WHEAT DISEASES

SHUMSUN NAHAR
Lecturer
Dept. of Crop Science and Technology
Rajshahi University
 RUST DISEASE OF WHEAT
Rusts of wheat (i.e., black, brown and yellow) are the most important and destructive of all the
plant diseases. They are the potential causes of enormous economic losses in all wheat growing regions
of the world. They are the earliest known diseases of crop plants. Early Romans and Greeks knew
about the rust of wheat and barley.
There are three different rust diseases that affect wheat—leaf rust (also known as brown rust or
orange rust), stripe rust (commonly known as yellow rust), and stem rust (commonly referred to as
black rust of black stem rust). Rusts are notorious for their ability to spread rapidly and reduce wheat
yield and quality. It all depends on the susceptibility of the variety, race of the pathogen present, timing
of infection, and the weather conditions. Damage to wheat depends on the growth stage at the time of
infection and the overall level of rust severity. Rust causes losses by reducing the number of kernels
per head and the size of the kernels, and by lowering test weight and the protein content of the grain.
Leaf, stripe, and stem rust are caused by Puccinia recondita f. sp. tritici, Puccinia striiformis f.
sp. tritici, and Puccinia graminis f. sp. tritici, respectively. Black and orange rusts are particularly
found all over the world, yellow rust is more restricted, being absent, for instance, from South Africa
and Australia.
Symptoms of Rust diseases

Fig. Leaf rust Fig. Stripe rust Fig. Stem rust

1. BLACK OR STEM RUST OF WHEAT
 Causal organism: Puccinia graminis tritici

 Systemic position:
Class: Basidiomycetes
Order: Uredinales
Family: Pucciniaceae

 Stem rust or black rust of wheat is distributed through the world. This is probably the most damaging
disease of wheat and develops in epiphytotic form in the drier areas during most seasons. Yield of the
grain is reduced. The composition of the grain is also modified.
Symptoms
 Plants do not usually show obvious disease symptoms until 7 to 15 days after infection when the oval
pustules (uredinia) of powdery, brick-red urediniospores break through the epidermis.
 The on set of black rust is first marked by an eruption of elongated, brown pustules on the stalk, leaf
sheaths and leaves, the stalk being often most attacked.
 These pustules(uredosori or uredia) may be a quarter of an inch or more in length and frequently
coalesce with one another.
 Soon they burst and expose brown uredospores.
 These uredospores re-infect the host and repeat the cycle of infection several times during a season
and are called ‘repeating spores’.
 As the plant matures, the the pustules produce mahogany-brown teliospores and the sori develop
black colour and often reffered to as black stem rust.
 As a result, one can see the pustules gradually changes from brown to black. At this stage the
epidermis ruptures(very typical of stem rust) and expose a black bed of teleutospores.
Symptoms

Fig. Black rust or stem rust symptoms of wheat. Infected culms of wheat showing urdial stages
 Symptoms

Fig. Stem rust may infect any part of the aboveground Fig. Black rust or stem rust symptom on later stage
portions of the wheat plant showing black pustules on stem
Pathogen/ Etiology

 It is heteroceious in nature.
 Uredial and telial stage occurs on wheat.
 The pycnial and aecial stage play role on barbarry plant.
 The uredospore are single celled, stalked, thick walled, oval spores and brown in colour.
 Uredospore are turned into teliosori producing only teliospore.
 Teliosori are black in colour and elongated.
 Teliospore are stalked, bicelled, spindle shaped, dark brown with pointed apex.
 It is a sexual stage in which kariogamy and meiosis occurred.
 Basidiospores are formed by germinating of teliospores.
 It is a macrocyclic rust.
Pathogen

Fig. Urediniospores

Fig. Teliospores, two celled, thick walled

 Disease cycle
The fungus overwinters on wheat as teliospore stage. Teleiospores remaining on the crop residue,
germinate and the diploid nucleus divides meiotically and produces a four-celled basidium. The
basidium produces four uninucleate, haploid basidiospores. This development occurs in the
overwintered grain straw. The basidiospores are blown away by wind and fall on the young barbarry
leaf (alternate host). They germinate and infect the leaf. On the barberry the fungus produces
pycniospores in tinny flask-shaped spermagonia or pycnia. Subsequently, a binucleate (dikaryotic)
condition is initiated by the fusion of compatible mycelia. This binucleate mycelium produces aecial
cups and binucleate aeciospores on the lower surface of the leaf. Aeciospores are blown away by
wind on wheat plants. Soon after infection, uredosori with binucleate, oval shaped uredospores are
formed. These uredospores cause secondary spread of the disease. As the grain matures binucleate,
two-celled, thick-walled teliospores are formed. The young teliospores are binucleate and they fuse
immediately before germination and formation of basidium occure.
Barberry plants play a very important role in the life history of P. graminis var. tritici. New races
of the pathogen are produced on barberry. The pathogen is a heteroecious fungus and requires two
hosts, barberry and wheat for completing life cycle. In our country there is no barberry plant. The
fresh infection every year, probably, starts from aeciospores blown by the northwind during winter
from the Himalayas. It helps the local propagation of newly introduced races of pathogen.
Contd.

Figure. Aecia of the wheat stem rust fungus produced on infected Fig. Microscopic view of aciospores.
barberry leaf.
Epidemiology

 Optimum temperature for germination of uredospore is between 18 and 20⁰ C.

 A film of water on the leaf surface is essential for germination and penetration.
 Epidemics are favoured by the presence of large of acreage of susceptible wheat.
 Physiological races capable to attack the wheat varieties.
 Wind and humid weather.
 Infection occurs through stomata
Control/ Management of the disease

 Successful chemical control has yet not been possible. Destruction of barberry plant
and growing of resistant varieties are the principal methods of control. Most of the
high yielding Mexican varieties have been found to be resistant to the disease.
2. BROWN, ORANGE OR LEAF RUST OF WHEAT
 Pathogen: Puccinia recondita f. sp. tritici
Puccinia triticina
Puccinia rubigo-vera var. tritici

 Systemic position:
Class: Basidiomycetes
Order: Uredinales
Family: Pucciniaceae

 Leaf rust is a common disease of wheat and is found throughout the world. This disease causes
severe damage to crop in Bangladesh. Leaf rust is a heteroecious rust. Thalictrum sp. acts as
alternate host for aecial and pycnial stages.
Symptoms

 The uredial sori appear on the leaves, rarely on sheath and stem.
 These pustules (uredia) are always scattered on the leaf surface and they never form rows but
they may be grouped in small clusters or irregularly scattered.
 The scattered uredia and their orange colour form the most characteristic distinguishing
features of the brown rust.
 The uredisori burst early and shed their uredospores.
 Teleutosori are rarely formed, some years they may not be present.
 When telia formed they are small, oval, to linear, dull black and covered by the epidermis.
Symptoms

Fig. A part of infected leaf with scattered uredia

Symptoms

Fig. Orange, brown or leaf rust infested wheat field. Fig. Infected leaf through uredium showing stalked
uredospores
Pathogen/ Etiology
 It is heteroecious in nature.
 Uredial and telial stage occurs on wheat.
 The pycnial and aecial stage on Thalictrum sp.
 The urediospore are brown spherical, minutely echinulate
and bearing 7-10 germ pores.
 Infect the wheat leaf through stomata.
 Uredosori are turned into teliosori producing only teleiospore
for a short period.
 Teliosori are rare, if formed it confined to lower surface only.
 The teletospores are two-celled, smooth, oblong, thick-walled and brown with a rounded apex.
 It is a sexual stage in which karyogamy and meiosis occurs.
 It is a macrocyclic rust.
Nature and recurrence of disease/Disease cycle
 Uredospores overwinter on crop residues and self-sown plants in the hills. The
uredospores are carried over by wind from hills and cause primary infection to plants in
the plains. Within a few days uredosorus and uredospores are formed on the leaves. Under
favourable conditions uredospores are formed several times and help in spreading the
disease. In Siberia the fungus produces five types of spores and completes its life cycle.
Teliospores produce basidiospores. These spores disseminate by wind and produce
pycnium and pycniospores on the upper surface of the leaf of alternate host and
aeciospores on the lower surface. These aeciospores then attack wheat plants and produce
uredospores again.
Disease cycle
r
Life cycle of leaf rust disease:
Disease cycle
Epidemiology

 Leaf rust is adversely affected by cool temperature at high altitude.

 High humidity increases disease severity.
 Generally the disease does not occur above 80⁰ F. If occurs only a few plants are
attacked.
Control measures:

 Self-sown plants and the crop residues should be destroyed to eradicate the sources of infection.
 Early maturing varieties should be grown.
 Avoid excess use of nitrogen fertilizers.
 The rust resistance is increased by the application of potassic fertilizers.
 High humidity favours the rust and therefore, the field should be irrigated timely and properly.
 Light irrigation during January and February keep the rust under control.
 Suitable resistant varieties should be cultivated. HD 2278, HD 2281, Akbar, Barkat, Balaka,
Kanchan, BAW-42, VAW-46, BAW-47 etc. are moderately resistant to leaf rust.
3. YELLOW OR STRIPE RUST OF WHEAT
 Pathogen: Puccinia striiformis f. sp. tritici

 Systemic position:
Class: Urediniomycetes
Order: Uredinales
Family: Pucciniaceae

 Gadd first described stripe rust of wheat in 1777. In 1953, Hylander et al. revived the name
Puccinia striiformis. The yellow rust is limited to northern and eastern India. In comparison to
other rust diseases of wheat it appears earlier. The disease is seen in middle of January and if there
are heavy rains it does much damage to the crop. Yellow rust is infrequent in Bangladesh, but does
occur sporadically.
Symptoms:
 Initially, symptoms are yellowish flecks on leaves.
 Mature pustules will break open and release yellow-orange masses of urediniospores.
 Pustules are clustered on seedling leaves, while pustules on mature leaves occur in a linear,
stripe-like pattern.
 Later in the season, yellow-orange fungal spores turn black and remain attached to leaf tissue.
 The infected tissues may become brown and dry as the plant matures or becomes stressed.
 The uredia are chiefly formed on the leaf blades, but when the attack is severe, they also appear
on the leaf sheaths, stalks and glumes as well.
 Sometimes the rust pustules also seen on the pericarp and kernels.
 Symptoms can be present from seedling stages through ripening.
 Stripe rust pustules form a noticeable striped pattern on mature leaves and are more yellow than
stem rust spores.
 Symptoms

Fig. Yellowish flecks on leaves Fig. Yellow stripe (uredpspores) on leave

(initial symptom)
Fig. Mature symptoms of stripe
rust. Infected plant tissue
become brown and dry
symptoms

Fig. Yellow rust affected wheat field Fig. Uredospores

 Pathogen/ Etiology
 It is heteroecious in nature.
 Uredial and telial stage occurs on wheat.
 The uredospores are nearly round and not oval or elliptical as in black rust.
 Uredosori are turned into teliosori producing only teliospore.
 The telio or teleutospores are dark brown, two-celled, often
flattened or oblique at the top.
 Teliosori are filled numerous brown paraphyses.
 It is sexual stage in which kariogamy and meiosis occurred.
 Basidiospores are formed by germinating of teliospores.
 The yellow rust is heteroecious, but the alternate host is still unknown,
and therefore, the pycnial and aecial stages have not been observed.
Nature and recurrence of disease/ Disease cycle

 The disease is air borne. The inoculum (uredospores) causing the annual recurrence is
brought from the hills to the plains every year. The uredospores of Puccinia striiformis
over-summer on the hills at 7,000 feet and above.
Disease cycle
EPIDEMIOLOGY

 Stripe rust is most common in higher elevations and cooler climates. The pathogen is
best sustained when night time temperatures are <60⁰ F (15⁰ C).
 Stripe rust can develop on wheat at lower temperature than other rusts. Optimum
uredospore germination occurs at 44-59⁰ F(7-15⁰ C).
 Heavy dew or intermittent rain can accelerate the spread of the disease.
 Uredospores are spread via wind currents to healthy plants where they can initiate new
infections.
Control measures

 Mixed cropping and crop rotation.

 Avoid nitrogenous fertilizers.
 Sulphur dusting @ 35-40 kg/ha.
 Spray Mancozeb @ 2g/lit.
 Growing resistant varieties
4. LOOSE SMUT OF WHEAT

 Pathogen: Ustilago nuda

Ustilago tritici

 Systemic position:
Class: Basidiomycetes
Order: Ustilaginales
Family: Ustilaginaceae

 This is an example of floral (embryo) infection type of smut disease. The disease is fairly
common in wheat growing areas of Bangladesh and cause appreciable damage to the crop in
northern districts.
Symptoms:
 The symptoms of the disease may be seen only on the emergence of the ear from the boot leaf.
 Diseased ears emerge earlier than healthy ones and the entire panicle is replaced by loose,
black, powdery masses of smut spores called chlamydospores or teliospores.
 The diseased heads are blackened and clearly visible among newly emerged green healthy
heads.
 All the parts of the spikelet are being converted into smut spores except awns.
 In the beginning the smut sori remain covered with thin silvery membrane, by the time the ear
emerge from the boot leaf the membrane disintegrates or bursts and the smut spores are
liberated in the atmosphere.
 These spores are blown off by winds or rain and other agencies and the rachis or central axis
remains barren.
 Significant reduction in height and number of tillers.
 High respiration.
 Low dry weight of plant.
Symptoms

Fig. Loose smut of wheat (Ustilago nuda). Fig. Loos smut infected wheat field.
Smutted ears showing typical symptoms
Symptoms

Fig. Infected ear with smut sori and showing barren rachis.
 Pathogen/ Etiology
 Internally seed borne fungal disease.
 It causes systemic infection.
 The chlamydospores (teliospore) of the fungus are minute, pale olive-brown, spherical to oval about 5-9 micro in diameter
and are adorned with minute echinulations on the wall.
 Hyaline mycelium grow through the plant.
 The mycelium cell transformed into spherical teliospores or chlamydospores.
 Chlamydospore germinate and form basidium.
 Cells of basidium germinate and produce uninucleate hyphae, it unite to form
dikaryotic mycelium.

Fig. Spores of Ustilago nuda

Disease cycle/ Nature and recurrence of disease
 The disease is seed-born (internally seed born). The chlamydospores are released from
the infected ears when normal plants are flowering. They are spread by the wind, rain,
insects and lodge on the feathery style of the healthy wheat flowers and germinate
producing promycelium (basidium). The binucleate stage is established through clamp
connection between compatible cells of the septate promycelium. Infection hyphae
develop from these binucleat cells and enter into style and grow downward
intercellularly until the ovary is reached. The binucleate hyphae remain dormant in the
seed during storage. When the infected seeds are planted the fungus again becomes
active as the seeds germinate. The fungus grows systemically and replaces the ovary at
flowering time producing smutted heads.
 Disease cycle
Infection hypha infects ovary and n+n Mycelium remains dormant in the embryo and overwinters
penetrates the embryo
7 1
n+n n+n
Binucleate stages is established by clamp
connection between compatible cells and Dormant mycelium becomes active during germination of seed
infection hypha develops and grows within seedling systemically and infects the ear.

6 n
2
Chlamydospores germinates and produces septate n+n
promycelium.

5 n+n

Chlamydospore form smutted plants

disseminated to the stigmas in healthy plants n+n
4 Mycelium forms chlamydospores and they replace the overy. 3
Disease cycle
Epidemiology

 Cool weather with light showers or dews during pollination time favoures infection.
 Cold climate (16-22⁰ C)
 Humid weather- 60-85% RH.
 Dormant mycelium act as a primary inoculum and chlamydospores or teliospores act as a
secondary inoculum.
Control/Management
 Resistant varieties: This is the simplest and most important method of control. Resistant varieties
such as Kalyan 227 may be grown.
 Rogueing: The infected ears should be burnt outside the fields, so that, the smut spores may be
destroyed.
 Seed selection: Since the disease is seed borne, the seeds should be collected from smut free
localities.
 Hot Water Treatment: The wheat grains are at first soaked in water kept within a range of
temperature between 26°C-30°C. They are allowed to remain there for about 4-5 hours. In the
softened grains the dormant mycelium becomes active. The temperature of water is then raised and
kept constant at 54°C for about 10 minutes. At this temperature the activated mycelium is killed. This
method requires strict care and supervision. The temperature should be carefully controlled. At a
range a little too low, it will fail to kill the mycelium and at a degree or so too high it will kill the
embryo. In this case the embryo is killed at 56°C. The margin of error either way is thus very little.
After the treatment the water is drained off. The grains should then be dried and sown.
Control/ Management

 Sometimes, seeds are presoaked in water for 6 hours and placed in air tight container for a period
of time depending upon the temperature. In this method, the fungus dies for want of oxygen but
the seeds remain viable.
 Solar treatment: This the modification of hot water treatment. The seeds are soaked in water for
4 hrs, and then the seeds are dried up on the floors in the open sun in very thin layers from 12.00
noon to 4 P.M. in the months of May and June. The dormant mycelium becomes activated on
soaking the seeds in the water for 4 hrs, and dies when the seeds are spread in thin layers in the
hot sun and the seeds become pathogen free.
 Chemical treatment: Systemic fungicides, such as Vitavax and Benomyl at 25% has been
reported to be effective as seed treatment.
5. FLAG SMUT OF WHEAT
 Pathogen: Urocystis tritici
Urocystis agropyri

 Systemic position:
Class: Basidiomycetes
Order: Ustilaginales
Family: Ustilaginaceae

 Flag smut or stem or stripes smut, of wheat was first observed in South Australia in 1868.
Symptoms:
 The disease is usually found on the leaf blades.
 It also common on the sheaths and occurs sometimes on the stem and very rarely on the ears.
 The seedling infection leads to twisting and drooping of leaves followed by withering.
 The complete plant dries up.
 Very frequently, the ears are replaced by a twisted mass of leaves.
 The ears do not bear any grains.
 Whenever grain is formed, it is always much shriveled and useless.
 On the infected leaf blade long, grey, slightly swollen bands appear parallel to the veins of the
leaf.
 Ultimately these elongated sori rupture and expose a black, powdery mass of spores.
Symptoms

Fig. Typical symptoms of Flag smut of wheat

Pathogen/ Etiology

 The pathogen is seed borne as well as soil borne.

 The spores are formed in tiny balls consisting of from 1-4 fertile brown spores.
 These spores remain surrounded by a layer of light coloured sterile cells.
 The spores are globose or oval.
 Basidiospore germinate to produce primary mycelium
Nature and recurrence of disease/ disease cycle

 The disease is both seed-borne and soil-borne. Infection occurs below ground. The spore
balls are adapted to retain their power of germination for a long time. On germination
they infect the primary shoot. The fungus is systemic and later produces the characteristic
spore bearing sori
Epidemiology

 Temperture of 18-24⁰ C
 Relative humidity 65% and above.
 Primary infection occurs by sowing infected seeds or by resting spores present in the
soil.
Control measures

 Resistant varities: The sowing of resistant varieties seems to be moat practical method.
Pusa 4 and WG 377 are resistant to this disease.
 Seed treatment: Treat the seeds with Carboxin (Vitavax) or tebuconazole (Folicur) @
2g/kg.
 Crop rotation: This practice has also been effective in controlling this disease.
6. ROUGH-SPORED BUNT OR STRIKING SMUT OF WHEAT
 Pathogen: Tilletia caries

 Systemic position:
Class: Basidiomycetes
Order: Ustilaginales
Family: Tilletiaceae

 Bunt is an important disease of wheat, and occurs in all wheat growing countries. The name
‘bunt’ comes from a dialectic contraction of the term ‘burnt ears’ to ‘bunt ear’ and finally to
just ‘bunt’. It is also called ‘Common Bunt’ and ‘Hill Bunt’ disease of wheat. It is a typical
covered-type inflorescence smut and is an example of seedling infection type of smut disease.
Symptoms
 Infected wheat plants are slightly shorter than healthy plants.
 The symptoms are seen only on ears.
 Infected plants ripen usually more rapidly than healthy plants and ears become of dark green
colour and more open.
 Smutted heads are bluish-green while healthy heads are yellowish-green.
 Infected flowers produce longer pistils and longer and broader ovaries compared to healthy
flowers.
 Diseased ovaries look green while healthy ones are white.
 The ears remain erect and rigid, instead of bending over like the healthy ears.
 The grains are completely filled up with a greasy, black powdery mass of chlamydospores or
teliospores, smelling strongly of rotten fish.
 The spore-mass becomes hard and it ruptures at some period during threshing, and then the
spores adhere to the healthy grains.
Symptoms

Fig. Bunted ear of wheat Fig. Contaminated grains

Symptoms

Fig. Bunt affected wheat field

 Pathogen/Etiology
 The spores possess rough and reticulate wall.
 The spores are generally round, measuring 15-20 micro meter in diameter.
 On germination, the spore produces a stout promycelium (basidium).

Fig. Bunt spore (Tilletia caries) Fig. Forming H shaped structure

Nature and recurrence of disease/ disease cycle

The disease is externally seed-borne and systemic. These two smut fungi survive between growing seasons
as teliospores on the surface of healthy seed or in the soil. They can remain viable in either location for a
number of years, perhaps ten years or more, particularly if the spores remain dry on the seed surface. When
seeds are sown and environmental conditions are favorable, each teliospore germinates, producing sporidia
(basidiospores). After compatible sporidia anastomose (fuse) to form the H-shaped structure, the resulting
dikaryotic, infectious hypha penetrates the young coleoptile in the region of the root node of a seedling. As
the plant grows, the fungal hyphae also grow, keeping pace with the apical meristerm. Seedling infections is
followed by systemic development of binucleate mycelium in the host and at the time of flowering, the
fungal hyphae concentrate in the floral parts, transforming the grain into smutted tissue. Eventually, the
hyphae replace the cells of the seed, and the individual cells of the smut fungus become teliospores. During
harvest, the smut spores are released from infected heads as the heads pass through the combine used to
harvest the grain. They contaminate other seed being harvested or are spread by the wind to the soil surface,
later to be incorporated into the soil mass during cultivation.
Disease cycle
n+n Dikaryotic sporidia may produce secondary sporidia
4
n+n
Secondery sporidia germinate and Sporidia fuse and become dikaryotic
infect seedling 3
5
n+n Chlamydospores germinate and produced sporidia
Mycelium grows with the plant systemically
and reach the ovary 2
6
n+n
Mycelium destroys the ovary n+n Chlamydospores lodge on the grains or healthy plants or
and fills with chlamydospores fall in the ground and overwinter there
7 1
Disease cycle
Factors affecting disease development/Epidemiology

 Maximum infection occurs at soil temperature of 5-15⁰ C with moisture content ranging
from 15-60% of the field capacity. Disease severity depends on depth of seedling,
length of day and soil fertility.
Control

 Planting of seeds during the periods of warm temperature permits the seedlings to
escape infection.
 Collect healthy seeds from disease free area and dust them with seed treating
fungicides.
 Seed treatment with systemic fungicides like carboxin, vitavax and benlate @ 2g/kg
seed and Tilt (propioconazole) 25 EC @ 0.1% are used for seed treatment. A
combination of vitavax with thiram is very effective for disease control
 Burning of soil residues in the field after harvesting reduces the inoculum potential in
the soil.
 For effective and economical control the resistant varieties should be grown such as
HB-383, Kalyan sona etc.
7. SMOOTH-SPORED BUNT OF WHEAT

 Pathogen: Telletia foetida

 Systemic position:
Class: Basidiomycetes
Order: Ustilaginales
Family: Tilletiaceae
Pathogen/Etiology
 The spores posses the smooth wall and measure 16-25 micro miter in diameter.
 On germination, the spore produce a stout promycelium (basidium).
 Primary sporidia which unite to form ‘H’ shaped structure.
 These structures give rise to secondary sickle-shaped sporidia.

Fig. pathogen spore

8. KARNAL BUNT OF WHEAT
 Pathogen: Tilletia indica (barclayana)
Neovossia indica

 Systemic position:
Class: Basidiomycetes
Order: Ustilaginales
Family: Tilletiaceae

 First reported by Mitra in 1931 from Karnal and since then this has been named as ‘Karnal bunt
of wheat’.
Symptoms
 This disease can be observed in the fields only when the ear are emerged out, and grains are
formed.
 In an infected plant, neither all spikes nor all the spikelets in a spike are infected. In an infected
ear, only a few grains not more than five to six, are being infected and changed into sori.
 The sori are always irregularly distributed on the infected ear.
 On the maturity of the grains, the outer glumes in a spike spread out, and the bunted grains may be
observed.
 The bunt balls (spore-mass) remain covered by the pericarp in the beginning, but later on they
burst and the spore mass is exposed.
 The major symptoms of KB are the presence of dark sori (black colored mass of teliospores) on
the ears and the rotten fish smell emitted by the infected grains in field as well as in storage.
 Rotten fish smell occurs due to the presence of trimethyl amine secreted by teliospores.
Symptoms

Fig. Karnal bunt infected spike Fig. Karnal bunt infected spikelets
Symptom

Fig. Karnal bunt infected wheat grains

Pathogen/ Etiology

 The spores are spherical, smooth-walled and measuring 22-49 micrometer in diameter.
 Teliospores are resting spore, remain viable in the soil.
 Primary sporidia produces when teliospore germinates under favourable conditions.
 Secondary sporidia prouduces by primary sporidia.
 Secondary sporidia carried out work of secondary infection while primary infection performed by
teliospore.
Etiology/ Pathogen

Fig. Spore of Tilletia indica Fig. Spores of Nevossia indica

Nature and recurrence of disease /Disease cycle

 The disease is soil-borne as well as air-borne. The spores found in the soil germinate, forming
a large number of needle-shaped sporidia (basidiospores), and sickle-shaped secondary
sporidia. The sporidia are being carried to the inflorescence through air currents, where they
infect the ovaries and the development kernels. Infection take place only when the flowering
occurs.
Disease cycle of karnal bunt
Epidemiology

 15-20⁰ C temperature
 60-80% RH
 Intermittent rain
 High nitrogen dose
 Close planting
Control
 Use healthy seeds
 Crop rotation
 Use of resistant varieties such as Kalyan sona, HD 2012
 Infected head destruction
 Use of systemic fungicides such as carboxin, vitavax and benlate @ 2g/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
9. BLACK POINT OF WHEAT/ LEAF BLIGHT/LEAF SPOT
 Pathogen: Bipolaris sorokiniana
Alternaria spp.
Fusarium sp
Aspergillus
Penicillium
Curvularia
Chaetomium
Gloeosporium
Nigrospora
Rhizopus
Stemphylium
 It is considered as a number one disease of wheat in Bangladesh. This disease was first observed in 1924,
and since then the plant pathologists are busy in various investigations. This disease is also called leaf
blotch or spot blotch. It is also very dangerous in semi-arid region. It reduces yield upto 30%.
Symptoms
 Early symptoms are small, oval, chlorotic lesions that are irregularly scattered on the lower leaves.
The lesions enlarge, become irregular in shape, and develop into dark brown or grey sunken.
 Lesions may have a bright-yellow marginal zone, and can grow up to 1 cm or more in diameter.
Lesions progressively develop from lower to upper leaves, and blighting may extend to whole leaf
and head due to coalesce of several lesions.
 Under moist conditions, lesions may be covered by black powdery conidia. Under severe
conditions the symptoms can also be seen on the leaf sheath, awns and glumes.
 At the dough stage of wheat development, heavily infected fields appear dull and bronzed with a
burnt appearance when seen from a distance.
 Diseased kernals are discolored and appear weathered, black- pointed, or smudged.
 Black point associated with the darkened pericarp and sometimes shriveled embryo end of the
seed.
 When embryos are invaded, germinability of the seeds decreases.
Symptoms

Fig. Irregular lesions surrounded by a bright yellow Fig. Sooty mold, a superficial growth of
halo. black, dark green, or even pink or
white molds on wheat heads.
 Symptoms

Fig. Black powdery conidia of the fungus on leaf

Fig. Black necrotic lesion developed
at the embryonic site of the wheat
grain and grain becomes shriveled.
Pathogen

Different stages of Bipolaris sorokiniana infection in wheat: (a) bipolar germination of conidia; (b)
branching of germ tube and differentiation; (c) development of appressoria, penetration peg and
invasion of mesophyll cell; and (d) conidia with conidiophores for air dispersal.
Nature and recurrence of disease/disease cycle

 This is a seed as well as soil-born disease. The organism mainly transmits through seeds.
The inoculum is found to be deep seated in the seed. Seven to fifteen days old seedlings
are not susceptible. As the plants become older, they become more susceptible to the
disease. If the suitable conditions of moisture and temperature prevail, the ten week old
plants are heavily infected by the disease. The pathogen live in the stubbles of the crops
upto next season and can infect the seedlings during germination through mycelia,
conidia and chlamydospore.
Disease cycle of Bipolaris sorokiniana
Epidemiology

 Temperature: 20-25⁰ C
 RH -20% (in storage) and 90% (in field) favoures the disease
 Continuous leaf wetness (10 hrs)
 Soil moisture > 20% enhance black point disease
 Zinc deficiency in the field
 High doses of nitrogen
Control
 Spray Propiconazole / Hexaconazole at the time of maturing heads for two times at 7-10 days
interval is found effective.
 Spray Trichosuspension or BAU Biofungicide (Trichoderma harzianum) or Trichoderma viride @
0.2% or Pseudomonas fluorescens (0.5%) and neem leaf extract (73.57%) and Tilt @ 0.2%.
 Seed treatment with Provax @ 2.5 g/kg seed can improve the germinability and decrease infection of
seedlings grown from diseased kernals.
 Store the seeds in well ventilated dry places to reduce the storage molds development.
 Use cultivars which are resistant or tolerant to black point infection.
 Black point can be partially controlled by reducing irrigation frequency after heading and by
reducing nitrogen rates, without sacrificing either yield or quality.
 Since the disease is soil-borne too, after harvest, plant debris should be collected and destroyed by
burning it.
 10. POWDERY MILDEW OF WHEAT
 Causal organism: Erysiphe graminis f. sp. Tritici

 Systemic position:
Class: Ascomycotina
Order: Erysiphales
Family: Erysiphaceae

 The powdery mildew of wheat is commonly found in those regions, where is enough of moisture
during sowing time.
 Symptoms

 Powdery mildew is characterized by a powdery white to gray fungal growth on leaves, stems and
heads. The fluffy white pustules are first detected on the upper surface of the lowest leaves of
plants.
 As the plant matures, the white powdery growth changes to a grey-brown color. The leaf tissue on
the opposite side of the leaf from the white mold growth becomes yellow, later turning tan or
brown.
 Small, black fruiting bodies (cleistothecia) develop on leaves as plants mature (usually at earing
time). Cleistothecia are recognized as distinct round, black dots within older, grey colonies of
powdery mildew.
 Cleistothecia contain spores (ascospores) that serve to infect in the fall and early spring.
 In severe cases the leaves become crinkled, twisted or variously deformed.
 From much discolouration and coverage of the host epidermis by the fungus, photosynthesis is less
and there is much chlorosis, which makes the plant weak.
 If the disease incidence takes place at the milk stage, the grains are dried and shriveled.
Symptoms

Fig. White powdery cottony masses of the fungal growth

Symptoms

Fig. Mature lesions may have dark,reproductive Fig. Small black fungal fruiting bodies (cleistothecia)
structures with black speckles mixed with immersed in the gray fungal tissue can be observed
the white, cottony growth of the fungus later in the season
Pathogen/Etiology
 Pathogen is obligate parasite.
 Mycelium is ectophytic (superficial) branched with small appresoria and haustoria.
 Infection is initiated by germination of conidia (conidiophore) on leaf surface.
 Infection hyphae / penetration peg breach epidermal cell wall and produce haustoria.
 Superficial septate hyphae form a web and cover the host surface.
 Conidia form in chain by conidiophores in acropetal manner.
 The conidia are oval or barrel-like, hyaline, single-celled, uninucleate and are capable
of germinate within a short time.
 Disease cycle/Nature and recurrence of disease

 The recurrence of the disease takes place through the cleistothecia (the perennating bodies). The
cleistothecia perennate on the straw and plant debris after harvest, and provide the necessary
inoculum (ascospores) for the next season. The primary infection is brought by ascospores, and
the secondary infection is from the air-borne conidia.
Epidemiology

 Mild temperatures (15–22°C) and high humidity (in excess of 70%),

 Dense crop canopies, where air circulation is poor and in damp, shaded areas, dense
canopies are closely correlated to high seeding rate and/or high nitrogen nutrition
 Good soil moisture profile which promotes canopy humidity
 Extended periods of humid and damp canopy
 Control measures

 Spray Propiconazole + Tebuconazole or Propiconazole + Azoxystrobin or Propiconazole @ 0.2 to

0.3% as soon as the symptoms appear in few plants.
 Use resistant varieties
 Cultural practices:
•Do not over-fertilize with nitrogen since this encourages heavy, succulent, susceptible
growth.
•Lighter seeding rates improve air circulation and decrease disease.
•Crop rotation and clean plowing reduce the amount of overwintering pathogen structures in
the field, although air-borne inoculum can negate these practices.
11. FOOT ROT OF WHEAT

 Causal organisms: Fusarium graminearum

Fusarium culmorum
Pythium graminicolum
P. arrhenomanes
Symptoms
 The first visible symptoms of common root rot are the appearance of stunted seedlings with
chlorotic symptoms in the field as irregular patches.
 The symptoms of common root rot include dark brown to black lesions in roots, sub-crown
internodes and stem bases.
 The primary and secondary roots may appear brown or blackened.
 The diagnostic symptoms of the Fusarium foot rot is cottony pink mycelium that may appear on the
stem bases.
 Infected plants may die prematurely, resulting in white heads. If heads survive, seed will likely be
shriveled.
Symptoms

Fig. Chlorotic symptoms due to foot rot disease. Fig. Black lesions on roots due to foot rot of wheat.
Symptoms

Fig. Brown or blackened roots due to foot rot Fig. Pink mycelium appear on the base of the stem.
of wheat.
Symptoms

Fig. Infected plants may die prematurely, resulting in white heads. If heads survive, seed will
likely be shriveled.
Epidemiology

 High humidity
 Wet weather
 Warm, moist and poorly drained soils

Disease cycle: Through soil and irrigation water.

Control
 Maintain balanced fertilization particularly by reducing the application of nitrogenous fertilizer.
 Proper weeding to eliminate the alternate hosts and weeds may predispose the plant roots to
infection.
 Use certified or fungicides treated seeds.
 Rotate crops to reduce the Fusarium inoculum by avowing the planting wheat following corn or
wheat.
 Seeds treatment with Provax (Carboxin + Thiram) or Tebuconazole or Mancozeb + copper
oxychloride @ 2.5 g/Kg seeds.
 Soil can be drenched with 0.2-0.3% solution of Mancozeb + Carbendazim at the seedling stage.
12. BLAST OF WHEAT
 Causal organism: Magnaporthe oryzae Triticum pathotype (MoT)

 Systemic position:
Domain: Eukaryota
Kingdom: Fungi
Phylum: Ascomycota
Subphylum: Pezizomycotina
Class: Sordariomycetes
Subclass: Sordariomycetidae
Family: Magnaporthaceae
Genus: Magnaporthe
Species: Magnaporthe oryzae Triticum pathotype
History

First sighted in Brazil in 1985s, blast is widespread in South American countries including
Argentina, Uruguay, Bolivia and Paraguay wheat fields, affecting as much as 3 million hectares in the
early 1990s.
In February or March 2016, a new fungal disease was spotted in wheat fields across eight
districts in Bangladesh. Wheat blast symptoms first appear in Chuadanga and Meherpur districts.
DAE informed that, the epidemic spread to an estimated 15,000 hectares, about 16% of the cultivated
wheat area in Bangladesh, with yield losses reaching up to 100%.
Symptoms
 The wheat blast pathogen can infect all above ground parts of the wheat plant, but head infection
is the most common symptom in the field.
 Highly susceptible cultivars can be infected at the seedling stage. The predominance of wheat
head blast symptoms without leaf lesions in the field represents a major difference between wheat
blast and rice blast.
 Infected heads become bleached with blackened rachis and either produce shriveled seeds or no
seed at all.
 Wheat leaf lesions in the field vary:
Type 1 Lesion: Small dark brown spots without light centers,
Type 2 lesion: Round or eye-shaped lesions with small light centers
Type 5 lesion: Larger, eye-shaped lesions with light tan centers and dark brown margins
 Sporulating leaf lesions appear gray from the color of the spores. The potential for individual
lesions to sporulate depends on the relative area of the light tan region (the sporulating region)
inside the darker brown margins.
 Uniformly dark brown Type 1 lesions represent an enlarged resistance reaction and fail to
produce spores.
Symptoms
Symptoms

Fig. Infected heads become bleached Fig. Symptoms of wheat blast disease
 Dissemination of wheat blast
 The disease is generally spread by infected seeds and air-born conidia, and the fungus can
survive in infected crop residues and seeds.
 Wheat blast mainly seed-borne disease.
 The disease is migrated from Brazil to Bangladesh during the seed import.
Pathogen

Fig. Laboratory culture of the pathogen (Magnaporthe oryzae triticum pathotype)

Epidemiology

 Environmental Conditions such as warm and wet weather

 Several days of continuous rains and temperatures from 18-25 °C during flowering, followed by hot,
sunny and humid days
 Minimum temperature for infection is 10°C and the maximum is 32°C, with optimum between 25
and 30°C
 High nitrogen fertilization and aerobic soils and drought stress
 Global climate change, one report suggests that rising CO2 levels enhances rice blast disease.
 High relative humidity which is required for sporulation.
 Rain and/or heavy dew are required for appressorium function and spore release.
 High humidity promotes lesion expansion.
 Control
Short term strategies:
 Use blast resistant wheat varieties such as BARI gom 33.
 Crop rotation with alternative crops such as oil seed crops and pulses in stead of wheat is one of the
important cultural practices which can reduce the pathogen inoculums from the field.
 Eliminating crop residues through burning immediately after harvesting of wheat.
 Keeping crop fields weed-free will destroy the alternative hosts of the blast pathogen because inoculums can
also survive on weeds and in crop residues.
 Spray Trooper(Tricyclazole) /Nativo (Tebuconazole+ Trifloxystrobine) at 7-10 days interval starting at early
flowering stage. Early planting can reduce the wheat blast incidence because delaying the planting date
significantly reduced yield losses due to wheat blast where the disease was previously endemic.
 Application Silicon (Monosilicic acid (H4SiO4), 250-1000kg/ha) in the soil enhances resistance to wheat
blast by making the epidermis harder.
Control
Long term strategies:
 Conventional and molecular breeding (CRISPR Cas9 techniques) to develop blast resistant wheat
varieties.
 Genetic approaches (pathogen population analyses) and epidemiological research (mode of pathogen
overwintering, transmission, environmental factors and hosts) to strengthen knowledge on the fungus
and its interactions with wheat and other host plants.
 Monitoring of disease appearances, movement, and evolution, in coordination with international
(CIMMYT), Universities (BAU) and local extension agencies (DAE, NGOs) and research agencies
(WRC), as well as predictive models
COVERED SMUT OF BARLEY

 Causal organism: Ustilago hordei

 Systemic position:
Class: Basidiomycetes
Order: Ustilaginales
Family: Ustilaginaceae

 The covered smut of barley is world-wide in its distribution. It is found in all those countries
where the barley crop is grown.
Symptoms
 The presence of the disease is first noticed at ear emergence when the ears appear dark grey due to
the masses of teliospores covered by a thin membrane of tissue.
 All the ears of a diseased plant become infected and all the developing grains turn into smut sori.
 The membrane splits at maturity, or during threshing, releasing the spore mass into the atmosphere.
 The spores are not readily wind-dispersed if the membrane ruptures before harvest as they stick
together due to the presence of an oily coating.
 Infected plants may be slightly shorter than their healthy neighbors.
 Affected ears may emerge later than the surrounding crop and in some cases remain trapped within
the sheath of the flag leaf.
 Infected ears are readily identified by their dark color and shriveled awns.
 Each smut sorus remains covered by a white, shining, silvery membrane, which is partially
developed from host tissue and partially from fungus. Due to this compact covering, the smut
spores are not blown off, and thus the disease in named covered smut.
 Sori can occasionally be found in stripes on leaves and stem galling has also been reported.
Symptoms

Fig. Covered smut infected ear of barley

Pathogen/ Etiology
 The smut spores are rounded to ellipsoidal, brown, smooth and upto 9 micro meter in diameter.
 In mass, the spores appear black, but actually they are brown in colour.
 On germination every spore (teliospore) produce promycelium or basidium.
 Later produce basidiospores.

Fig. Teliospores/ smut spores (Ustilago hordei)

Nature and recurrence of disease/disease cycle

 When the masses of spores are broken open as the barley is threshed after harvesting, innumerable
spores are released. Many of the spores lodge on healthy kernels and remain dormant until the
seed is sown. On germination, every smut spore (teliospore) produces a promycelium or basidium.
The diploid nucleus of smut spore divides meiotically forming four haploid nuclei. The basidium
become septate and basidiospores or sporidia are produced (two ‘+’ strain, and two ‘-’ strain
develop).The two sporidia of opposite strain (+ and -) fuse together, and a dikaryotic hypha is
resulted. Infect the seedling along the epicotyl by dikaryotic infection hyphae. After the fungus has
entered the seedling, its hyphae continue to grow with the shoot and eventually replace the grains
by masses of spores. A warm, moist, acid soil favours seedling infection. During threshing the
smut sori break, the smut spores are released, and they make the seeds contaminated again.
Control
 Spray Mancozeb/Tebuconazole @ 0.2 to 0.3% starting just before emergence of the heads
continue for two or three times if the disease is severe.
 Treatment of barley seeds with Provax @ 2.5 g/kg seeds successfully controls the disease.
 Use of disease resistant varieties also helps to reduce losses.
 Sowing seeds in a moderately dry soil will reduce the disease incidence, since moist soils are
favourable for infection.
 The rate of covered smut infection can be reduced when barley is raised in a neutral or alkaline
soil than in an acid soil.
 Rogueing: The infected plants may be uprooted and burnt.