lack one or more stages and may be referred to as
microcyclic (which produce only teliospores and
basidiospores)
• demicyclic (which do not produce urediniospores)
• Gynoconia peckiana is an autoecious demicyclic rust and
Gymnosporangium juniperivirginiane is a heteroecious
demicyclic rust.
• endocyclic (which produce only spermatia and aeciospores).
Diseases of Lentil
 1. Rust of Lentil
• Symptoms: The disease symptoms are necrosis
and deformity of stem and affected plants often
die.
• Yellowish powdery pustules are developed on
leaves, stem and petioles and even on pods.
• These yellow spots have aecia in round and
elongated clusters.
• Uredopustules develop on both side of leaves,
petiole and stem as powdery light brown pustules.
Dark brown or black teliospores also develop in the same
sorus at later stages.
Later the aecidia and pycnidia develop.
It is autoceous rust.
• Pathogen:
• The causal pathogen is Uromyces fabae (Pers.) de
Bary.
• The pathogen belongs to Basidiomycotina.
• Aeciospores developed in aecia are round to elliptical,
yellowish in colour and measure 14-22 micron.
• Uredospores are round to ovate, light brown and
measure 20-30 x 18-26µ in size.
• Teliospores are subglobose to ovate, brown in colour
and measure 25-38 x 18-27µ.
• This rust is not common in India.
• The disease generally starts from low-lying
patches in the paddock and radiates
towards the border.
• Rust is an autoecious fungus, completing
its life cycle on lentil.
• High humidity, cloudy or drizzly weather
with temperatures 20 to 22°C favour
disease development.
• The disease generally occurs during the
flowering /early podding stage.
• Disease Cycle:
• The dissemination of lentil rust pathogen takes place by
aeciospores which form secondary aecia after infection of
leaves.
• The secondary aecia are formed at a temperature of 17-22°C
but at 25°C the infection causes development of uredia.
• The aeciospores and probably the uredospores do not
survive during off season.
• The teliospores can withstand the summer heat and hence
the lentil rust perpetuates in its telial stage in the left over
diseased plants trash or on seed as external contaminant
and infects the new crop in the next season.
• Aeciospores from lentil have also been found to infect pea
and Vicia faba and Lathyrus.
• However, another species of U. pisi (Pers) Wint. is a
heteroceous rust and commonly occur on cultivated pea.
• The aecial stage of this pathogen develops on
Euphorbia cyparissias L.
• Control:
• Destruction of diseased plant trash after harvest
• crop rotation
• seed treatment with fungicides are the effective control
measures.
• Use of foliar fungicides as Hexaferb and Dithane M-45
give best control.
• Mancozeb (0.2% a.i.), Bayleton (0.05% a.i) and Calixin
(0.2% a.i.)
• Foliar spray of benomyl, carboxin, metalaxyl, oxycarboxin,
thiram, triademafon either alone or in combination of
Dithane M-45 are also effective.
• Lentil varieties Pant L-639, Pant L-406, Pant L-6, pant L-7
and Pant L-8 are resistant.
 Wilt of Lentil
• The disease is common in India on lentil
crop.
• In India lentil wilt was first reported from
undivided Bengal in 1934.
• The pathogen causes serious disease
and is widespread in India.
• It is a soil borne, root pathogen colonizing
the xylem vessels and blocking them
completely to cause wilting
• Symtoms: The disease appears in the field in
patches at both seedling and adult stages.
• Seedling wilt is characterized by sudden drooping,
followed by drying of leaves and seedling death.
• The roots appear healthy, with reduced proliferation
and nodulation and usually no internal discoloration
of the vascular system.
• Adult wilt symptoms appear from flowering to late
pod-filling stage and are characterized by sudden
drooping of top leaflets of the affected plant, leaflet
closure without premature shedding, dull green
foliage followed by wilting of the whole plant or
individual branches.
• Seeds from plants affected in mid-pod-fill to late
pod-fill are often shriveled.
• Pathogen:
• Fusarium oxysporum fsp lentis.
• It belongs to family Tuberculariaceae,
order Moniliales and sub-division
Deuteromycotina.
• The pathogen is present both inter and
intracellularly in vascular bundles of the
host and produces macro and
microconidia over there.
• Disease Cycle: The pathogen is a facultative parasite and
lives saprophytically on organic matter in the soil.
• When the crop is harvested, the roots remain in soil and
pathogen survives on these roots for several years.
• The pathogen may produce chlamydospores which may
face adverse soil conditions and become active and
infect plants when next crop is sown.
• The fungus is soil borne, which can survive in the soil and
plant debris in the absence of its host for a period of 3-4
years.
• The disease is favoured by low soil temperature, 30 per
cent soil water holding capacity and increasing plant
maturity.
• Yield losses depend on the stage at which the plant wilts;
it can be 100 per cent when wilt occurs at pre pod stage,
about 67 per cent when it occurs at the pre harvest stage.
• Management:
• Soil amendment with organic matter enhances
antagonism with other soil microflora.
• Ploughing of the field during summer.
• Following crop rotation with cereal crops which are
not affected by wilt pathogen.
• Seed treatment with benornyl (0.3%) or thiram +
benomyl (1:1, 0.3%)
• Using antagonistic microflora like Bacillus subtilis,
Trichoderma harzianum, T. viride @ 4 g/kg seed etc.
• Resistant varieties, Pant L-4, Pant L-6, Pant L-8 and
Noori.
• Macrocyclic all five stages of the life cycle
• macrocyclic heterceious – Pgt.,
• macro autoceious – Pea rust, lentil rust.
• rust fungi lack one or more stages and may be referred to as
microcyclic (which produce only teliospores and
basidiospores)
• demicyclic (which do not produce urediniospores)
• Gynoconia peckiana is an autoecious demicyclic rust and
Gymnosporangium juniperivirginiane is a heteroecious
demicyclic rust.
• endocyclic (which produce only spermatia and aeciospores).
 Diseases of Potato

1. Late blight of potato

Symptoms

It affects leaves, stems and tubers. Water-soaked spots appear on leaves, increase in
size, turn purple brown & finally black colour. White growth develops on under surface
of leaves. This spreads to petioles, rachis & stems. It frequently develops at nodes.
Stem breaks at these points and the plant topples over. In tubers, purplish brown spots
and spread to the entire surface. On cutting, the affected tuber shows rusty brown
necrosis, spreading from surface to the center.

Causal Organism: Phytopthora infestans

Etiology and Disease cycle:

Mycelium of the fungus is coenocytic, hyaline, much branched and intercellular with club shaped
haustoria. Sporangiophores are slender, hyaline, branched and indeterminate in growth. The
branches of sporangiophore show bulbous enlargement at certain interval that indicates the
positions where sporangia were attached. Sporangia are multinucleate (7-30 nuclei), thin walled,
hyaline, oval or pear shaped with a distinct papilla at the apex. The sporangium may germinate
either directly by means of germ tube (above 15°C) or indirectly by means of zoospores (up to
15°C). Sexual reproduction is not very common in nature. The pathogen can survive as dormant
mycelium in the tubers left in the field where temperature do not rise above 30°C. In other area
the persisting mycelium in seed tubers stored at low temp. is the main source of primary
inoculum. The spread of disease is through sporangia or zoospores, disseminated by rain or
irrigation water, contact among leaves and in dry condition by wind through sporangia alone.
 Management:

• Selection of disease-free seed tubers from reliable source.

• Use resistant varieties – Kufri Jyoti, K. Giriraj, K. Himalini, K. Shailja, K. Kanchan for hill and
Kufri Chipsona-1 2&3, K. Anand, K. Pukhraj, K.Badshah for plain.

• Commonly recommended fungicides are mancozeb (0.2 %) 7-10 days interval.

• If disease appear early in the season and weather condition are favourable one spray of
combination of metalaxyl + mancozeb @ 0.1% may be given. A sticker like Triton AE @
0.1% must be added with fungicides solution.

2. Early blight of Potato

Symptoms

Disease appears as mall, isolated & scattered

pale-brown spots on leaflets. In necrotic tissues
concentric rings develop to produce target board
effect. Lower leaves, attacked first & the disease
spread upwards. Several spot coalesce & spread all
over the leaf. Affected stems show brown to black
necrotic lesions & may leads to collapse the
branches.

Causal Organism: Alternaria solani

Etiology and Disease cycle:

Mycelium of the fungus is branched, septate, intercellular or intracellular, light
brown and become darker with the age. Conidiophores emerge through stomata from
the dead center of spots. Conidia are beaked, muriform, 5-10 transverse and few
longitudinal septa, dark coloured and borne singly. The pathogen survives in soil on
diseased crop debris as mycelium and conidia and serves as primary source of inoculum.
Contamination of tubers with conidia or mycelium is another source of primary
inoculum. Secondary spread of disease occurs through conidia developed on primary
spots. These conidia are disseminated by wind, water and insects.
Management:

• Removal and destruction of diseased crop debris.

• Resistant varieties: Kufri Pukhraj, K. Badshah, K. Lalima, K. Naveen, K. Sinduri, K.
Jeevan etc.
• Spray mancozeb or difolaton @ 0.2% at 15-20 days after planting.
• A sticker like Triton AE @ 0.1% must be added with fungicides solution.
 3. Black scurf- Rhizoctonia solani
Symptoms
Appearance of irregular, black encrustation on the tubers due to formation of
sclerotia of the fungus which reduces their market acceptability. The sclerotia are
normally skin deep only and do not cause any damage to the tuber inside. At the time of
sprouting dark brown necrosis appear on the tips of the sprouts and sunken lesions
appears on stolon, roots & stems. Infected plants are stunted and develop a purplish
and chlorotic discolour.

Causal organism: Rhizoctonia solani

Etiology and Disease cycle:

The perfect stage of pathogen is Thanatephorous cucumeris (Basidial stage). The

mycelium is stout, branched, septate, and initially white and later become brown with
typical dolipore type septa. The lateral branches from the main hypha are constricted at
the point of origin and a septum occurs in the branch near the junction with main axis.
Fungus produces moniloid or barrel shaped clamydospores. Seed tubers are source of
spread. Moderately cool , wet weather and temp 23 °C are the favourable for the
development of disease

Control

• Use certified potato seed.

• Long crop rotation should be followed, i.e. more than 3 yrs.
• Seed treatment with boric acid @ 3% for 30 min.
• Soil application of brassicol @ 20-30 kg/ha

4. Viral Diseases of Potato

(I) Mosaic: There are two types of Mosaic disease appear in potato.

(i) Latent mosaic

Symptoms:

Affected plants looks healthy but carry the virus. There is very slight symptom appears like
interveinal mosaic in early stage of plant growth.
Causal organism: Disease is caused by Potato Virus X (PVX) or Potato Mild Mosaic Virus.
Etiology and disease cycle:

The virus belongs to potex virus group. Pathogenic virus is filamentous particle and highly
contagious. The virus survives on other host like tomato, tobacco, brinjal, dhatura etc. The insect
vector is not known but the spread in field by contact or by cutting of seed tubers.

(ii) Severe mosaic:

Symptoms:

The characteristic symptoms include severe mosaic, necrosis along the veins and may also
induce rugosity and drooping of leaves. Plants of infected mother tubers are stunted with brittle
and crinkled leaves.

Causal organism: Potato Virus Y (PVY) or Potato Severe Mosaic Virus is the causal organism.
Etiology and disease cycle:

The virus belongs to poty virus group. It has flexuous filamentous and helically structured
particles. PVY is mainly survives on other solanaceous host like tobacco and dhatura. It is
transmitted by aphids (Aphis gossypii and Myzus persicae).

(II) Potato leaf roll :

Symptoms:

Primary symptoms are seen as chlorosis of top leaves. Late in season the top leaves show
rolling and erect habit. The secondary symptoms includes stunting of shoots, upward rolling of
older leaflets which may turn chlorotic, leathery and brittle.

Causal organism: Potato Leaf Roll Virus.

Etiology and disease cycle:

It belongs to Lutero Virus group. It has isometric particles which are confined to phloem
tissues. It can also infect the other host like tomato, dhatura, and gomphrena. It is transmitted
by several aphids like Aphis gossypii, Macrosiphum euphoorbie and Myzus persicae).

Control:

• Field sanitation by removal and destruction of diseased crop debris.

• Obtained certified seed tubers and plant them early in the season.

• Spray mancozeb or difolaton@ 0.2% at 15-20 days after planting .

• Rogue out the diseased plants as soon as locatted.

• Remove foliage (Detopping or dehaulming) in 3rd or 4th week of December when aphid
infestation start and leave the tuber to mature.
• In late planted crop use of systemic insecticide like metasystox (0.1%) as spray to check
insect vector.
 Diseases of Cruciferous vegetables,
Onion & Garlic, Turmeric and Coriander
 Diseases of Cruciferous vegetables
1. Alternaria Leaf Spot of Crucifers

Symptoms:
• Symptoms of Alternaria Leaf Spot on cabbage may first develop on young
plants in seedbeds, where leaf spots, stunting, or damping off may occur.
• The Alternaria fungus produces round, brown lesions on infected leaves
and oval or elongated lesions on stems.
• Dark brown to black leaf spots may appear on tissues of any age and vary
in size from pinpoint to 2-inches in diameter.
• The leaf spots enlarge in concentric circles and mature lesions have a
bull’s eye type appearance (presence of concentric rings within the dead
tissue).
• The black spores easily detach from the leaf if touched and are visible on
the leaf surface, fingers and tools.
 Causal Organism: Alternaria brassicae and Alternaria brassisicola
Etiology and Disease Cycle:
• Mycelium of the pathogenic fungus is branched, septate, hyaline at first,
later brown or olivaceous brown.
• Conidia of Alternaria brassisicola are pale to dark brown in colour, have 1-11
but usually less than 6 transverse septa and up to 6 longitudinal septa. The
beak length in conidia is almost 1/8 of the length of the conidium.
• Conidia of Alternaria brassicae are pale or very pale olive or greyish olive in
colour, consists usually 11-15 transverse and 0-3 longitudinal septa. The
length of beak is about 1/3 of the length of conidium.
• The source of initial disease, may be infected seed, transplants, or infested
crop residue that overwinters in midwestern fields.
• In warm, wet conditions, lesions on infected plant material produce spores
that may be windblown or rain-splashed to other plants or fields.
• The spores result in new infections that continue the cycle of lesion
development, spore production, dissemination, and infection.
• The fungus may survive in Indian fields only in association with infected
crop residue.
• Temperature between 21 and 28 C with high relative humidity (at least 95%)
favours for disease development.
 Management:
 Disease-free planting material should be used.
 Crop rotation should be followed.
 Spraying of chlorothalonil (0.2%) as soon as the disease
appears.
2. Black Rot of Crucifers

Symptoms:
• Young seedlings are particularly susceptible to black rot.
• Initial infections on the cotyledons (seed leaves) may seem to disappear when these leaves fall
off, but the bacteria remain present in plants at low levels.
• Infections become systemic as the bacterium spreads through leaf veins.
• Close spacing and overhead watering of transplants worsen plant-to-plant spread.
• As disease progresses, plants become stunted and chlorotic and may drop leaves prematurely
before eventually dying.
• On mature plants initial symptoms appear as distinct, yellow V-shaped lesions along leaf margins,
with the bottom of each “V” pointing inward.
• Lesions turn brown as they become necrotic, enlarging until entire leaves yellow, wilt, and fall
from plants.
• Leaf veins in affected areas turn from green to dark-brown to black. Black discoloration is evident
in the vascular system when stems or heads are cut lengthwise (Fig. D).
• Soft-rotting bacteria often invade and colonize diseased tissues, resulting in a slimy, foul-smelling
decay of stalks and/or heads.
Causal Orgaism:- Xanthomonas campestris pv. campestris.
Etiology and Disease Cycle:
• The bacterial cells are single, straight rods and usually 0.4 x 1.0
micon in size.
• They are gram negative and motile by single polar flagellum.
• The most common source of the pathogen is infested seed lots or
infected transplants, but it can also survive from season to season
in plant debris left in the field or garden.
• While the pathogen only infects crucifers (cole crops), a number of
related weeds are also host and can serve as reservoirs of
inoculum.
• Infection can occur through wounds or insect damage, but most
common is entrance through natural openings, such as stomata
and hydathodes.
• Spread within fields occurs via splashing rain, insects, wind-blown
plant debris, or handling plants with infested tools or human hands.
• Warm (25° to 30 °C), humid or rainy weather favours infection and
 Management:
 Use only certified disease-free seed.
 At least two years crop rotation should be followed.
 Seed treatment with Agrimycin or streptomycin (0.01%) or hot water
treatment at 52℃ for 30 minutes.
 Three sprays of 50 ppm streptomycin at transplanting, curd
formation and pod formation.
 Diseases of Onion & Garlic
1. Purple Blotch
Symptoms
• Symptoms first appear on leaves and stalks as small water-soaked lesions that quickly
develop white centre.
• Under favourable condition, the lesion enlarge, coalesce, become zonate and brown to
purple that extend upward and downward.
• In moist weather, the surface of the lesion, may covered with black fruiting bodies of
fungus.
• The older leaves are more susceptible than younger leaves and younger leaves relatively
more susceptible when they emerge close to the bulb maturity.
• Similar lesion may form on seed stock, as a result of seed either do not develop or are
shrivelled.
• Severely infected foliage of onion and garlic may exhibit dieback.
• The bulb can also be affected at harvest when the fungus enters through the neck or
injurious, causing storage rot.
Causal Organism: Alternaria porri
Etiology and disease cycle:
• Mycelium -branched, coloured and septate.
• Conidiophores arise singly or in groups, septate, pale to mid brown.
• Conidia are solitary, straight or curved.
• The pathogen overwinters in crop residue on or near the soil surface.
• The fungus can also survive in diseased onion leaves and debris for 12 months buried at 5- 7.5 cm
depth wherever the chlamydospores of the fungus are formed they can also serve as source of
perennation.
• Invasion of the fungus takes place either through stomata or directly through the cuticle, to form
an intercellular mycelium, which turn form conidiophores and conidia.
• Spores are produced and new plants infected during periods of warm (77-85°F) and humid
weather.
• Symptoms appear 1-4 days after infection and black spores are produced by fresh lesions within 5
days.
• Spores are produced at night and released in the morning as humidity decreases.
Management:
 Use of healthy seed/planting material.
 Crop rotation with non-host crop.
 Collection and destruction of infected crop debris after harvest.
 Good drainage and summer ploughing.
 Hot water seed treatment at 50oC for 20 min. for reducing seed
inoculum.
 Use of resistance varieties like Pusa red, IHR-56-1, Hybrid
PVM-7 etc.
 Seed treatment with thiram @ 2.5g/kg of seed.
2. Onion Smudge
Symptoms:
• The disease is characterized as subcuticular, small dark green to
black smudge (minute stroma of the fungus) that appear on the bulb,
neck or green leaves that are clinging to the bulb after digging.
• The black colour may be uniform on the lesion but normally the
circular lesions show concentric rings of dark stroma and mycelium.
• The outer scale are also attacked if the outer scales have peeled
off but the lesions on inner scales are small, sunken and yellow.
• During the moist conditions, acervuli of the fungus develop on the
infected areas and spore masses and the setae can be easily
recognized fleshy scales resulting in yellow depressions on the bulb.
Causal Organism: Colletotrichum circinans
Etiology Disease Cycle:
• Mycelium of the fungus is narrow, septate which are
initially hyaline but later become slightly dark.
• Acervuli are formed abundantly on the affected host
surface.
• Conidiophores, conidia and setae are formed in the
acervuli.
• The fungus can over-winter in the soil and can be
introduced on infected bulbs.
• Warm moist conditions favour conidial production and
wind and rain splash spread the conidia.
• These conidia infect mature bulb scales and cause
disease when free moisture and optimum temperatures
for infection occur.
Management:
 Plant debris should be collected and burnt to prevent the introduction
of pathogen into other fields.
 Yellow and red skinned varieties can be used in areas where disease
pressure is high.
 Cultural practices like, good drainage and use of healthy planting
material.
 Practice a three years or longer crop rotation.
 Protect the produce after harvested from rains, provision of well-
ventilated storage also reduces the incidence of the disease.
 Pre-harvest spray of Carbendazim (0.1%) or Mancozeb (0.2%) reduce
the infection of this disease under storage conditions.
 Leaf Spot of Turmeric
Distribution:-
The disease is prevalent in almost all of the turmeric-growing
regions, and often it can occur in epidemic form. Several
investigators have extensively studied the disease, in various
species of turmeric, such as Colletotrichum capsici, C.
curcumae and C. gloeosporioides.
Symptoms:-
The disease appears in the form of elliptic or oblong spots
of variable size. In the initial stages of infection, the spots
are small and measure only few centimeters in length and
are 2–4 cm in breadth, which later may increase in size. In
advanced stages of infection, two or more leaf spots
coalesce and develop into irregular patches which occupy a
major portion of the leaf, which eventually dries up. The
center of the spot is grayish white and thin with numerous black
dots called acervuli, springing up on both upper and lower
surfaces, and arranged in concentric rings. The grayish white
portion is surrounded by a yellow halo around it. The
central region of the spot may become papery and easily tear.
The infection is usually confined to lamina and may occasionally
extend to leaf sheaths. The pathogen survives on infected leaf
debris for at least 1 year, which forms the pri-mary source for
succeeding infection.
Causal Organism:- Colletotrichum capsici
Favorable condition:-
• The disease is usually appears in October and November.
• Relative humidity of 80% and temperatures of 21 – 230C favours the primary infection.
Disease cycle:-
The fungus is carried on the scales of rhizomes which are the source of primary infection during
sowing. The secondary spread is by wind, water and other physical and biological agents. The same
pathogen is also reported to cause leaf-spot and fruit rot of chilli where it is transmitted through seed
borne infections. If chilli is grown in nearby fields or used in crop rotation with turmeric, the pathogen
perpetuates easily, building up inoculum potential for epiphytotic outbreaks.
Management:-
• Select seed material from disease free areas.
• Treat seed material with mancozeb @ 3g/litre of water or carbendazim @ 1 g/litre of
water, for 30 minutes and shade dry before sowing.
• Spray mancozeb @ 2.5 g/litre of water or carbendazim @ 1g/litre; 2-3 sprays at
fortnightly intervals.
• The infected and dried leaves should be collected and burnt in order to reduce the
inoculum source in the field.
• Spraying Blitox or Blue copper at 3 g/l of water was found effective against leaf spot.
• Crop rotations should be followed whenever possible.
• Cultivate tolerant varieties like Suguna and Sudarshan.
 Stem gall Coriander
Distribution:-
The disease is prevalent in all coriander-growing areas of India and
is considered as a limiting factor for the successful cultivation of the
crop. It is one of the largest-known diseases on coriander in the
world. This disease has been reported from all coriander growing
areas of the world such as Scotland, Ireland, Norway, Denmark,
Sweden, Germany and in North America, North Africa and South
Asia where the favorable temperature is present.
Symptoms:-The infection of stem gall disease takes place at an early
stage of seed germination, but the symptoms appear much later. The
fungus cause swellings (hypertrophy and hyperplasia) on stems,
leaves, flowers, fruits and other aerial parts of tissues of plants. The
disease appears in the form of swellings of leaf veins, leaf stalks,
peduncles, stems and on fruits. The swellings on the veins give a
swollen hanging appearance to the leaves. These tumors are initially
glossy but later rupture and become rough. The swellings are mostly
elongated, and their size varies according to the size of the infected
part, those on the stem being usually larger than those on the flower
stalk. Systemic infection provides greater distortion to the plant and
plant parts. The inflorescence may show outgrowth on the surface,
and uniform invasion of the fruit makes it abnormally large, but
partial invasion may lead to distortion. The disease is usually
apparent in early spring when the greatly distorted leaves first
appear. On veins, mid-ribs, and petioles, the gall appears as
translucent yellow-white swellings that are often elongated and
blister-like.
Causal Organism:- Protomyces macrosporus
The mycelium was intercellular , coenocytic , septate , and branched . The chlamydospores (resting
spores) of P. macropsorus were yellowish brown, spherical or globose to oval, single-celled, smooth and
measured 40 to 81 μ in diameter. A mature chlamydospore was protected externally by hard, thick and
unsculptured exospores enclosing a medium thick mesopore and membraneous endospore.
Disease Cycle:-
The disease is seed and soil borne in nature.
In soil the fungus over winters in the form of chlamydospores.
The chlamydospores germinate in the presence of water by rupturing the outer wall.
The inner wall is pushed out to form vesicle, which appears in continuation with the mouth of the crack.
The protoplasm passes into this vesicle and the nucleous divides several times forming 100 to 200
daughter nuclei.
The protoplasm also devoides by cleavage into several uninucleate masses.
On maturity, these spores separate and collect into the centre of the vesicle. The latter burst and the
spores are set free.
These spores further multiply by budding in yeast like fashion and cause infection of the host.
Minimum/maximum atmospheric temperature and relative humidity play an important role in in
initiation and development of this disease.
Potassium and nitrogen fertilizers reduced stem gall incidence while phosphoric fertilizers increase it.
A pH of 7.5 is most suitable for infection while minimum infection occurred at pH 5.5.
Favourable Conditions:-
Relatively high soil moisture and soil temperature are favourable for infection.
Management:-
The disese affects less in the early and late sown crop. Sowing crop around 16 October to 16
November give minimum yield losses.
Use of clean and healthy seed and follow suitable crop rotation.
Use resistance cvs/lines like Jd 1, G-5365-91, Pant Haritma, UD 20, Rcr 41, Pant-1, CIMAP 2053.
Seed treatment with Captan/Thiram (0.3%) followed by their foliar sprays were foun effective in
managing this disease.
 Diseases of Rose and marigold
1. Black Spot of Rose
Symptoms:
Black, nearly circular spots ranging in diameter from just under one-tenth of
an inch to about one-half inch occur on the upper leaf surfaces. They have
characteristic feathery margins. Infected leaflets usually turn yellow and drop from
the plant. Lower leaves are usually infected first, followed by middle and upper leaves.
Excessive defoliation weakens plants and increases the risk of winter injury from cold
temperatures. In resistant cultivars or during dry weather, only small spots may form
without defoliation. Symptoms also can occur on canes. They usually occur in the form
of raised purple blotches on immature wood of first-year canes, which later become
blackened and blistered. Branches are rarely killed by lesions on canes; however, the
pathogen survives the winter in these lesions. Inconspicuous, reddish-purple spots
may result from infection of petioles, stipules, peduncles, fruit and sepals.

Causal Organism: Diplocarpon rosae

Etiology and Disease Cycle:

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 micron in diameter.
Stroma thin, conidiophores are hyaline short and cylindrical. Conidia are hyaline, two celled,
fusiform or allantoid to obclavate, upper end round, base narrow, 18 – 25 x 5 – 6 micron meter.

The black spot fungus overwinters as mycelia or spores in infected canes and leaves. In the spring,
overwintering mycelia or spores cause primary (initial) infections on new shoots. Within about two
weeks after primary infections, fruiting structures form within lesions and produce spores which
cause secondary infections throughout the growing season. At least seven hours of continuous
wetness is required for spores to cause infection. Temperatures ranging from 72°F to 86°F favour for
disease development.

Management:

 The first step is to select disease resistant cultivars.

 Removal and destruction of infected canes and fallen leaves
 Planting roses in sunny locations and spacing plants adequately to allow good air circulation
will promote quick drying of foliage.
 If possible, avoid sprinkler irrigation.
 Spraying with Mancozeb (or) Chlorothalonil 0.2% (or) Benomyl 0.1% or a copper dust.
 2. Powdery Mildew of Rose
Symptoms:

This disease is recognized by the white, powdery growth on leaves, shoots, and buds. Early
symptoms of disease appear as chlorotic or reddish areas or patches on leaves that eventually
develop the characteristic white, powdery appearance. This diagnostic, powdery, white
growth is usually found on the upper surfaces of leaves, but it can occur on both upper and
lower leaf surfaces. When newly emerging shoots are infected when young, shoots can be
distorted and twisted. Young leaves may curl upward and may be deformed. Flower buds
infected with powdery mildew often fail to open. Unlike other fungi that require free water in
order to infect, the powdery mildew fungus does not require moisture on the tissues for
infection. This fungus also produces small, black, pepper-like resting structures called
cleistothecia. Cleistothecia are overwintering structures, these are found in plant debris and
are often the primary sources of inoculum in the spring. The powdery mildew fungus can also
survive the winter as hyphae or fungal strands in infected buds.

Causal Organism: Sphaerotheca pannosa

Etiology and Disease Cycle:

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 to 29.0 x 12.9 to 14.5 micron in size.
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.
The disease cycle of rose powdery mildew starts when the sexual spores (ascospores) of
the pathogen which produced inan ascocarp. The specific ascocarp is a cleistothecium, and
has a circular shape to it. Under the right conditions the cleistothecium break open to reveal
the asci, which are tube like structure containing the ascospores. These ascospores are then
released and spread by wind, insects, and rain until they land on a susceptible rose for a host
and land attach, and germinate on the plant. They also produce conidia, the sexual spores of
Sphaerotheca pannosa, which will spread throughout the summer. It is these long chains of
white conidia which give the fungus its characterstic ‘Powdery’ appearance. Late in the year
as the plant is dying cleistothecia again form when the ascogonium recieves the nucleus from
the antheridium. The fungus overwinters as mycelium in dormant buds and shoots spread is
through wind-borne conidia. The disease is favoured by dry weather with maximum day
temperature of 20 to 25°C with cool nights.
Management: Use of resistant varieties like paradise, dwarf queen, super starcrimison glory.
 The diseased and fallen leaves should be collected and burnt.
 Four sprayings at 10 days interval with wettable sulphur 0.3% or dinocap 0.07% or
carbendazim 0.1 % manage the disease effectively.
 Wettable sulphur or sulphur dust should not be used when the temperature is above 30°C
as it may cause scorching.
3. Di back of Rose
Symptoms:
Drying of twigs from tip to down wards.
Blackening of the twigs. The disease
spreads to root and causes complete killing
of the plants.

Causal Organism: Diplodia rosarum

Etiology and Disease Cycle:

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.
The fungus survives in dead twigs and
the stalks of the withered blooms.
Management:
 Pruning should be done so that lesions on the young shoots will be eliminated.
 Apply chaubatia paste on the pruned surface.
 Spray with Difolatan 0.2% or Chlorothalonil 0.2% or Mancozeb 0.2%.

4. Botrytis Blight or grey mould of Marigold

Symptoms:

Botrytis blight, also known as grey mould, is a

fungal disease. This disease is particularly
troublesome during periods of extended cloudy,
humid, wet weather. 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.
A covering of grey fuzzy fungal growth and spores
appears on infected plant tissue.

Causal Organism: Botrytis cinerea

Etiology and Disease Cycle:
The hyphae are septate and 8-16 µm wide. The tall, erect, conidiophores arising from the
mycelium are hyaline towards the tip but dark below. The tips rise to sporogenous ampullae,
each ampulla produces numerous conidia. Conidia are septate, ovate and 11-15x8-11 µm in
size. Generally, the sclerotia appears like a crust on woody part of the host.
 Botrytis fungi overwinter as sclerotia on dead plant debris in the garden. In the spring,
spores form and spread by wind or splashing water to infect dying, wounded, or extremely
soft plant tissues. Fungal mycelial strands (web blight) from previously infected plant parts
can grow onto healthy plant parts and infect them. The fungus is capable of invading tissue
during all periods of the growing season and multiplies rapidly in declining foliage, hence, the
need for good sanitation. A moist, humid environment is ideal for pathogen sporulation and
spread.

Management:
 Remove and destroy all infected plant parts as soon as they are observed.
 Give adequate space between plants to allow for good air circulation.
 Avoid fertilizing with excessive amounts of nitrogen. This can cause tender growth that is
very susceptible to the fungus.
 Water on foliage and flowers from overhead irrigation, especially on cool, cloudy days,
promotes the disease. Try to keep buds and flowers dry. Water early in the day so the plants
have enough time to dry off completely.
 Spray fungicide like chlorothalonil, mancozeb or thiophanate methyl at 10-15 days interval.

5. Blister blight of Tea

Symptoms:
Small, pinhole-size spots are initially seen on young leaves less than a month old. As
the leaves develop, the spots become transparent, larger and light brown. About 7 days
later, the lower leaf surface develops blister with dark green water-soaked zones
surrounding the blister. After releasing the fungus al spores, the blister becomes white
and velvety. Subsequently the blister turns brown and young infected stems become bent
and distorted.

Causal Organism: Exobasidium vexans

Etiology and Disease Cycle:

Basidia are hyaline, club shaped, thin walled with two short sterigmata at the end and
arise from the hymenial layer intermingled with sterile hairs. Each basidium bears 4-8
hyaline and oval to oblong basidiospores. The basidiospores form hyaline, elliptical,
straight or slightly curved conidia like blastospores which also germinate and infect the
leaves.
 The disease cycle repeats continuously during favourable (wet) conditions, and the spores
are readily dispersed by wind. Spores that land on a leaf with adequate moisture will
germinate and infect it, producing visible symptoms within 10 days. The fungus can
directly penetrate the leaf tissue. The basidiospores have a low survival rate under
conditions of drought or bright sunlight. The life cycle of the fungus is 3–4 weeks.
Management:

 Removal of affected leaves and shoots by pruning and destruction of the same have been recommended.
 Spraying of Bordeaux mixture or Copper Oxy Chloride 0.1%
 A mixture of 210g of Copper oxy Chloride + 210g of nickel chloride per ha sprayed at 5 days interval from June to
October to November
 Spray Tridemorph at 340 and 560 ml/ha is satisfactory under mild and moderate rainfall conditions

6. Coffee rust

Symptoms

It mostly affects leaves or some time leaves and tender shoots.

In earlier stage, 2- 3 mm size yellow spots develop on the lower
surface of leaves. Rust lesions develop as orange yellow spots on
lower surface of leaves. The upper surface of the leaves just above
the lesion, become yellow to brown. At later stages, yellow rusty
appearances are found on the entire under surface of the leaf. The
orange yellow spots are followed by black spots followed by
necrosis. Infected leaves defoliate and branch remains without any
leaves. The plants remain stunted with reduced yield.
Causal Organism: Hemileia vastatrix
Etiology and Disease Cycle:
The pathogen produces urediniospores which are cuniform with the convex surface
ornamented with spines or warts. The fungus occasionally produces teliospores which germinate
and produce basidium and basidiospores. They do not infect coffee plant and alternate host has
been not found.
For a tropical evergreen perennial shrub like coffee, it would appear that there is no need of
alternate host, despite its role in sexual recombination. The carry over of inoculum between rainy
season is critical, the longer dry season would reduce fungal survival. At the beginning of rainy
season new leaves are produced, which are most susceptible when they are maturing. The rate of
infection is high during the mid to late rainy season but with onset of dry weather, the infection
ceases.

Management
 Collection and destruction of diseased leaves.
 Grow S 238, S 395 resistant varieties.
 Spraying of Bordeaux mixture 0.5% before flowering, during rainy and after rainy seasons.
 7. Coconut wilt
Symptom:

The characteristic symptom of the disease is slow wilting of the foliage. Tapering of terminal portion of the
trunk and reduction of leaf size. Abnormal bending or Ribbing of leaf lets termed as flaccidity. Flowering is
delayed and also yield is considerably reduced. This is the earliest visual symptom. In the beginning
yellowing is restricted from the leaf tips to the middle of the leaves, necrosis of leaflets and deterioration
and decay of root system are other salient features of the disease. The leaflets curve inwardly to produce
ribbing so that the whole frond develops a cup like appearance. Abnormal shedding of buttons and
immature nuts are also noticed.

Causal Organism: MLOs (mycoplasma like organisms)

Etiology and Disease Cycle:
The disease is transmitted by insect vectors such as lace bug (Stephanitis typica), leaf hopper (Sophonia
greeni) and plant hopper (Proutista moesta). Electron microscopic observation of the lace bug that had a sufficient
acquisition plus incubation period on diseased palms (18-23 days) showed the presence of MLOs in the salivary
glands and brain tissues, which were not observed in the bugs collected from healthy palms. In case of hoppers, the
acquisition plus incubation period is more than 40 days.
Management:
• Cut and remove diseased, uneconomical palms yielding less than 10 nuts per palm per year.
• Grow green manure crops - cowpea, sunhemp (Crotalaria juncea), Mimosa invisa, Calapagonium
mucanoides, Pueraria phaseoloides etc. may be sown in coconut basins during April-May and
incorporated during September-October.
• Adopt suitable inter/mixed cropping in coconut gardens.
• Provide adequate drainage facilities.
• Magnesium may be supplied @ 500 g per palm per year
• To manage the insect vectors, phorate 10 G (200 g) or powdered neem cake (250 g.) mix withal
quantity of sand and place around the base of the spindle.
8. Bud rot of coconut
Symptom:

Palms of all age susceptible, but normally young palms are more susceptible, particularly during
monsoon. In seedlings, the earlier symptom is the yellowing of one or two younger leaves. Basal
tissues of the leaf rots quickly and can be easily pulled out from the crown. In the later stages the
spindle withers and drops down. The tender leaf base and soft tissues of the crown rot into a slimy
mass of decayed material emitting foul smell. Ultimately the entire crown falls down and the palm
dies In adult palms, the first visible symptom is the colour change of the spear, which becomes
pale and breaks at the base and hangs down. The rotting slowly progresses downwards, finally
affecting the meristem and killing the palms. This is accompanied by drooping of successive
leaves. Even then, nuts that are retained on the palm may grow to maturity.

Drooping
Causal Organism: Phytophthora palmivora
Etiology and Disease Cycle:

The pathogen of bud rot is found to survive on infected palmyrah and coconut palms as dormant
mycelium. Whenever the seasonal conditions favourable, the dormant mycelium germinates and
spreads to the nearby palms. The primary source of inoculum was found to exist on dead palms of
palmyrah existing in coconut gardens. The disease appears mostly during first fortnight of June of
every year i.e., with the onset of the monsoon and maximum disease incidence occurs during the
months of July to October when the maximum and minimum temperatures were 33.20°c and
25.27°c and relative humidity were 96.52 and 60.69 respectively.

Management:
 Provide adequate drainage in gardens.
 Adopt proper spacing and avoid over crowding in bud rot prone gardens.

 Remove all the affected tissue of the crown region and drenching the crown with Copper
oxychloride 0.25%. Apply Bordeaux paste and protect it from rain till normal shoot emerges.
(Dissolve 100 gm of copper sulphate and 100 gm of quick lime each in 500ml. water separately
and mix to form 1 litre of Bordeaux paste).
 Spray 0.25% Copper oxychloride or 1 % Bordeaux mixture on the crown of the neighbouring
palms as a prophylactic measure before the onset of monsoon. Palms that are sensitive
(Dwarf palms) to copper containing fungicides can be protected by mancozeb 0.2%.
 Leaf axil filling with Sevidol 8G, 25 g mixed with 200g sand is recommended to manage red
palm weevil infestation of affected palms.

.
 Anthracnose of Mango
Symptoms:
Numerous, oval or irregular spots appears on the leaf surface. Under humid conditions
these spots increase rapidly and form irregular necrotic areas. The young leaves are most
susceptible to this disease. The wither tip or die-back symptoms appear at the tip of young
branches. Black necrotic areas are formed on the affected twigs which dry from the tip to
downward accompanied by defoliation of the branch. The pathogen causes blossom blight in
which minute black spots appears on the flower which dry and shed. On fruits black spots of
various forms develop which may be slightly sunken or may show surface cracks. These spots
may coalesce to form larger spots. The spots are often concentric at the stem end and some
times in streaks towards one side of the fruit.

Causal Organism: Colletotrichum gloeosporioides Perfect stage – Glomerella cingulate

Etiology and Disease Cycle:
Mycelium is narrow, septate which are initially hyaline but later become slightly dark.
Acervuli are formed abundantly on the affected host surface. In acervuli numerous
conidiophores arise, among them setae are also formed. One or more conidia are formed at
the apex of each conidiophore. The conidia are hyaline but in mass they look pinkish. They
are oval to oblong with rounded ends, non-septate and some times contains 1-2 oil globules.
Conidia germinate by means of germ tube and form dark appressoria. The perfect stage of
the fungus produces perithecia. The perithecia are sub-spherical with prominent ostiolar hair.
Asci are sub-clavate and slightly pedicellate. Ascospores are hyaline and single celled. They
are difficult to distinguish from conidia.
The fungus has a long saprophytic survival ability on diseased leaves and twigs in soil.
The conidial production in acervuli favoured by temperature 10-30℃ and relative humidity
95-100%. The humid and misty conditions are most favourable for disease development.

Management: 1. Apply recommended dose of fertuilizers and watering during summer.

2. Diseased twigs should be pruned and burnt along with fallen leaves.
3. Two to three sprays of Fytolan or Zineb (0.2%) between January to July effectively manage
the disease.
4. Post-harvest treatment of fruits in hot water at 50℃ for 15 minutes effectively check the
fruit rot.
 Bacterial blight of Mango
Symptoms:
Minute wate soaked lesions appears in groups towards the tip of the leaf blade. They
increase in size to about 1-4 mm, turn brown to black in colour and surrounded by chlorotic
halos. Large necrotic patches may be formed by coalescing of several lesions. These patches
are often rough and raised due to heavy bacterial exudate. On tender branches and fruits
water-soaked lesions appears which later become raised and turn dark brown to black with
longitudinal cracks mostly filled with bacterial oozes.

Causal Organism: Xanthomonas campestris p.v. mangiferaeindicae

Etiology and Disease Cycle:
The bacterium is straight rod and 0.36-0.54 x 0.45-1.44 micron in size. The bacterial
cells are single or in short chains. No capsule or spores are formed. It is motile by single
polar flagellum. It is gram negative and aerobic.
The pathogen survives from one season to the next in localized lesions on leaves and
twigs. From these lesions the bacteria are washed to adjacent tissues. Patogen spread from
one tree to another during rain by splashing of water droplets. Maximum infection occurs
when temperature ranged between 22-26℃. Rainfall is a major weather factor affecting
infection.

Management:
 Orchard sanitation
 Pruning and destruction of infected plant parts.
 Spraying of Agrimycin (0.1%) followed by Plantomycin or Streptomycin sulphate
(0.25%) followed by Aureofungin (0.25%) found effective in controlling the disease.
 Malformation of Mango
Symptoms:
Symptoms appears at two stages i.e. vegetative malformation and floral
malformation. Vegetative malformation is more pronounced on young seedlings but may also
appear on mature trees. In the initial stages of symptom development, vegetative buds in the
axils of the leaves or at the apex of seedlings swell and produce small shoot lets bearing small
scaly leaves. In such seedlings apical dominance is lost and as a result numerous vegetative
buds sprout, producing hypertrophied shoot lets, bearing very small leaves at short
internodes. The leaves get crowded so that shoot lets and their branches are not
distinguishable and the whole mass of rudimentary leaves gives a bunch like appearance,
which also referred to as bunchy top stage. In floral malformation, the flowers in diseased
panicles are greatly enlarged, which constitutes a malformed inflorescence. At maturity such
panicles appear hypertrophied, heavier and generally much greener as compared to healthy
one.

Causal Organism:
The actual cause of the disease has been very controversial. Several workers have
suggested various causes.
 Fungal cause: Fusarium moniliforme var subglutinans
 Acarological cause: Aceria mangiferae (Eriophyid mite)
 Physiological cause: Imbalance of auxin and anti-auxins hormones. Increment in
carbohydrates, mangiferin, malformin and phenols. Deficiency of iron, zinc and
copper.
Etiology and Disease Cycle:
The sufficient information on the causal organism, it’s biology and infection court,
mode of entry, mechanism of dissemination have not been generated and still unknown.
Management:
 Use disease free planting materials.
 Seedlings should be raised in the soil free from fungal pathogen.
 It should also be ensured that scions selected from a tree free from malformation.
 Pruning of diseased parts along with basal 15-20 cm healthy portion.
 Spraying of NAA (0.02%) during October.
 Spraying of carbendazim or benomyl (0,1%) and phosphamidan (0.1%) at pre-bud
burst, after emergence and pre-blossom stage.
 Powdery mildew of Mango
Symptoms:
The disease appears at flowering time (Jan-March). The characteristic symptoms are
the presence of white, superficial, powdery growth on all the aerial parts like inflorescence,
leaves, stalk of inflorescence and young fruits. Flowers are attacked before fertilization which
results in dropping of infected flowers. Young fruits are covered entirely by powdery growth
and it results in pre-mature fruit drop at pea stage.

Causal Organism: Oidium mangiferae

Perfect stage: Erysiphe polygoni

Etiology and Disease Cycle:

Pathogen produces branched conidiophores from the superficial mycelium. Conidia
are borne singly but some times in pairs or in chain. Conidia are single celled and oval shaped.
The pathogen survives in intact malformed infected panicles mostly hidden under
dense foliage where conidia are produced. Abundant conidia are produced and blown over
to the new flushes on young panicles. Conidia germinate by germ tube which produces
haustoria inside the host cells.

Management:
 Orchard sanitation.
 The intact malformed panicles should be removed from the tree and burnt.
 Spraying of carbendazim (0.1%) or dinocap (0.2%) or triadimefon (0.05%) have given
effective management.
 Citrus Canker
Symptoms:
Necrotic brown spots having a course raised surface appeared on all the aerial parts including
leaves, twigs and fruits. On young leaves, the lesions appear as small white specks and later develop
into brown necrotic spots. The lesions further enlarge and become white or greyish which give a
rough, corky and crater like appearance. The lesions are surrounded by a yellow halo. The cankers are
irregular, rough and more prominent on twigs and branches. The lesions on fruits are almost similar
to those on leaves, however the yellow halo is absent

Causal organism:
Xanthomonas campestris pv. citri , now known as Xanthomonas axonopodis.
Etiology and Disease cycle
The bacterium is straight rod and 1.5-2.0 x 0.5-0.75 micron in size. It forms chains and
capsule but no spores and motile by single polar flagellum. It is gram negative and aerobic.

The bacterium does not survive in the soil or on infected plant parts fallen on the ground.
Attacked twigs bearing old lesions on the tree are the main source of perennation of the
pathogen. The bacteria from the cankers are mostly disseminated by driving rains, by insect such
as citrus leaf minor (Phyllocnistis citrenella) and by man himself through infected nursery stock.
The bacterium enters the host through stomata and through wounds such as those caused by
insects or movement of thorns. It multiplies rapidly in the intercellular spaces, dissolves the middle
lamella and establishes in the cortical region. The disease is favoured by mild temperature (20-
30℃) and wet weather.

Management:

 Fallen and pruned canker affected leaves and twigs should be collected
and burnt.
 Use, disease free nursery stock for planting in new orchard.
 Vigour of the plant should be maintained by proper irrigation and
fertilization.
 Spraying of streptomycin sulphate (500-1000ppm) at 15 days interval.
 Citrus Gummosis
Symptoms:
Primary infection normally occurs at the base of the trunk near ground level. Then the
infection spreads upwards and downwards to the roots. The bark and wood both are affected.
The main symptom is oozing of gum from affected parts. During the raining season the gum
is washed down or near the ground it get mixed with soil hence symptom may not be clear.
During summer gum deposits make the symptom very clear. Bark on the affected trunk and
branches cracks and dries. Leaves of the affected trees show symptoms of nutritional
deficiency. Their veins turn yellow and there is premature leaf fall.

Causal organism:
Phytophthora citrophthora, P. parasitica and P. palmivora
Etiology and Disease cycle:

The mycelium of the pathogen in soil soon converted into oospores and
chlamydospores. In the presence of host roots, nutrients, optimum temperature and
moisture these resting spores germinate by germ tube and by sporangia and zoospores. These
zoospores initiate the infection. The fungus also survives on fallen fruits, twigs, leaves and
cracks on the standing tree. Dispersal of sporangia and zoospores is by wind, rain drop
splashes, irrigation water and insects. Heavy soil, high soil moisture, soil pH of 5.4-7.5 and
temperature around 24℃ are conducive for disease development.
Management:

 The site selected for citrus orchards should be on well drained land.
 Resistant root stock such as Khatta and trifoliate orange may be used.
 Fallen fruits, leaves and twigs should be collected and burnt.
 The trunk should be painted every year with Bordeaux paste up to a height
of about 70 cm.
 Spraying and drenching of Ridomil MZ-72 or Blitox-50 (0.25%) during
summer and rains.
 Diseases of Grape vine
1. Downy Mildew of Grape
Symptoms:

Irregular, yellowish, translucent sports on the upper

surface of the leaves, these are about 10mm diameter often
with a chocolate halo. Correspondingly on the lower surface,
white, downy (cottony) growth on leaves. Affected leaves
become, yellow, brown and gets dried and premature fall.
Infection on young shoots, stems and tendrils is seen as oily
brown areas. These oily patches may spread into leaf stalks,
which turn brown and may die. After warm humid nights
spots on upper leaf surface
these oily patches may also sporulate and be covered with
white downy growth of the fungus. Infection on
inflorescences, young berries and bunches, are seen as oily
brown areas. Infected inflorescences and young bunches
rapidly turn brown and wither. Infected young berries stop
growing, harden and may later develop a purple in colour.
They turn dark brown, shrivel and fall from bunches.
Lower leaf surfece
Causal Organism: Plasmopara viticola
Etiology and Disease Cycle:
Mycelium is intercellular with spherical haustoria, coenocytic, thin walled and hyaline.
Sporangiophores arise from hyphae in the sub stomatal spaces. It branched at right angle
to the main axis and at regular intervals. Secondary branches arise from lower branches.
Ssporangia are thin walled, oval or lemon shaped. The Zoospores are pear shaped,
biflagellate and 7 – 9 µm. The oospores are thick walled which are the survival and resting
stage of the pathogen.
The pathogen survives in the winter
as oospores embedded in dead leaves
and other host tissue on the vineyard
floor. Oospores may be released from the
decaying plant material on the soil
surface. Oospores typically produce
sporangia. These sporangia, produce
zoospores. Sporangia and zoospores are
splashed by rain or carried by wind to the
lower leaves and tissues of the grape-
vines. The condition necessary for
oospore germination are wet soils with
temperatures above 10ºC. Once
zoospores form and are dispersed to host Disease Cyc le

wny
of Do

Mildew
tissue, infection will occur. Zoospores encyst and then germinate and penetrate through
stomates. After infection, the pathogen grows intercellularly, producing haustoria.
Secondary infections occur through sporangia, produced on sporangiophores that emerge
through stomata of infected leaves and other grapevine tissues. Optimum temperature
20-22°C and relative humidity 80-100 per cent favours for disease development.

Management:
• When establishing vine-yards the location, drainage, type of irrigation and trellising
system should also be selected to reduce the risk of disease.
• Avoid increasing humidity and leaf wetness at night to mitigate secondary infection.
• Spray the crop with Bordeaux mixture 1 % or Metalaxyl + Mancozeb 0.4 %.

2. Powdery mildew

Symptoms:
The powdery mildew fungus can infect all green tissues of the vine. Small, white or
grayish-white patches of fungal growth appear on the upper or lower leaf surface. These
patches usually enlarge until the entire upper leaf surface has a powdery, white to gray
coating. The Severely affected leaves may curl upward during hot, dry weather.
On young shoots, infections are more likely to be limited, and they appear as dark-
brown to black patches that remain as dark patches on the surface of dormant canes.
If blossom clusters are affected, the flowers may wither and drop without setting fruit.
Infected cluster stems may wither and dry up, resulting in berry drop. Affected berries
may have patches of fungal growth on the surface similar to those on the leaves, or the
entire berry may be covered with the white, powdery growth. Infected berries often are
misshapen or have rusty spots on the surface. Severely affected fruit often split open.
Late in the season, many black specks may develop on the surface of infected areas.
These are the sexual fruiting bodies (cleistothecia) of the fungus.
 Causal Organism: Uncinula necator
Etiology and Disease Cycle:
White growth consists of mycelium, conidiophores and conidia. Mycelium is
external, septate and hyaline. Conidiophores are short and arise from external
mycelium. Conidia are produced in chain. They are single celled, hyaline and barrel
shaped.
The powdery mildew fungus
overwinters as chasmothecia (tiny,
round, black fruiting bodies), in bark, on
canes, left-over fruit, and on leaves on
the ground. Spores (ascospores) from
the overwintering chasmothecia are
released in the spring after a rainfall of
at least 2.5 mm. For primary infection
to occur the spores require at least 12-
15 hours of continuous wetness at 10-
15 °C to infect developing plant tissue.
Once the primary infection has occurred
the disease switches to its secondary
phase. Patches of white powdery Disease Cycle
mildew develop in 7 to 10 days. These produce millions of spores (conidia) which are
spread by wind to cause more infections. Free moisture is not needed for secondary
infection; temperature is the most important environmental factor. The disease
spreads quickly in early summer when temperatures are moderate. The incubation
3.time can be as short as 5 to 6 days under optimal temperatures. Shaded and
sheltered locations favour for powdery mildew development. High temperatures and
sunlight are inhibitory to powdery mildew.
Management:
 Manage canopies to increase air drainage and light penetration by removing lateral
shoots in dense canopies. If necessary, remove leaves in the fruiting zone. Dense
canopies provide low light intensity, which favours powdery mildew development.
 Use an under-vine irrigation system (drip or micro-jet).
 Manage irrigation carefully. Excessive irrigation leads to excessive vigour and higher
disease potential.
 Select varieties that are less susceptible to mildew.
 Spray Inorganic sulphur 0.25 % or Chinomethionate 0.1 % or Dinocap 0.05 %.

3. Anthracnose/Bird’s Eye Spot

Symptoms:

The symptoms of disease appear on shoots and berries, fruit stems, leaves, tendrils and
petioles. Disease is more dangerous when it occurs on young leaves. Infected leaves are
usually full of spots with grey centers and brown to black margins, with round or angular
edges. Grey center of the spots eventually dry and drops out, so leaves look like they were
shot through. If spots cover the entire leaf or affect leaf veins the whole leaf eventually dries
out. Symptoms on shoots first appear as small, round, reddish spots. Eventually, the spots
enlarge, and generate grey centers with reddish brown to black margins and round or
angular edges. On infected lesions, shoots can crack and become brittle, or die out. The
symptom of disease on the berry appears first as dark red spots. Later, these spots are
circular, sunken, ashy- grey and in late stages these spots are surrounded by a dark margin
which gives it the “bird’s eye” appearance. The spots vary in size from 1/4 inch in diameter
to about half the fruit.

Causal Organism: Gloeosporium ampelophagum (Elsinoe amphelina)

Etiology and Disease Cycle:

 Mycelium is septate and dark coloured. Conidia single celled oval and hyaline. The fungus
overwinters in the vineyards as sclerotia (fungal survival structures) on infected shoots. In
the spring, sclerotia on infected
shoots germinate to produce
abundant spores (conidia). Conidia
are spread by splashing rain to new
growing tissues and are not carried
by wind alone. Conidia are by far the
most important source of primary
inoculum in the spring. In early
spring, when free moisture from rain
or dew is present, conidia germinate
and infect succulent tissue. Conidia
germinate and infect. Heavy rainfall
and warm temperatures are ideal for
disease development and spread.
Once the disease is established, asexual fruiting bodies called acervuli form on diseased
areas. These acervuli produce conidia during periods of wet weather. These conidia are the
secondary source of inoculum and are responsible for continued spread of the fungus and
the disease throughout the growing season.

Management:

 Prune out and destroy (remove from the vineyard) diseased plant parts during the dormant
season.

 Eliminate wild grapes near the vineyard.

 Any practice that opens the canopy to improve air circulation and reduce drying time of
susceptible tissue is beneficial for disease control.

 Where the disease is established, especially in a commercial vineyard, the use of fungicides
is recommended e.g. Copper oxychloride 0.2% or Mancozeb 0.25%.
 Peach Leaf Curl
Identification (Symptoms):
 Diseased leaves are 2-3 times larger than healthy leaves.
 Affected leaves show curling inwards.
 Infected leaves are twisted, thickened, puckered and often greatly distorted.
 In the beginning affected leaves looks pale green or yellowish but finally change to
reddish or purple colour.
 Old infected leaves become necrotic, wither and have premature fall.
 Infected twigs become swollen and ultimately killed.

Histopathological studies:
 The disease is caused by Taphrina deformans.
 Mycelium of the fungus form just below the epidermis of the upper surface of the
leaf.
 The mycelial cells contain two nuclei, which may develop into ascogenous (stalk) cell.
 Asci produced from the stalk cells in a naked layer on the host surface.
 A mature ascus is typically clavate.
 An ascus contains eight, uninucleate round or oval ascospores.
 The ascospores multiply by budding inside or outside the ascus, producing conidia.
 Citrus Canker
Identification (Symptoms):
 Necrotic brown spots having a course raised surface appeared on all the aerial
parts including leaves, twigs and fruits.
 On young leaves, the lesions appear as small white specks and later develop into
brown necrotic spots.
 The lesions further enlarge and become white or greyish which give a rough,
corky and crater like appearance.
 The lesions are surrounded by a yellow halo.
 The cankers are irregular, rough and more prominent on twigs and branches.
 The lesions on fruits are almost similar to those on leaves, however the yellow
halo is absent

Histopathological studies:
 The causal organism is Xanthomonas campestris pv. citri , now known as
Xanthomonas axonopodis.
 The bacterium is straight rod and 1.5-2.0 x 0.5-0.75 micron in size.
 It forms chains and capsule but no spores and motile by single polar flagellum.
 It is gram negative and aerobic.
 Citrus Gummosis
Identification (Symptoms):
 Primary infection normally occurs at the base of the trunk near ground level.
 The infection spreads upwards and downwards to the roots. The bark and
wood both are affected.
 The main symptom is oozing of gum from affected parts.
 During the raining season the gum is washed down or near the ground it get
mixed with soil hence symptom may not be clear.
 During summer gum deposits make the symptom very clear.
 Bark on the affected trunk and branches cracks and dries.
 Leaves of the affected trees show symptoms of nutritional deficiency. Their veins
turn yellow and there is premature leaf fall.

Histopathological studies:
 Phytophthora citrophthora, P. parasitica and P. palmivora are associated with the disease.
 The mycelium of the pathogen is coenocytic and petaloid colony pattern.
 In soil the mycelium, soon converted into oospores and chlamydospores.
 In the presence of host roots, nutrients, optimum temperature and moisture these
resting spores germinate by germ tube and by sporangia.
 The sporangia are papillate, obpyriform or ovoid in shape and 36.5-64.4 x 23.6-38.6
m in size.
 These sporangia, produces zoospores which initiate infection.
 Blister blight of Tea
Identification (Symptoms):
 Small, pinhole-size spots are initially seen on young leaves less than a month old.
 As the leaves develop, the spots become transparent, larger and light brown.
 About 7 days later, the lower leaf surface develops blister with dark green water-
soaked zones surrounding the blister.
 After releasing the fungus al spores, the blister becomes white and velvety.
 Subsequently the blister turns brown and young infected stems become bent and
distorted.

Histopathological studies:
 The disease is caused by Exobasidium vexans.
 Basidia are hyaline, club shaped, thin walled with two short
sterigmata at the end and arise from the hymenial layer
intermingled with sterile hairs.
 Each basidium bears 4-8 hyaline and oval to oblong
basidiospores.
 The basidiospores form hyaline, elliptical, straight or
slightly curved conidia like blastospores which also
germinate and infect the leaves.
 often the primary sources of inoculum in the spring. The powdery mildew fungus
can also survive the winter as hyphae or fungal strands in infected buds.

Leaf spot of Strawberry

Identification (Symptoms):
 Small, round and purple spots appeared on the leaves.
 Older spots are circular in out line, 2.5-3.0 mm in diameter with greyish-white centre
and surrounded by a reddish-purple margin.
 In advance stage, the spots coalesce with each other giving a blighted appearance.
 Same type of spots developed on the petioles, fruit stalks and calix.

Histopathological studies:
  The causal organism is Ramularia tulasnei.
 Perfect stage of the fungus is Mycosphaerella fragariae.
 The fungus produces conidia in pycnidia.
 Conidia are hyaline, cylindrical and 0-4 septate.
 In perfect stage the fungus produces black and globose perithecia.
 Asci are cylindrical to clavate, that contains hyaline and one septate ascospores.

Collection and Preservation of Plant Disease

Specimens for Herbarium
Collection:
The specimens of diseased plants or plant parts are collected and taken to the
laboratory for the following purposes.
1. To complete microscopic and other work to confirm the diagnosis.
2. To complete the identification.
3. To enrich the herbarium stock.
4. To preserve the excess specimens for exchange with other laboratories.
5. To send for identification and confirmation to specialist taxonomist if necessary.
Additional samples of the healthy plant may also be taken for taxonomic
identification of the host, if it is new.

Preservation:
There are two types of preservation which are followed to preserve the diseased
specimens i.e. dry preservation and wet preservation.
1. Dry preservation:
The representative specimens preferably indicating all the stages of the disease,
choses and spread out on blotting paper sheet or used news papers and pressed.
Preliminary drying may be done at the spot of collection itself. The leaves of grasses may
be dipped in water to get them stretched back to normal and then spread and dried. The
blotting papers should be changed frequently to avoid discolouration or mouldy growth.
The dried specimens are labelled and packed in packets of brown paper, between folds
of blotting papers or prepared with herbarium sheets. A specimen label should indicate
the followings.

 Name of laboratory
 Name of disease
 Name of pathogen
 Name of host
 Name of Location
 Date of collection
 Name of person (responsible for collection and identification)

1. Wet preservation:
A diseased sample may be preserved in FAA (Formalin, Acetic acid and Alcohol)
solution. The recipe of FAA is as follows.

 Formalin: 50 ml
 Acetic acid (Glacial): 50 ml
 Alcohol (50%): 100 ml
For colour preservation the following methods are available.
i. Saturated copper acetate method:
Make a super saturated solution of copper acetate in 5 % acetic acid. Dilute
the solution 3 to 4 times with water. Boil the solution and immersed the specimen
in the hot solution which first loses and then regains the green colour. The
specimen is then washed in clean water and kept in 2-4 % formalin.
ii. Scully’s method:
Sample keep in 5 % solution of CuSo4 for 6-24 hours, wash in running water
for few hours, then preserve in solution containing Sulphuric acid (H2So4) – 16 ml,
Sodium sulphate – 21 g and Water – 1000 ml. Glycerol @ 20-30 ml may be added
when fruits are to be preserved.
iii. Turtox method:
Specimen preserve in a solution containing Phenol – 20 g, Lactic acid – 20 g,
Glycerol – 40 g, Cupric chloride – 0.1 g, Cupric acetate – 0.2 g and Water – 1000
ml.
iv. Keefe’s method:
Sample preserve in the solution containing Ethyl alcohol (50 %) – 90 ml,
Formalin – 5 ml, Glycerol – 2.5 ml, Acetic acid (glacial) – 2.5 ml, Cupric chloride –
10 g, Uranium nitrate – 1.5 g and Water – 1000 ml.
Field visit to NEBCRC, VRC and HRC for diagnosis and collection:

Stains and Staining Methods for Bacteria and Fungi

Introduction:
Bacteria and fungi are microscopic organisms. They are colourless for the
most of the part. In order to visualize them to studies their structure, shape and
other structural characteristics, it becomes necessary to make them more easily
visible. This means that the structures have to be contrasted from their environment
so that they can be easily seen.
Stain:

Stain is a dye used to colour the living or dead organelles.

Types of stain:
1. Acidic stain – Acidic stains, in their ionized form, have a negative charge and bind
to positively charged cell structures and give colour e.g. Eosin, Rose Bengal,
Indian ink and Acid fuchsine etc.
2. Basic stain – Basic stains have positively charged basic radicals combines with
negatively charged particles in cytoplasm and give colour e.g. Methylene blue,
Basic fuchsin, Crystal violet, Safranine and Malachite green etc.
3. Neutral stain - Both positively and negatively charged imparts different colours to
different components e.g. Geimsa’s stain, Leishman’s stain and Wright’s stain
etc.
Staining Methods:
1. Positive Staining: Where the actual cells are themselves coloured and appear
in a clear background. This method is of two types.
A) Simple staining – A stain which provides colour contrast but gives same
colour to all bacteria and cells e.g. Loeffer’s methylene blue, Polychrome
methylene blue and Diluted carbol fuchsin.
 B) Differential staining – A stain which imparts different colours to different
bacteria is called differential stain which contains more than one stain.
e.g. Gram’s stain, Acid fast stain and special stain.
2. Negative Staining: Negative staining is useful for those bacteria which are
difficult to stain by simple staining.

Gram’s Staining:
Gram stain is developed in 1884 by the Danish physician Hans Cristian Gram. Is
the most widely used method in bacteriology.

Principle:

 Violet dye and the iodine combine to form an insoluble, dark purple
compound in the bacterial protoplasm and cell wall.
 This compound is dissociable in the decolourizer, which dissolves and
removes its two components from the cell.
 The removal is much slower from Gram-positive than from the Gram-
negative bacteria, so that by correct timing the former stay dark purple while
the latter become colourless.
 The difference between the two typ
 es of bacteria is that the Gram positive have thicker and denser
peptidoglycan layers in their cell walls, which makes them less permeable to
the stain than those of the Gram-negative bacteria.
 The iodine has a critical role in enhancing this difference.
 It seems to bind temporarily to peptidoglycan and make it even less
permeable to the dye.
Procedure:
Step 1- Crystal violet (primary stain) for 1 minute then water rinse. Cells stain
purple.
Step 2- Iodine (mordant) for 1 minute then water rinse. Cells remain purple.
Step 3- Alcohol (decolourizer) for 10-30 seconds then water rinse. Gram-positive
cells remain purple while Gram-negative cells become colourless.
Step 4- Safranin (counter stain) for 30-60 seconds then water rinse and blot dry.
Gram-positive cells remain purple while Gram-negative cells appear red. Cells
stain purple.

Lactophenol cotton blue staining:

Lactophenol cotton blue stain is commonly used for making a semi-
permanent microscopic preparation of fungi. It stains the fungal
cytoplasm and provides alight blue background against which walls of
the hyphae can readily be seen. It contains four constituents, phenol
serves as fungicidal agent, lactic acid act as a clearing agent, cotton
blue stains the cytoplasm of fungus and glycerine gives the semi-
permanent preparation. A permanent preparation is made by
incorporating polyvinyl alcohol in place of glycerine.