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Wheat: Triticum aestivum L. Family: Poaceae 1. FLAG SMUT
Flag smut of the wheat is found in all most all the wheat growing areas of the world. The
disease occurs in some European countries and in the major wheat producing
countries of the world such as
Symptoms: Theses appears in springs
on leaf sheath and leaf blades but occasionally it may be found on the stem and
ear tissues. At early stage of disease development, the lesions are long& light
green stripes that room after became grayish black. These streaks are
sub-epidermal smut sori that develop between the leaf veins and cause leaves to
become twisted and rolled .the infection is more sever on upper surface of the
leaf blade than the base. The epidermis of the leaves splits along the sori
liberating a powdery mass of black colour spores that disintegrates leaf
tissues. The disease plants are dwarfed, tiller expressing reducing inter node
length and rarely head out. However the head do not formed any grain. The
diseased plant leaves and the whole plant will die.
Causal Organism: The flag smut of
wheat is caused by Urocystis agropyri
(Preuss) Schreet Koern. The spores are formed in tiny balls consisting of one to
six fertile cells covered with bright brown coloured layer of sterile peripheral
cells. The sterile peripheral cells are irregularly oblong or sub-spherical in
shape. The spore balls are 18-53 µm in diameter. They germinate to produce a
short promycelium with or without septation. Three to four hyaline cylindrical
sporidia are produced near the apex. The basidiospores are oblong, thin walled
and measure 12-15 x 3 µm. They germinate to produce slender infection hyphae
while attached to the promycelium.
Disease cycle: Flag smut is caused by
the pathogen Urocystis agropyri
(Preuss) Schreet koern (Syn. U.
tritici), belong to class
Basidiomycetes, order- Ustilaginales and family- Ustilagenaceae. The fungus form
small spore ball consisting of 1to 4 teliospores are red brown, smooth and
round. They germinate a produce a short hypha with 3-4 sporidia were the tip and
infect wheat coleoptile prior to there emergence. They germinate in the soil at
the temperature ranging from 40-86F. The optimum germination occurs at 64 – 77
F. Infection is optimum at soil moisture of 10 to 15% of field capacity. The
fungus over winters as mycelium in seedlings, then systematically invades and
sporulates within the upper portion of the plant, producing sori in which hyphal
tips differentiates into teliospores. After few days or when wheat is harvested,
the sori erupted liberated the teliospores that contaminates seed and soil.
Disease Management:
2. HILL BUNT OR STINKING SMUT
The Stinking smut or Hill bunt of wheat occurs in major wheat growing areas of
the world. In
Symptoms:
The stinking smut or hill bunt is caused by two closely related
species of fungi, Tilletia foetida
(smooth spore) and Tilletia caries
(rough spore). Both fungi have similar life cycles and may even occur together
in a plant or a grain. The symptoms of the disease are not easily identified
until the earhead emerges. The infected plants may be slightly to severely
stunted with bluish green cast on heads that appeared dark green than healthy
ones. The diseased heads have a more open appearance due to the expanding of the
smutted kernels causing spreading of the glumes. During the head development,
the kernel is replaced by a smut ball that is dull, gray-brown, short and plump.
The smut balls consists of a mass of oily, foul smelling, dark brown spores. The
smut balls crushes during threshing and liberate the spores to adhere on healthy
grains. A single smut ball may contain up to 8 million teliospores.
Causal Organism: The spores of
Tilletia caries (D.C.) Tul. are rough
walled, reticulate and measure 15-20 µm in diameter. The resting period is not
occurred and spores germinate immediately in favourable condition on suitable
surface. The spores produce uninucleate, primary sporidia which fuse in pairs to
form H shaped structures. After fusion, these primary sporidia become
binucleate. Primary sporidia germinate by giving out hyphae which bears sickle
shaped secondary sporidia. The infection can be found only when the germ tube of
a primary or secondary sporidium comes in contact with young seedlings of host
plants. The pathogen is heterothallic with more than 20 known races. The
pathogen is externally seed borne and usually infects all spikelets in an ear.
The spores of Tilletia foetida
(Waller.) Lira. are reticulate, smooth walled and measure 15-25 µm in diameter.
The spores can germinate frequently in moist environment. Spores produce a
basidium, which formed a cluster of 8-15 long, narrow and curved sporidia. The
sporidia fuse laterally and form H shaped structures. On germination, these
structures give rise to secondary sickle shaped sporidia. The infection can be
found only when the germ tube of a primary or secondary sporidium comes in
contact with young seedlings of host plants. The pathogen is heterothallic with
more than 10 known races. The pathogen is externally seed borne and usually
infects all spikelets in an ear.
Disease Cycle: The pathogen
overseasons as teliospores on contaminated wheat grains and germinate at the
same time the wheat seed germinate. Bunt spores germinate to form a basidium on
which 8-16 basidiospores (primary sporodia) develops. The basidiospores fuse
near their middle in compatible pairs to form H shaped structures. They then
germinate to form short hyphae on which sickle shaped secondary sporodia are
borne. On germination, the secondary sporodia penetrate wheat plants and cause
infection. After infection, the mycelium grows systemically in the meristmatic
tissues of the growing point. The smut mycelium invades the developing head and
displaces all kernel tissues within the pericarp. Eventually teliospores are
formed within the kernel tissues. It is estimated that the spores remain viable
up to 25 years under dry conditions.
Disease Management:
3. FUSARIUM HEAD BLIGHT
Head scab of wheat or Fusarium head blight (FHB) is a destructive disease in the
humid and semi humid wheat growing areas of the world like north central USA,
eastern Canada, eastern and western Europe, the regions of the former USSR,
China, Brazil, Romania and India. Disease affects the ears of the host. FHB is
currently not a severe problem in
Symptoms: Initial infections appear
as small, water soaked spots at the base or middle of the glume, or on the
rachis. Water soaking and discoloration then spreads in all directions from the
point of infection. A salmon pink fungal growth may be seen along the edge of
the glumes or at the base of the spikelet. Infected grains become shriveled with
a floury discoloured interior. Premature death or bleaching of spikelet is also
a common symptom and can be seen on emerged immature heads where one or more
spikelets or the entire head may be affected. In severe infection, the peduncle
may turn dark brown. Infected grains become smaller, shriveled in appearance and
white to pale pink in colour especially when infected with
F.
graminearum. At the later stage of
infection, small black perithecia grow in the same diseased area.
Causal Organism and Disease cycle:
Fusarium head blight has been associated with up to 17 causal organisms, of
which Fusarium graminearum Schwabe
(teleomorph Gibberella zeae [Schwein]
Petch) is the principal pathogen responsible for head blight in many countries.
Other related species such as F.
culmorum (Smith) Sacc.,
F.
avenaceum (Fries) Sacc.,
F.
moniliforme Sheldon,
F.
oxysporum Schlect.,
F.
poae (Peck) Wollenw and Microdochium nivale
(Fries) Samuel and Hallett may contribute to the head blight complex but are
generally less important than F.
graminearum. In addition to these,
F.
semitectum,
F.
compactum (Wollenw) Gordon, F.
subglutinans,
F. equiseti,
F.
solani,
F.
pallidoroseum (Cke) Sacc. have also been associated with head scab of wheat.
All Fusarium species and M. nivale
that infect wheat are capable of surviving saprophytically on crop residues.
Fusarium graminearum can survive as
mycelium, ascospores, macroconidia and chlamydospores. There is considerable
evidence that continuous wheat cropping or wheat following corn in a rotation
system significantly increases the incidence and severity of FHB. The highest
percentage of infection occurred through extruded anthers and during the
flowering period. Anthesis may be the period of greater susceptibility because
the high levels of choline and betaine produced in the extruded anthers
stimulate the growth of F.
graminearum and promote the infection
of wheat spikes by the pathogen. F.
graminearum infects wheat spike
tissues primarily through anthers then spreads to the epidermis of glumes and to
the ovaries. The fungus can also directly invade the external and internal
epidermis of the glumes and penetrate the external epidermis of anthers through
natural openings. From the infected floret, fungus mycelium enters adjacent
florets in the same spikelet and through the rachis enters adjacent spikelets in
the same spike. The optimum disease development caused by
F.
graminearum occurs at 26° C. Conidia
produced on diseased heads serve as secondary inoculum.
Disease Management:
4. ALTERNARIA LEAF BLIGHT
The leaf blight disease of wheat was first time reported from
Symptoms: The disease appears when
the crop the crop is seven to eight week old and the leaves are in direct
contact to soil. At early stage of disease development, leaves showed scattered,
small, oval, irregular and highline lesions with bright yellow margins. Two and
more lesions collapsed with each other and covered large areas of the leaf. The
older leaves are more easily infected by the pathogen. At latter stage, these
lesions become brown or grey coloured. The wet and humid environmental
conditions favors with 22 -26°C temperatures. The fungus produced black colour
conidia on older lesions. The disease appeared on leaf sheath, leaf blade,
heads, owns and glumes.
Causal Organism: The disease is
caused by Alternaria triticina Prasada
and Prabhu. The mycelium of the pathogen is hyaline in early stages but becomes
olive buff at later stages. The mycelium is branched and septate which produce
septate, unbranched or rarely branched, erect, single or in groups conidiophores
that emerge out from stomata measure 17-28 x 3-6 µm. Conidia are borne singly or
in chains (2-4), light brown to dark olive brown, smooth, irregularly oval,
elliptical and beaked. Each conidium possess 1-10 transverse, 0-5 longitudinal
septa and measure 15-89 x 8-30 µm. The maximum disease incidence is found at
absolute relative humidity and 25 °C temperature.
Disease cycle: The pathogen is seed
born as well as soil born, surviving as conidia on seed as mycelium in seed.
Pathogen over season in soil and within infected soil residue, the possible
source of primary inoculum. At advance stage of seed formation the seed
infection may also takes place, to make a source of internal seed born
infection. The fungus sporulated under dark conditions. The secondary inoculum
is provided by conidia produced in lesion and disseminates by wind to other
susceptible hosts.
Disease Management:
5. SHARP EYE SPOT
The sharp eyespot of wheat is a common disease throughout the temperate regions
of the world and is capable of infecting many numbers of grass family including
barley oat and rye. The disease itself does not cause such yield loss. The
disease is frequently occurring in combination with take all root rot and
Cephalosporium stripe disease. It is
found that acidic soil increases the disease risk as do cool spring
temperatures. The symptoms were found more severe on plants around the wet and
water logged area. Sharp eye spot is not a major yielding limiting disease of
wheat but it can reduce yields considerably under condition conductive to its
establishment up to maximum of 18 percent.
Symptoms: The name sharp eye spot
comes from the characteristics disease symptoms that occur on the lower stems.
The lesion on the lower stems showed dark sharp margins and lens shaped. The
growth of fungal pathogen with in the lesion is more superficial. The centers of
these lesions are pale to straw
colored and often studied with mycelium. The compact masses of small
black colored sclerotia may develop in the space between culm and leaf sheath.
The infected tillers of mature plants producing white head and die prematurely.
The plants with diseased roots are prone to lodging.
Causal Organism and Disease cycle:
Sharp eye spot disease is caused by the soil born fungus
Rhizoctonia cerealis. This fungus has been found to have a sexual stage,
Ceratobasidium cereale, but the
perfect stage is not important in the disease cycle.
Rhizoctonia cerealis produces no spores, but
survive in the soil and live on crop residues as mycelium and hardened
structures called sclerotia. The sclerotia are very small and irregular is
shape, produce white to brown mycelium on germination. The disease is favored by
wet and cold conditions. The fungus infects the roots and calms of the host
during growing season particularly in light dry soils. The seedlings may be
killed but some survive through the growing session by producing the new roots
to compensate the loss.
Disease Management: Management
practices that favors vigorous plant growth like proper seed bed preparation,
soil drainage, well fertilized soil and crop rotation may generally limit the
loss due to disease.
6. KARNAL BUNT
Karnal bunt or partial bunt is a minor fungal disease of wheat, durum and
triticale (a hybrid of wheat and rye). The disease was first reported in 1931 in
wheat growing areas near the city of
Symptoms: Karnal bunt is not easily
detected in the field because few florets are typically infected in the area of
the kernel affected might be small and facing in wards. Individual kernels most
commonly have a great tint on the embryonic end but can be fully encompassed
with a grey black color. In the bunted kernels, telutospores remain covered by
the pericarp at the early stage of disease. The sori (bunt-balls) cracked and
liberate the spores. A fishy order that be detectable from heavily infected
grain is common to karnal bunt as well as several other bunt diseases and is
caused by aromatic alkaloids present in the spores. Spores can move in the wind,
they are relatively heavy and are not believed to be carried long distance.
Causal Organsim: The causal pathogen
of karnal bunt is Neovossia indica
(Mitra) Mundkur. The spores are smooth walled, spherical and measuring 22-49 µm
in diameter. The spores require a long resting period before germination. On
germination, the spores produce a short stout basidium. The sporidia are produce
in large numbers (60-180) at the top of the basidium. The sporidia are flexible
and needle shaped. The secondary sporidia are sickle shaped. The sporidia
germinate by producing germ tubes that acts as infection threads. The pathogen
is soil and air borne, usually affecting only a few spikelets in an ear.
Disease cycle: Disease spread from season to season occurs
when teliospores become dislodged from infected kernels during harvest, become
airborne and settle in the field or spread to adjacent areas with wind currents.
These teliospores lie in the soil until conditions become favorable for
germination. During a period of cool, wet weather, the teliospores near the soil
surface can germinate and produce airborne spores called primary sporidia. If
the flowering of wheat occurs simultaneously with the production of primary
sporidia, the fungus can infest the ovary in the wheat flower. At maturity, the
kernels becomes blackened with a mass of teliospores and damaged by concurrent
bunting or eroding of the embryo end of the kernel. The black teliospores my be
internal and covered by the pericarp of the kernels. The spores on and in
infected mature seed, hay or agricultural equipments are capable of spreading
the infestation to other fields in which they come in contact.
Disease Management:
7. LOOSE SMUT
Loose smut is a common disease of wheat throughout the humid and semi-humid
areas of the world. In
Symptoms: The disease is easily
recognized at the time of ear emergence by the characteristic dusty black
appearance of diseased ears. The infected ears emerge from the boot leaf,
usually 1-3 days earlier than those of healthy plants. Usually all the glumes
and grain in a smutted ear are completely transformed in to black powder. This
sooty mass is composed almost entirely of millions of microscopic smut spores
(teliospores). Large clouds of black dust can often be seen due to release of
spores in to the air as a result of the thin membrane cover being ruptured
during the harvest or blown off by wind, leaving behind the erect bare rachis.
Causal Organism: The loose smut of
wheat is caused by Ustilago nuda tritici
(Pers.) Rostr. is now known as Ustilago
segetum (Pers.) Roussel var. tritici.
The chlamydospores are produced in great abundance are pale, olive brown,
spherical to oval, 5-9 µm in diameter and have minutely echinulate walls. The
promycelial cells fuse and give rise to the germ tubes that enter in the ovary
through stigma and infection become established in the embryo, which remain
dormant until seed germination. Its presence is shown only when the mature plant
emerges smutted ear. The physiological races of the fungus are known. The
diseased plants has greater rate of photosynthesis and respiration than healthy
plants during the early stages of growth of the pathogen but declines at later
stages that results in reduced dry weight of affected plants.
Disease Cycle: Wheat plants are
infected only during the flowering periods. Wind, rain, insects and other
agencies carry the black teliospores from a smutted head to the open flowers of
a healthy head. Dispersal of spores at flowering is critical to the perpetuation
of loose smut because infection usually takes place during the two days after
flowering. At the presence of moisture with a temperature of 16° to 22° C, the
spores quickly germinate and grow down to the stigma and pistil to invade the
young embryo. Plants become resistant to infection one week after flowering.
After establishing in the embryo of the kernel, the mycelium of the fungus
becomes dormant. When an infected kernel is sown and begins to germinate, the
mycelium of the smut fungus again becomes active and grows systematically in to
the young shoots to the growing point. At heading time, the spike lets in an
infected wheat head are completely transformed, except the rachis and the
pericarp membrane in to a dusty mass of teliospores. The pericarp membrane holds
the spore mass together until the head emerges from the boot. The delicate gray
membrane tear away and the masses of teliospores are released in the wind,
leaving the rachis barren.
Disease Management:
8. STRIPE RUST
Stripe rust or yellow rust was first discovered in
Symptoms: The yellow coloured
uredinia (the spore producing structures of the pathogen) appear in rows,
somewhat linearly along the axis of the leaf and hence the name ‘stripe rust’.
When disease severity increases, the pustules may be found on the leaf sheaths,
stem, spikelets, glumes and grains. The uredini sori are embedded in
sub-epidermal layer and covered with epidermal layer of leaf that cracks on crop
maturity. Thousands of urediniospores can arise from a very small area of
infected leaf tissue. These urediniospores can be spread by wind to other plants
to initiate other subsequent infections. The teleutosori appeared at end of the
growing season. It is observed that the teleutospores may be formed in the
uredosori which are black, elongated and sub-epidermal. The aecial and pycnial
stages of the fungal life cycle are still not known.
Causal Orgaism: Yellow rust of wheat
is caused by Puccinia striiformis
West. The urediniospores are unicellular, binucleate, almost globose, measure
23-35 x 20-35 µm and spore wall is minutely echinulate. They have 6-16 germ
pores. The teleutospores are dark brown, two celled, oblong to cuneiform,
measure 35-63 x 12-30 µm, slightly constricted at the septum and the apex is
less thickened and pointed than in Puccinia graminis. The teleutosori are filled
with spores interspersed with many unicellular, brown coloured long paraphyses.
The teliospores have ability to germinate immediately on maturity. The fungus
has more than 40 races worldwide.
Disease Cycle: The pathogen survives
from one season to the next on volunteer wheat plants or as latent infections in
dormant wheat plantings in its uredial stage in
Disease Management:
9. PYTHIUM ROOT ROT
The Pythium root rots are distributed
throughout the world on wheat, other cereals and grasses. The disease is
reported from
Symptoms: The disease appeared after
seedling emergence with characteristic symptoms of the disease showing
light-brown soft rot of rootlets and roots and the pale-green stunted growth of
tillers, followed by wilting of plants. The severe development of disease causes
browning of the leaves and a soft rot of the leaf sheaths and cortical tissues
of the crown below the soil surface. Under moist soil conditions and continuous
cereal and grass cultivation, the disease cause considerable damage of yield up
to 20-25 percent of an average.
Disease Cycle: The fungus, which is
present in all agricultural soils, inhabits as chlamydospores, oospores,
zoospores and dormant mycelia. The oospores survive for 5 years or more in soil
and host residues as oospores. When the crop is sown, oospores germinate and
form germ tube that attacks the host plant roots. The fungal hyphae invaded the
host plant tissues and spread inter and intra-cellularly. As the disease
increases, the pathogen spread in upwards and downwards direction of the
vascular system, causing wilt. Under wet environmental conditions, the fungus
produces numerous sporangia having zoospores that are spreading further
infection after releasing from it. The disease severity is found maximum at the
soil temperatures of 10° to 25° C and in wet areas that are deficient in
phosphorus and organic matter.
Disease Management:
10. STEM RUST
Stem or black rust of, caused by fungus
Puccinia graminis Pers. f. sp. tritici
Eriks. & E. Henn., is a highly damaging disease of wheat that primarily occurs
in warm weather and can cause great damage to susceptible crops. The first
detailed reports of wheat stem rust were given independently by Italian
scientist
More than 50 numerically catalogued resistant (Sr) genes confer resistance to
the various races of the stem rust pathogen. However, virulence for a large
proportion of these genes is common. Additionally, the wheat breeding community
particularly relied on the use of the Sr31 gene, which gave continued protection
against stem rust all over the world. However in 1999, a new race designated as
Ug99 with virulence to Sr31 and other important genes, was discovered in
Symptoms:
The flecking of leaf, leaf sheaths, culms and floral structures are
the first symptoms of black rust. The uredosori are oblong, reddish brown
pustules and merging with one-another and producing brown coloured uredospores
on bursting. The affected plant parts shows brown appearance when large number
of uredosori bursts. The teleutosori are produced in later season which are
linear or oblong, conspicuous, dark brown to black and producing linear patches
of black lesions. The teleutosori produced dark brown mass of teleutospores. The
diseased plants are stunted and produce small spikes and shriveled or no grains.
Causal Organism:
Puccinia graminis f. sp. tritici Erikss. and
Henn. is a macrocyclic, heterocious and obligate parasitic rust fungal pathogen
which infect two alternate host plants i.e. Barberry and Wheat in their life.
The rust fungus has five stages or types of spores in their life cycle i.e.
pycnial, aecial, uredial, telial and basidial. Airborne spores infect young
tissues of the alternate hosts, where binucleate stage is started by sexual
fusion. The mycelium is slender and septate which ramify in intercellular spaces
of the host tissues and obtain nutrition from host cells by small tubular
haustoria.
On Barberry, the pycnial stage is found as small, flask shaped cups rupturing
upper epidermis of host leaf. After sometimes, on the undersurface of leaf,
aecial cups arised by rupturing lower epidermis is similar manner. The
aeciospores are somewhat spherical and vary from 14 to 60 µm in diameter.
Aeciospores are echinulate (spiny), arise in chains from the base of the aecial
cup with six germ pores. Aeciospores can infect grass family host i.e. wheat.
Uredospores and teleutospores are produced on wheat plants in the early spring
to late spring. The uredospores are brown, oval and 25-30 x 18 µm having single
thick wall with tiny spines. The teleutospores are two celled, deep brown, 40-60
µm long and 15-22 µm broad with thick smooth wall and persistent pedicel. The
apex of teleutospore is pointed with a single germ pore through which
promycelium extrudes.
The germ pore of lower cell is situated just below the septum. The teleutospores
have long resting period and before germination, meiosis division occurred. On
germination, they form four celled promycelium and each cell of promycelium
develops a sterigma. Each sterigmatic cell bears a haploid basidiospore. These
basidiospores are ejected out violently and blown by air. The basidiospores can
germinate immediately in moist environment but unable to infect cereal crops.
Basidiospores, fallen on barberry leaves, germinate in favourable environmental
conditions with germ tube. The germ tube penetrates through epidermis and form
mycelial mat below upper epidermis. The fungal mat produces pycnia on the upper
surface of the leaf.
Disease Management:
11. POWDERY MILDEW
Powdery mildew has been recognized as a disease problem on wheat as well as
other cereals and grasses for centuries over worldwide. This important foliar
disease of wheat is caused by the fungus
Blumeria graminis (DC) E. O. Speer f. sp.
tritici Em. Marchal (Syn.
Erysiphe graminis DC f. sp. tritici
Marchal). It is common in wheat growing areas with a humid or semiarid
environment. The disease is important in the cooler regions of
Symptoms: Powdery mildew occurs on
all aerial parts of the wheat plant, but it is most conspicuous on the upper
leaf surfaces and leaf sheaths just above the soil line. Symptoms may develop
anytime after seedling emergence. The disease is most commonly seen in late
winter to early spring. The fungus produces white to gray, cottony growth mostly
on the upper leaf surfaces, although some pustules may develop on the lower side
of the leaf. Pustules begin as small white circular patches of fungal mycelium
often surrounded by chlorosis. Pustules often join together to form large masses
of fungal growth on the upper leaf surfaces and at later stage, tissue around
older pustules die and become brown. After few days, these pustules produce
large quantities of small asexually produced oidia (also called conidia) in long
chains, which are dispersed by wind and water. These single celled spores
(oidia) are oval and colorless. As the wheat and the mildew colonies mature, the
fungus produced sexual stage or cleistothecia. Ascospores develop within the
cleistothecia and serve as the long term survival structures.
Causal Organism: The pathogen
responsible for powdery mildew of wheat is
Erysiphe graminis f. sp. tritici
(D.C.) Marchal. The primary mycelium of pathogen is superficial, branched and
conidia are elliptical, hyaline, single celled, white to pale brown or grey in
colour measuring 20-30 x 8-10 µm in diameter. Haustoria are elliptic and long
finger shaped appendages and penetrate in the epidermal layer to obtain
nutrition. The pathogen is ectoparasite, spreading on host surface and produce
long chains of conidia on short conidiophores. The dark black globose
cleistothecia are 135-250 µm in diameter, wall cells small, indistinct, have
short appendages and contain 9-30 asci. The ascus is cylindrical to oblong, have
long pedicels and measure 70-110 x 25-40 µm. The ascus contains eight oblong,
hyaline, thin walled ascospores measuring 20-25 x 10-13 µm. Ascospores germinate
immediately on falling suitable host under favourable environmental conditions.
Disease Cycle: The fungus over
winters as cleistothecia on plant debris. In warmer climates it can also survive
as conidia (oidia) or mycelium on infected plants. Ascospores and conidia serve
as primary inoculum. Ascospores and conidia, produced on wheat plants are wind
dispersed. Conidia germinate and infect plants under cool, moist conditions.
Infection does not require free water on the plant surfaces but high relative
humidity (near 93 to 100 percent) favours infection. Optimum development of
powdery mildew occurs from 10° to 22° C and is declined above 25° C. Host tissue
is invaded directly by the germ tube. Haustoria are formed inside invaded cells
and mycelium is formed on the surface of these cells. Conidia, produced on the
mycelium, are serving as secondary inoculum. Under optimum environmental
conditions, the fungus can complete a repeating cycle in 7-10 days. Other
factors that favour disease development are: susceptible cultivars, dense
plantings and increased use of nitrogen fertilizers.
Disease Management:
12. LEAF AND GLUME BLOTCH
The leaf and glume blotch are two different diseases caused by two different
species of Septoria. The
Septoria fungi destroy nearly 2 percent of the world’s wheat annually. The intensity of
the disease depends entirely on the time of onset of infection and the weather.
Both species of the fungi are found throughout the world. In
Symptoms:
Septoria tritici blotch is ordinarily only found on the foliar parts of infected plants,
while Septoria nodorum (Stagonospora nodorum) can be found on
all above ground parts of the plant including the glumes around the grain.
Symptoms appear first as small, chlorotic flecks restricted by veins. These
subsequently develop in to spots that tend to develop longitudinally to form tan
to reddish brown, irregular shaped blotches which are often surrounded by a
yellow margin. As the disease advanced, these blotch’s centers become light
brown to ashen, appearing small black specks (Pycnidia). Pycnidia are the
asexual reproducing structure of the fungus and are diagnostic of this disease.
Pycnidia are sphere or ball-shaped, gelatinous and gray brown. The white to
cream masses of spores can be seen oozing from matured pycnidia. Severely
infected leaves turn yellow, wither and die prematurely. Glume blotch develops
mainly in areas where the weather is warm and moist. It appears as small,
irregular gray to brown spots or blotches on the glumes, although infections may
also occur at the nodes. When the lesions enlarge, a sprinkling of pycnidia
develops. The whole area of glumes may be covered with dark brown to dark purple
with ash gray areas. This stage of the disease is called ‘glume blotch’. Severe
leaf blotch and glume blotch infections may lead to light weight and shriveled
kernels.
Causal Organism: These two diseases
are caused by the fungi, S.
tritici and
S. nodorum with their sexual stages,
Mycosphaerella graminicola and
Leptosphaeria nodorum, respectively,
that may occur in the disease cycle. S. tritici forms subepidermal, round or
sub-globose, open with ostiole and gray-brown coloured pycnidia. Conidia are
cylindrical, 3 to 6 septate, hyaline, thin walled, slightly curved and measures
as 56-65 x 3.7-5.0 µ. The conidia are extruded from the pycnidia in milk white
to buff-coloured cirrhi. The conidia of S.
nodorum are shorter and broader than
those of S. tritici, having 2-3 septa and rounded ends. The cirrhi are pink.
Disease Cycle: The disease cycle of
S.
tritici is similar to that of
S.
nodorum, although
S. tritici can go through its life cycle at
slightly lower temperature (15-20° C optimums) and requires longer periods of
high humidity to initiate infection. Septoria fungi are over summers as mycelium or pycnidia on infected plant debris and on
volunteer wheat. The pathogen may infect wheat seedlings soon after emergence.
Infection may occurs during cool, wet weather and continues to increase and
spread until the temperature is below 40 F. The perithecia and pycnidia produce
an abundance of ascospores (sexual spores) and pycnidiospores (asexual spores)
during cool, wet weather in early spring. These spores are dispersed by either
wind or splash rain during the wheat growing season and can initiate infections
under favourable environmental conditions. Temperature between 60- 70 F and 12
or more hour’s leaf wetness is optimum for infection and spread. The disease
cycle can be completed in 10-14 days during such conditions.
Disease Manageemnt:
13. TAKE ALL
This is one of a complex of disease attacking the roots, crown and basal culm of
cereals and grasses. The disease is widespread and destructive in major wheat
growing areas of temperate world. The yield loss from Take –all disease is
ranging from 0- 50%.
Symptoms: Take – all is a wheat
disease but may be causes disease in other cereal crops and grasses that infects
the plant’s roots, blocking the conductive tissue and reducing water uptake.
Under relatively moist conditions, the conspicuous symptoms of take- all appear
at about the time wheat is heading. Localized area occurs in which growth is
checked, the green colour fades and the leaves, culms and heads bleach. Affected
plants are easy to pull out of the ground due to poor root development the main
root, crown, and basal culms tissues show a dry not accompanied by a dark brown
to black surface mat of thick walled coarse fungal mycelium. The leaf sheath
shows small black raised spots having the neck of fungal perithecia.
Causal Organism and Disease cycle:
The Take – all disease of wheat is caused by the fungus
Gaeumannomyces graminis var.
tritici. The fungus produces
ascospores in asci in specialized structures called perithecia. These black perithecia are embedded
in leaf sheaths with protruding necks. The fungus survives in infected cereals
and grass residues. Upon germination fungal ascospores produces mycelium which
spread the disease through the soil to plants. The superficial mycelium invades
the cortex and the vascular system of plants and invades roots are killed. Take
all disease is most severe in porous infertile alkaline and poorly irrigated
soil under cool temperature between 12- 180C.
Disease Management:
1.
Crop rotation involving legumes, other dicotyledonous
crops, oats or corn are important in reducing damage.
2.
A balanced fertility with a good availability of
phosphate and potash reduces loses.
3.
Use systemic fungicides for seed treatment like
triadimenol up to 75% that can reduce the disease.
14. WHEAT STREAK MOSAIC VIRUS
Wheat streak mosaic, caused by the wheat streak mosaic virus (WSMV), is a
serious and widely distributed disease of winter wheat. Wheat streak mosaic also
occurs on spring wheat and barley, corn, rye, oats, and a number of annual and
perennial grasses. It was first recognized in
Disease symptoms: Infection of winter
wheat often occurs in the fall, but disease symptoms may not appear until
spring, when temperatures begin to increase. Infected plants have a general
appearance of yellowing and stunting. Plants infected with WSMV initially have
light green streaks in the leaves which later develop into yellow stripes
running parallel to the leaf veins. Heads on infected plants can be sterile and
contain no seed, or only small and shriveled grain. Infected plants usually
appear first along paddock edges or in patches near volunteers. Small ‘islands’
of plants showing symptoms may then occur throughout the field as the growing
season progresses. Symptoms develop at temperatures above 10ºC, so may fail to
appear in infected plants during the winter months, especially in later sown
crops. The evidence of mite feeding can sometimes be seen on young leaf blades
which may curl tightly, trapping new leaves and resulting in rolled, twisted
seedlings. Heads may also be trapped in the boot.
Causal Organism: Wheat streak mosaic
virus, a member of the virus family
Potyviridae, is a flexuous rod-shaped particle that can be seen only under
high magnification using an electron microscope. Virus particles consist of a
central core of ribonucleic acid (RNA) wrapped in a protein coat. Each particle
is approximately 15 nanometers (nm) in diameter and 700 nm long.
Disease cycle: WSMV is spread by a
tiny (0.3mm) white, cigar-shaped mite called the wheat curl mite (Aceria tosichella). This mite has no
wings but has two pairs of legs near its head, and a fleshy body. It is not
visible to the naked eye. The mites do not walk far, but like many small
insects, they can be randomly distributed by wind. They can also hitch a ride on
other insects and animals, including humans. These mites are believed to be very
widespread across the cereal belt. The life cycle of the mite, from egg to
adult, is completed in seven to 10 days and need to continue feeding on live,
green plants to survive. As such their disease cycle is dependent upon a ‘green
bridge’ of live volunteer cereals and/or host grasses between seasons. The mite
vector feeds preferentially on the upper leaf surface and near the margin of
leaves causing the leaf edges to curl tightly inward and upward toward the upper
midrib. Such infected leaves tend to remain erect. The mites are enclosed
protectively within the rolled leaves.
The mites thrive on the lush, young growth of wheat, barley, corn, millet, and many annual and perennial grasses. Once the mite has fed on an infected plant, it transmits the virus as it feeds but does not pass the virus through the egg to its offspring. The optimum temperatures for mite activity and virus transmission are 24-27ºC.Seed transmission of the virus is possible but has not been reliably confirmed in wheat. If it does occur, it is expected to be extremely rare.
Disease Management:
15. BARLEY YELLOW DWARF VIRUS
Wheat is a natural host for many viruses. Approximately 55 viruses to which
Triticum aestivum is susceptible and around 30 viruses that naturally infect
wheat are reported. Infection by wheat viruses produces symptoms such as foliar
chlorosis (mottle, mosaic, streaks and yellowing), necrosis, stunting and
rosetting. Some of the symptoms, especially foliar discoloration, can easily be
confused with nutritional and abiotic disorders. Barley yellow dwarf is the most
widely distributed and the most economically important virus disease of wheat.
Barley yellow dwarf was first reported by Oswald and Houston in 1953. It is
caused by a group of luteoviruses called barley yellow dwarf luteoviruses
(BYDVs). Barley yellow dwarf viruses are not mechanically transmissible, nor
through the seed, but are transmitted by aphids in a persistent, circulative but
non-propagative manner. Aphids acquire and transmit BY-DVs while feeding on the
phloem sieve tube elements of host plants. Barley yellow dwarf viruses are
restricted to the Poaceae (Gramineae). Cultivated hosts include all the major
cereal crops: barley, maize, oat, rice, rye and wheat, as well as many annual
and perennial cultivated and wild grasses. BYD has been reported from over 50
countries (Lister and Ranieri, 1995) including
Symptoms: Yellow dwarf first appears
early in the season, usually along the margins of small-grain fields and later
develops within a field in more or less circular spots up to 25 feet or more in
diameter. As the season progresses, these diseased areas may enlarge and merge.
When aphid populations are high, entire fields may become affected. The typical
symptoms of BYDV disease on small grains may be confused with other causes,
e.g., mineral deficiencies, bacterial toxins, leaf breakage, low temperatures,
root and crown rots and others. The first symptoms on oats and to a lesser
extent on barley and wheat are the appearance of faint yellowish green blotches,
usually near the leaf tip. The blotches enlarge rather rapidly, merge and turn
various shades of red, purple, brown or yellow-orange. The yellowish green
blotches continue to appear on lower parts of the leaf before they change color.
Affected portions often die as the infection spreads through the entire plant.
The leaves may curl inward, are flexible and appear more erect than usual.
Symptoms generally appear first on the older leaves. Blasting of florets also
occurs, it may involve only a few florets or, if severe, plants may fail to
head. Kernels may shrivel and test weight may be reduced. In barley, the most
characteristic symptoms are dwarfing and the brilliant yellow coloring of the
leaves which extends from the tip towards the base. In wheat, severe dwarfing
and general yellowing are less common and the disease is more severe when
infection takes place in the fall than in the spring. Generally, the earlier the
infection, the more severe the disease with the root system damaged as severely
as the tops.
Causal Organism: BYDV is the type
member of the luteovirus group. These viruses are restricted to the phloem or
food-conducting tissue in infected plants. They are 25 nanometers (nm) in
diameter and icosahedral in shape, although sometimes they are referred to as
spherical. The genetic material in each particle is one single-strand RNA
molecule that has a molecular weight of about 2 million
Disease Cycle: The barley yellow
dwarf virus persists in small-grain cereals, in corn, in more than 75 species of
perennial and annual grasses, and in its aphid vectors. The spread of BYDV from
plant to plant and from field to field depends entirely on aphid movement.
During the growing season, each adult aphid may produce from 10 to 20 young each
day. The young aphids mature in eight to fifteen days. The wingless daughter
aphids reproduce and usually move only short distances by crawling from plant to
plant or by wind. When food is scarce, especially during the spring, winged
forms develop that migrate to other small grains and grasses, transmitting the
virus to these plants as they feed. Infected cereals and grasses serve as a
virus source for new generations of aphids. In the fall, the aphids migrate to
winter hosts – in the process, spreading the virus to fall-seeded small grains.
Infected winter barley, wheat, and oats, as well as perennial grasses become
important virus reservoirs for spread of the disease in the spring. BYD
epidemics are most common in cool (10° to 18° C), moist seasons that favor
growth of small grains and grasses as well as the multiplication and migration
of aphids. BYD infections occur throughout the growing season, but are most
common and damaging in spring in areas where the aphids over winter. Inoculated
plants become systemically infected and develop symptoms within two weeks at 20°
C, within four weeks at 25° C, but not at all above 30° C. The barley yellow
dwarf virus is not transmitted through eggs, newborn aphids, seed, soil, sap, or
other insects.
Disease Management:
1. BYDV cannot be fully controlled in the field. Damage in
oats as well as in other crops can be greatly reduced by growing tolerant
varieties. No major gene(s) for resistance to BYDV have been found in wheat and
oats. In barley, the gene Yd2 confers resistance.
16. SOIL-BORNE WHEAT MOSAIC FUROVIRUS
Soil borne wheat mosaic, caused by a soil borne virus, was first discovered in
Madison County, Illinois, in 1919. The disease occurs throughout the eastern and
central
Symptoms: The virus is carried inside
zoospores and persists inside the fungal resting spore for many years (Chen and
Wilson, 1995). The best conditions for disease transmission (as for vector
development) are high soil moisture, humid weather, soil temperature around 15°
to 18°C and slightly neutral to alkaline soil. The optimum temperatures for
symptom development are 15° to 20°C. Symptoms range from mild green to prominent
yellow leaf mosaics. The new unfolding leaves show mottles and streaks. Stunting
can range from moderate to severe, and certain strains of the virus can cause
rosetting of plants. The symptoms are more prominent in early spring growth and
rarely appear in autumn.
ROSETTING: The leaves and tillers remain short, growth is bunchy or compact, and
tillering is excessive (Figure 3). The leaves of such plants are usually bluish
green and may retain this color throughout the growing season. At other times,
rosetted plants die early without developing much green color.
LEAF MOTTLING: Soil borne wheat mosaic is best identified by an irregular
mottling, streaking, and blotching of the leaves when plants are growing rapidly
in very early spring before heading. The color of the mottling varies from a
hard-to-see pale green to a conspicuous lemon yellow that may involve most of
the leaf blade as well as the leaf sheaths and glumes. The mottling may persist
into late spring as long as the leaves are green – especially if the
temperatures remain abnormally cool.
Causal Organism:
Soil
borne wheat mosaic virus particles (called virions) are rigid hollow rods 20
nanometers (nm) wide of two principal lengths, 90 to 160 nm and 300 nm.
Particles of both sizes are necessary for infection. The virus is highly
variable and the length of the predominant short rods often changes as the wheat
plants grow. Infected cells often contain amorphous and crystalline inclusion
bodies that contain virions in a paracrystalline array. The virus also infects
certain cultivars of fall-sown rye, barley, emmer, and spelt, wild annual brome
grass (Bromus commutatus),
sorghum, and some species of
Chenopodium
have
been inoculated experimentally.
Disease Cycle: The virus causing soil borne wheat mosaic survives in the
soil and crop residues from season to season protected by its fungal vector or
agent, Polymyxa graminis, an obligate parasite in the roots of many
grasses and a few higher plants. During cool wet periods motile spores
(zoospores) are released by the fungus and infect roots of wheat plants. The
virus particles are either inside the spores of the fungus (both zoospores and
thick-walled resting spores) or tightly bound to the surface of these spores.
The fungus normally infects wheat roots shortly after planting in the fall. The
symptoms, however, do not normally appear until early spring. The virus is
transmitted from plant to plant by its fungal vector. The zoospores are produced
in virus infected roots or debris and carry the virus. The zoospores swim
through the soil solution to healthy root hairs and epidermal cells, penetrate
them, and thus inoculate the plant. The Polymyxa fungus survives
unfavorable periods in the form of resting spores clustered in the cortical and
epidermal cells within plant debris (Figure 4). These spores can survive in soil
for 10 years or more in the absence of wheat or other host plants. Because the
swimming zoospores of the fungus transmit the virus, soilborne wheat mosaic is
most common and severe in low, wet areas of fields in years when fall rainfall
is ample.
Disease Management: Control measures
include crop rotation, delayed sowing, increasing fertilizer application and the
use of resistant cultivars. Application of chemical sterilants and fungicides
can help reduce fungal inoculum but are not practical for large-scale field
control.
17. WHEAT SPINDLE STREAK MOSAIC BYMOVIRUS AND WHEAT YELLOW MOSAIC BYMOVIRUS
Wheat spindle streak mosaic bymovirus (WSSMV) and wheat yellow mosaic
bymovirus (WYMV), before considered to be strains of the same virus, were shown
to be distinct species through genome analysis (Namba et al., 1998). A
multiplex RT-PCR assay permits the discrimination of these two viruses (Clover
and Henry, 1999). Nucleotide and amino acid sequence comparison demonstrated
that the European and North American isolates were extremely similar and were
WSSMV, while the Chinese isolates were close to the Japanese isolates and were
WYMV.
Wheat yellow mosaic was first described in
Symptoms: They are both
sap-transmitted to wheat and naturally transmitted through the soil by the
fungus Polymyxa graminis. Symptoms develop only in spring when soil
temperatures are between 5°C and 15°C. The virus is usually detected earlier in
roots than in leaves. The optimum temperature for the development of P.
graminis in wheat roots is 15° to 22°C, for transmission of the virus 15°C
and for virus development 10°C (Slykhuis and Barr, 1978), perhaps the lowest
optimal temperature range of any plant virus disease. Wheat spindle streak
mosaic bymovirus and WYMV cause similar symptoms on susceptible plants.
The
first leaves produced in early spring develop yellow-green mottling, dashes, and
streaks. The discontinuous streaks are oriented parallel with the leaf veins and
taper at each end to form yellowish "spindles" (Figure 5). Symptoms are most
prominent on the lower leaves because warmer spring temperatures present their
development on younger leaves. As the leaves mature and when temperatures remain
cool, the center of the spindle may turn brown, streaking may progress to the
flag leaf, and the yellow-green areas tend to merge. Reddish streaking and
dieback of leaf tips or entire leaves sometimes occurs. Infected plants
can be mildly stunted and with few tillers. Autumn infections are most common,
and spring infection results in few symptoms.
Causal Organism:
Wheat
yellow mosaic virus particles are 14 to 18 nm wide and 200 to 2,000 nm long. The
infectious flexuous rods are about 600 nm long and apparently aggregate to form
particles up to three microns long. These particles are sparse in host cells of
wheat and are difficult to observe in leaf-dip preparations in the electron
microscope. They are found scattered and in loose to tight bundles in most
epidermal and parenchyma tissues in leaves showing symptoms of wheat yellow
mosaic. Infected host cells also contain prominent inclusion bodies which appear
as pinwheels and membrane proliferations.
Disease Cycle: There are several similarities between wheat yellow mosaic virus and soil borne
wheat mosaic virus. Both viruses are transmitted in nature by the same soil
borne fungus,
Polymyxa graminis. The
two viruses also survive in soil for years in the absence of wheat, apparently
in a stable, close association with their fungal vector. The
Polymyxa fungus survives in the form
of resting spores clustered in the cells of wheat root residue. In the fall, the
fungus produces large numbers of swimming spores (zoospores) in saturated soil
at cool temperatures. The zoospores carry the virus particles to wheat root
hairs and epidermal cells. The spores penetrate the cells of the root and infect
the plant, carrying the virus particle inside the plant. Wheat sown in infested
soil becomes infected soon after emergence (about 2 weeks after seeding) if the
soil temperature is near 15° C.
Infections of wheat yellow mosaic do not occur above 20° C, and
disease development is checked above 18° C. The optimal temperature for symptom
development is between 5° to 13°C. The optimum temperature for virus
transmission in the soil is 15° C.
Disease Management:
18. EARCOCKLE DISEASE
Wheat seed gall nematode was the first plant parasitic nematode observed by
Rev.Turbeville Needham in 1743 in
Symptoms: The nematode causes
earcockle disease of wheat. Nematode infected seedlings are more or less
severely stunted and show characteristic rolling, twisting and crinkling of the
leaves with consequent growth distortion. The affected earheads showed shorter
and thicker morphology. The glumes are arranged loosely and nematode galls
replaced the seeds. Galls or cockles are small, dark brown to black and
irregular in shape.
Disease Cycle: Seed galls mixed with
seeds contain approximate 3000-12000 second stage juveniles. In moist
conditions, the juvenile become active and move out from soil and invade the
germinating wheat seedlings. The juveniles adhere on the tip of growing point
and remain ecto-parasite during plant growth. Second stage juveniles become
endo-parasites at the time of flowering. These juveniles become adult and after
mating, the females start lying eggs inside the galls that replaces developing
seeds. On crop maturity, galls turn brown, hard and juvenile become quiescent.
These second stage juveniles may remain viable in the galls up to 32 years in
dry conditions. At harvest, seed galls also collected along with healthy seeds.
Control:
19. TUNDU
A more widely reported disease is yellow ear rot or tundu caused by
Corynebacterium tritici (ex
Symptom: The disease is characterized
by yellow slime on stem and inflorescence, which dries up to form sticky yellow
layers. Wheat ears covered by such slime become destroy or fail to emerge
properly and produce little or no grain. The nematode alone causes wrinkling,
twisting and other distortions on the leaves and stems. The grain with ear head
replaced with nematode galls that carry the causal bacterium. The diseased plant
showed shorter and thicker morphology than normal healthy plants. The disease
severity enhanced during rainy session. The diseased plant showed very early
emergence of the ear than the healthy plants. There is no, race variation in the
causal bacterium.
Disease cycle: The presence of the
nematode is considered essential for the establishment of the bacteria in the
plants and different attempts to inoculate wheat artificially in the absence of
the nematodes e wheat artificially in the nematodes have failed to produce
infection. The bacteria carried by galls can remain viable for at least five
years, while the nematodes with in the galls are known to remain viable for even
longer periods. The bacteria are not carried within the galls on or inside the
larvae, but probably on the gall surface.
Disease Management:
|
Wednesday 17 July 2013
Wheat; FLAG SMUT; HILL BUNT OR STINKING SMUT; FUSARIUM HEAD BLIGHT; ALTERNARIA LEAF BLIGHT
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