Diseases and Pests in

Wheat and Rice

WHEA
T

Principal

Barley yellow
diseases

dwarf
Common bunt
Eyespot
Wheat leaf rust

Barley Yellow Dwarf

Barley

yellow dwarf is a plant

disease caused by the barley yellow
dwarf virus, and is the most widely
distributed viral disease of cereals.
It
affects
the
economically
important crop species barley, oats,
wheat, maize, triticale and rice.

Biology
Barley

yellow dwarf virus

(BYDV) is a positive sense
single-stranded RNA
virus; the viron is not
enveloped in a lipid
coating. The virus is
transmitted by aphids,
and the taxonomy of the

Pathology
When

aphids feed on the

phloem of the leaf, the
virus is transmitted to
the phloem cells. Once
inside the plant, the
virus begins to replicate
and
assemble
new
virons.
This
process

Sources and spread

There

are two main sources by which a

cereal crop might be infected
1. By
non-migrant
wingless
aphids
already present in the field and which
colonise newly-emerging crops. This is
known as "green-bridge transfer".
2. By winged aphids migrating into crops
from elsewhere. These then reproduce
and
the
offspring
spread
to
neighbouring plants.

Control
"Green

bridge" sources must be ploughed in

as early as possible. Alternatively, a
desiccant herbicide should be applied 10
days prior to cultivation. Insecticide sprays
may be used at crop emergence.
Drilling dates prior to mid-October favours
attacks
from
winged
migrant
aphids.
However, yield penalties may be experienced
from late drilling. Insecticide sprays in this
instance are therefore aimed at killing the
aphids before significant spread can occur.

Common Bunt

The

bunts and smuts are

caused by fungi that affect
the seed of wheat and other
small grains and grasses.
Only loose smut and common
bunt occur in Oklahoma.
However, Karnal bunt, which
does not occur in Oklahoma,
is a concern because grain

Symptoms
Plants

with common bunt

may
be
moderately
stunted but infected plants
cannot
be
easily
recognized
until
near
maturity and even then it
is
seldom
conspicuous.
After initial infection, the

The

sorus is light to dark

brown and is called a bunt
ball.
The
bunt
balls
resemble wheat kernels but
tend to be more spherical.
The
bunted
heads
are
slender, bluish-green and
may stay greener longer
than healthy heads.
The bunt balls change to a

Disease cycle

Millions

of
spores
are
released at harvest and
contaminate
healthy
kernels or land on other
plant parts or the soil. The
spores
persist
on
the
contaminated kernels or in
the soil. The disease is
initiated when soil-borne, or

The

intercellular
hyphae
become established in the
apical meristem and are
maintained
systemically
within the plant. After initial
infection, hyphae are sparse
in
plants.
The
fungus
proliferates in the spikes
when ovaries begin to form.
Sporulation
occurs
in

Management

Control

of common bunt
includes using clean seed,
seed treatments chemicals
and
resistant
cultivars.
Historically, seed treatment
with
organomercury
fungicides reduced common
bunt to manageable levels.
Systemic
seed
treatment

Eyespot

Eyespot

is an important
fungal disease of wheat
caused by the necrotrophic
fungus Tapesia yallundae
and Tapesia acuformis. It is
also called Strawbreaker.
Eyespot is more severe
where
wheat
is
grown
continuously and when the

Sympt
oms

near
to
the
soil
surface. The lesions
are
straw
yellow,
often
with
black
pupil-like dots in the
centre,
and
are
bordered
by
greenish-brown
to
dark-brown rings. In
cases
of
severe
infection stems are

Development of infection
It

is more severe if wheat is

grown continuously in same
field over the same period.
The
fungus
grows
as
mycelium which penetrates
successive
leaf
sheaths
throughout
the
growing
season. High humidity, cool,
and damp weather at the

Invasion of fungi
Invasion

of

Pseudocercosporella
herpotrichoides'" in wheat
initiates with release of
enzyme for breaking the
plant cell wall. A specific
sequence of enzymes is
employed; without these
enzymes the fungus would

Plant defences
Wheat
cells
release
hydroxyproline
glycoprotein
(HRGP)
in
their cell walls. Secretion
of HRGP is dependent on
the signal induced by the
fungal elicitors stimulating
the transcription of genes

Method of control

I.

The
best
method
of
control
for
eyespot
disease is breeding for
resistance. Currently the
gene
conferring
resistance to eyespot is
the
Pch1
gene.
To
generate
resistant
culitvars
plants

II.

Crop
rotation
is
also
important in reducing the
extent of disease because
eyespot
fungi
live
on
debris of the previous
crop. Cropping the wheat
with alternate non-host
crops and with set-aside
periods of at least one
year
helps
to
lessen

Wheat Leaf Rust

Wheat

leaf rust, is fungal disease

that affects wheat, barley and rye
stems, leaves and grains. In
temperate zones it is destructive
on winter wheat because the
pathogen overwinters. Infections
can lead up to 20% yield loss exacerbated by dying leaves which

Symptoms
Small

brown pustules develop

on the leaf blades in a random
scatter distribution. They may
group into patches in serious
cases. Infectious spores are
transmitted via the soil. Onset
of the disease is slow but
accelerated
in
temperatures

Control
Varietal

resistance
is
important.
Chemical
control
with
triazole
fungicides may be useful
for control of infections up
to ear emergence but is
difficult
to
justify

RIC
E

Common Types of Diseases

Rice

Blast
Sheath Blight
Stem Rot
Tungro

 Rice Blast
Magnaporthe

grisea,
also
known as rice blast fungus,
rice rotten neck, rice seedling
blight, blast of rice, oval leaf
spot of graminea, pitting
disease, ryegrass blast, and
Johnson spot is a plantpathogenic
fungus
that
causes a serious disease

A Rice Leaf with Rice Blast

Symptoms
Initial

symptoms white to
gray-green lesions or spots
with darker borders produced
on all parts of shoot
Older lesions elliptical or
spindle-shaped and whitish to
gray with necrotic borders
Lesions wide in the centre

Causal agent or factor

A

fungus causes rice blast. Its conidiophores

are produced in clusters from each stoma.
They are rarely solitary with 2-4 septa. The
basal area of the conidiophores is swollen
and tapers toward the lighter apex.
The conidia of the fungus measure 20-22 x
10-12 m. The conidia are 2-septate,
translucent, and slightly darkened. They are
obclavate and tapering at the apex. They
are truncate or extended into a short tooth
at the base.

Mechanism of damage
Conidia

are produced on
lesions on the rice plant
about
6
days
after
inoculation. The production
of spores increases with
increase in the relative
humidity. Infection tubes
are
formed
from
the
appressoria and later the

Management
Manipulation

of planting time
and
fertilizer
and
water
management is advised.
Early sowing of seeds after
the onset of the rainy season
is more advisable than latesown crops.
Excessive
use of fertilizer

Planting

resistant varieties
against the rice blast is the
most practical and
economical way of
controlling rice blast.
Systemic fungicides such as
pyroquilon and tricyclazone
are possible chemicals for
controlling the disease.
Nitrogen should be applied

 Sheath Blight
The pathogen involved in this disease is
Rhizoctonia solani Kunh (anamorph),
Thanatephorus cucumeris (Frank) Donk
(teleomorph).

Symptoms
Initial

lesions are small, ellipsoidal

or ovoid, greenish-gray and watersoaked and usually develop near
the water line in lowland fields.
Older lesions are elliptical or ovoid
with a grayish white centre and
light brown to dark brown margin.
Lesions may reach the uppermost
leaf under favourable conditions.

Lesions

may coalesce forming bigger

lesions with irregular outline and
may cause the death of the whole
leaf.
Severely infected plants produced
poorly filled or empty grains,
especially those on the lower portion
of the panicles.

Confirmation
The

disease is easily distinguished by

the irregular lesions, which are initially
water-soaked to greenish gray and
later becomes grayish white with brown
margin. These lesions are usually found
on the leaf sheaths near the waterline
and on the leaves. The disease can be
confirmed by the presence of sclerotia.

Mechanism of damage
The

sclerotia germinate and initiate

infection once they get in contact with the
rice plant.
The fungus penetrates through the cuticle
or the stomatal slit. Infection pegs are
formed from each lobe of the lobate
appressorium of infection cushion.
The mycelium grows from the outer surface
of the sheath going through the sheath
edge and finally through the inner surface.

Economic importance
Rice

sheath blight is an increasing

concern for rice production especially
in intensified production systems. In
Japan, the disease caused a yield loss
of as high as 20% and affected about
120,000-190,000 hectares.
Studies at IRRI showed that sheath
blight causes a yield loss of 6% in
tropical Asia.

Management principles
Sanitation,

specifically removing of weeds,

can help control sheath blight considering
that the pathogen also attacks weeds which
are commonly found in rice fields.
Removal of infected stubbles or crop residues
from the field is also recommended to reduce
the amount of inoculum for the succeeding
cropping season.
Spraying infected plants with fungicides, such
as benomyl and iprodione, and antibiotics,
such as validamycin and polyoxin, is effective
against the disease.

 Stem Rot
The

pathogen involved in this

disease is Sclerotium oryzae
Cattaneo
(anamorph),
Magnaporthe
salvinii
(Cattaneo) R.A. Krause & R. K.
Webster (teleomorph)

Symptoms
Initial

symptoms are small,

irregular black lesions on the
outer leaf sheath near water
level.
Lesions expand as the disease
advances.
Visible numerous tiny white and
black sclerotia and mycelium
inside the infected culms.

Confirmation
Blackish,

dark, irregular
lesions are visible on the
outer leaf sheath. The
lesion later expands and
affects the inner culm. If
infected culm is dissected,
it
reveals
dark
gray
masses of fungi and small

Why and where it occurs

The

infection
bodies
or
sclerotia are found in the upper
soil layer. They survive in airdry soil, buried moist rice soil,
and in tap water. They can also
survive on straw, which is
buried in the soil. The sclerotia
float on irrigation water and
infect newly planted rice during

Economic importance
The

infection is seen on
the rice crop during early
heading and grain filling.
The leaf sheaths decay and
cause lodging and lower
grain filling. It can cause
heavy losses in many
countries. For example, in

Management principles
A

balanced use of fertilizer or

split application with high potash
and lime to increase soil pH
reduces stem rot infection and
increases yield.
The use of resistant cultivars
may be the best control measure
for stem rot.

 Tungro

Signs and symptoms

discoloration

begins from leaf

tip and extends down to the
blade or the lower leaf portion.
infected leaves may also show
mottled or striped appearance
stunting.
delayed flowering, which may
delay maturity - panicles small

Factors favouring

disease
presence development
of the virus
sources
presence of the vector
age and susceptibility of
host plants
synchronization
of
the
three above factors

Confirmation
There

are some serological

tools to detect tungro
viruses. These are Latex
agglutination test, Enzyme
Linked
Immunosorbent
Assay or ELISA, and Rapid
Immunofilter Paper Assay
or RIPA. The presence of

Causal agent or

Tungro
virus
disease
factor

is
transmitted by leafhoppers,
wherein the most efficient
vector
is
the
green
leafhopper,
Nephotettix
virescens
(Distant).
The
disease
complex
is
associated with rice tungro
baciliform virus (RTBV) and

Mechanism of
The insect acquires
damage

the virus
by feeding on the plant for a
short
time
in
an
8-hr
acquisition
access
period
(minimum of 30 minutes). It
can
transmit
the
virus
immediately
after
feeding.
Either or both viruses can be
transmitted during a 1 hour

Economic importance
Tungro

is one of the most

damaging and destructive
diseases
of
rice
in
countries
in
Southeast
Asia. Outbreaks of the
disease
can
affect
thousands of hectares in
many
countries.
Plant

Management
principles
There are three limitations

of
effective tungro management:
1. the absence of symptoms
at early growth stage of
the disease development,
2. lack of resistant varieties
to the tungro viruses,
3. vector adaptation on GLH-