THIS IS PPT FILE FOR BASIC DISEASES OF WHEAT CROP

2. Diseases of Wheat

3. Sr.
No. Diseases Of Wheat Causal Agent Primary Infection Secondary Infection
1. Wheat Rusts
a. Black/stem rust Puccinia graminis tritici
Urediospores present in
plant debris
Teliospores through air
b. Brown/leaf rust Puccinia recondita
c. Yellow/stripe rust Puccinia striformis
2. Loose smut Ustilago nuda Infected grains Teliospores through wind
3. Karnal bunt Neovossia indica Teliospoes in plant
infected seeds
Air borne sporidia
4. Powdery mildew Bumeria graminis Dormant mycelium in
plant debris
Wind borne conidia
5. Alternaria blight Alternaria triticina Infected seeds, plant
debris
Wind borne conidia
6. Ear cockle Anguina tritici Infected seeds Irrigation water
7. Leaf blotch Septoria tritici Plant debris Air borne conidia

4. 1. Wheat rust
 Black or stem rust - Puccinia graminis tritici
 Symptoms :
• Symptoms are produced on almost all aerial parts of the wheat plant but are most common
on stem, leaf sheaths and upper and lower leaf surfaces.
• Pustules (containing masses of urediospores) are dark reddish brown - occur on both sides of
the leaves, on the stems, and on the spikes.
• Pustules are usually separate and scattered, heavy infections -coalesce.
• Prior to pustule formation, "flecks" may appear. Before the spore masses break through the
epidermis, the infection sites feel rough to the touch.
• As the spore masses break through, the surface tissues take on a ragged and torn appearance

5. Black stem rust :
The pustules may be abundant and
produced on both leaf surfaces and
stems of host plants.
HOSTS: Wheat, barley and common
Barberry (Berberis,Mahoberberis,
and Mahonia spp.)

6. Microscopically
urediospores
spores are
covered with
fine spines
Teliospores of Puccinia graminis
tritci

7.  Diseaes Cycle: A. Black stem rust Puccinia graminis f.sp. tritici

8.  Survival and spread:
•Both survive on stubbles and volunteer crops, alternate host: Berberis spp. and primary spread occur through
uredospores from southern hills.
 Favourable conditions:
•Moisture and temperature above 20° C favours the development of disease.

9.  Brown or leaf rust - Puccinia triticina (P. recondita)
 Symptoms :
• The most common site for symptoms is on upper leaf blades, however, sheaths, glumes and
awns may occasionally become infected and exhibit symptoms.
• The pustules are circular or slightly elliptical, smaller than those of stem rust, usually do not
coalesce, and contain masses of orange to orange-brown Urediospores

10. Brown or leaf rust Rusty-red urediospores

11.  Diseaes Cycle: Brown or leaf rust

12.  Survival and spread
•Pathogen over-summers in low and mid altitudes of Himalayas and Nilgiris. Primary infections develop from wind
deposited urediospores in eastern Indo-gangetic plains in middle of January where it multiplies and moves
westwards by March
•Alternate host is Thalictrum sp.
 Favourable conditions
•Temperatures of 20-25° C with free moisture (rain or dew) cause epidemics. Severe infection causes upto 30
percent yield losses

13.  Yellow or stripe rust - Puccinia striiformis
 Symptoms :
1.Mainly occur on leaves than the leaf sheaths and stem. The first sign of
stripe rust is the appearance of yellow streaks (pre-pustules), followed by small,
bright yellow, elongated uredial pustules arranged in conspicuous rows on the
leaves, leaf sheaths, glumes and awns.
2.Bright yellow pustules (Uredia) appear on leaves at early stage of crop and pustules
are arranged in linear rows as stripes.
3. Pustules are yellow in colour in the beginning later on become dull black brown.
4. The stripes are yellow to orange yellow.
5.The teliospores are also arranged in long stripes and are dull black in colour.

14.  Survival and spread:
•The inoculum survives in the form of uredospores
/teliospores in the northern hills during off season on self
sown crop or volunteer hosts, which provide an excellent
source of inoculums and primary spread occur through
uredospores from hills
 Favourable conditions
•Disease is prominent when temperature is 10-20°C and
high humidity.

16. Etiology:
 Urediospores:
Uredospores are stalked, oval, unicellular, brown, thick walled with 4- round equatorial germ pores measuring outer layer25-
30 um 17-20 pm. The sporewall is thick with echinulate outer layer.
 Teliospores:
The teliospores are stalked, spindle-shaped, thick and smoothwalledwith round or pointed apex, 2-celled andslightly
constricted at the septum. Spores are chestnut brown in colour and measure about 15-20 um x 40-46 um.
 Basidiospores:
Basidiospores are unicellular, thin-walled and very small. After discharge from basidium by explosive mechanism, they are
disseminated by air current. The basidiospores can survive for a few days. They can infect only the leaves of
alternate host, the barberry, otherwise they die.
 Pycniospores:
The pycnium produce receptive hyphae and haploid, unicellular, uninucleate pycniospore of single mating type either
of + or - type. Within few days, the growing mycelium becomes aggregated under the epidermis and forms a
yellowish flask-shaped structure, called Pycnium or Spermogonium.
 Aeciospores :
The aeciospores are unicellular, binucleate (n + n), thin-walled and orange in colour. The young aeciospores are polyhedral
in shape, but becomes globose with maturity.

17.  Favourable Conditions:
• Low temperature (15-20°C) and high humidity during November – December favour
black and brown rusts. Temperature less < 10o favours yellow rusts.
 Disease cycle:
• Uredospores and dormant mycelium survive on stubbles and straws and also on weed
hosts and self sown wheat crops. Wind borne uredospores from hills are lifted due to
cyclonic winds and infect the crop in the plains during crop season.
 Management:
• Mixed cropping with suitable crops.
• Avoid excess dose of nitrogenous fertilizers.
• Spray Zineb at 2.5 kg/ha or Propioconazole @ 0.1 %.
• Grow resistant varieties like PBW 343, PBW 550, PBW 17

18. 2. Loose smut - Ustilago nuda tritici (Ustilago tritici)
Symptoms :
 Generally, diseased plants are indistinguishable from the healthy plants before heading but diseased plants produce
heads earlier than healthy plants.
 Terminal symptom in all the varieties is the production of black powder in place of wheat grains in the ears. Almost
every ear of the diseased plant is converted into black powder.The black powder is a mass of olive-green
microscopic spores of the smut fungus.
 When spores are blown to flowers of healthy plants, they germinate on the female organ (Ovary), stigma and lead
to infection of the developing seed.The smut fungus thus reaches in the mature grain and remains dormant there
until germination of the grain.
 From superficial examination at harvest time, infected grains are sown in the following season; the
fungus inside the seed becomes active as the germination starts.
 The fungus grows inside the plant first behind the growing point, keeping pace with apex of the growing shoot.
 As the ear formation starts, there is an accumulation of the fungus in the floral parts, which are completely
destroyed due to formation of the black powder.

20.  Etiology:
The spores are olive brown, lighter on one side, spherical or oval, 5-9 um india. They readily germinate in
water. Each spore (Teliospores) produces four celled mycelium. Germination of spores take place in
moist condition by germ tube. The pro-mycelium cells fuse to the germ tube that enters the ovary and
stigma established in the embryo and remain dormant until seed germinate.
 Disease Cycle of loose smut of wheat:
The disease is internally seed borne and systemic. The infected grains can not be distinguished apparently
from healthy grains. The pathogen remains dormant with in the mature grain. When such seed are sown, the
dormant mycelium becomes active and grows keeping pace with the growing tip of the host. Secondary
spread is by teliospores which are wind borne.
 Survival and spread
•The disease is internally seed borne, where pathogen infects the embryo in the seed.
•Primary infection occurs by sowing infected seeds.
 Favourable conditions
•Infection is favored by cool, humid conditions during flowering period of the host plant

21.  Disease Cycle of
loose smut of wheat

22. Management:
 Hot Water Treatment (54°C for about 10 min).
 Treat the seed with Vitavax @ 2g/kg seed before
sowing.
 Burry the infected ear heads in the soil,
so that secondary spread is avoided.
 Growing Resistant Varieties Viz, Np
710, Np 120, and Pb 90, Raj 2296, K-
8027, K-8251, HW-657, HW-240, Raj-
6276, VL-646, VL-719.

23. 3. Karnal bunt - Veovossia indica
 Symptoms:
 Karnal bunt attacks durum wheat, rye, and triticale, a hybrid of wheat and rye. Despite its preference for a
common crop, Karnal bunt can be extremely difficult to diagnose in the field for many reason.
 First, not all kernels on a plant head will be infected, and thus infected plants are not as readily
identifiable. This distribution is the reason for Karnal bunt's being referred to as partial bunt.
 Another factor which makes Karnal bunt difficult to readily diagnose in the field is the fact that most
infected kernels do not show symptoms prior to maturity.
 In an ear only few grains are infected. A portion of the grain is converted into black powdery mass. The
black powder which gives foul smell due to presence of Trimethyl amine is a mass of thick walled dark
brown spores of the fungus known as teliospores.
 The fungus is both seed borne and soil born and the infection occurs at flowering time by airborne
sporidia.

25.  Etiology:
The spores are dark brown, smooth walled measuring 20-49 um requires a long lasting
period, sporidia are produced in large number on short stout basidium. The primary
sporidia are needle shaped, secondary sporidia are sickle shape.
 Disease cycle:
Karnal bunt was reported as a soil borne disease by Mitra (1931), but now it is
considered as an air borne disease. The fungal spores are also transferred by means of
equipment, tools or by man moving from milling places. The spores remain viable for
several years in soil (Bonde et al. 2004), wheat straw and farm yard manure. Soil or
seeds are primary sources of inoculum. Environment plays a key role in disease
progression. Teliospores germinate at suitable temperature (15—250C) and humidity in
the soil. This condition generally dominates during February to March in North Indian
plains.

26.  Disease cycle
Karnel Bunt
 Survival and
spread
•The disease is seeds
borne and sowing of
infected seeds is the
source of primary
infection.
 Fabourable
conditions
•Temperature of 18-
20°C.
•High soil moisture

27.  Management of Karnal bunt (Neovossia indica)
1. Deep ploughing during summer
2. Crop rotation
3. Use of resistant varieties is the most effective method for controlling the disease.
E.g. PBW 502 and N-75-3 and N-75-5 are partially resistant
4, The incidence of Karnal bunt can be effectively reduced by the application of
foliar fungicides between late boot and flowering. Some effective fungicides are
Propioconazole, Agrozim and Bavistin (carbendazim) and Bayleton (triadimefon).
5. Integration of propiconazole with bioagent fungus (Trichoderma viride) gives almost
complete control.
6. The temperature of the soil rises considerably by practices of polythene mulching
and wheat straw burning after mechanical harvesting.

28. 4. Powdery mildew : (Erysiphe (Blumeria )graminis var. tritici)
 Symptoms:
 Powdery mildew appears as fluffy, white powdery growths of fungal spores on the leaf surface.
 Symptoms progress from lower to upper leaves.
 Un er severe disease pressure as the season progresses, the fluffy, white owdery growth can also affect
stems and heads. Fungal colonies eventually enlarge and merge together.
 The area surrounding the lesion and on the reverse side of the leaf turns ellow to brow Older infections
on leaves and heads turn grey and can develop black fruiting bodies, called cleistothecia, which appear
as black specks.
 Moderate to severe infections can result in leaf death.
 Young, succulent growth such as new tillers is usually more susceptible than older plant tissues.

 A powdery mildew infected crop will appear yellow from a distance, similar to a crop suffering from
water logging or nutrient deficiency.

30.  Etiology:
Powdery mildew, caused by Blumeria graminis f. sp. tritici (syn. Erysiphe graminis). The mycelium
can cover the plant surface almost completely, especially the upper sides of leaves. It is
asexually produced conidia and sexually formed ascospores (produced from cleistothecia).
Ascocarp is dark brown, globose with filamentous appendages, asci oblong. ascospores hyaline, ellipsoid, 20-30 x
10—13 tum in size. Anamorph produces on hyaline conidiophores catenate conidia of oblong to cylindrical
shape, not including fibrosin bodies, 32—44 x 12-15 um in size. Haustoria are palmate.
 Disease cycle:
Each mildew infection produces masses of tiny, white spores. These are readily blown
about by the wind, spreading the disease. The fungus needs a high humidity but not rain
or dew to infect the plant. Development of powdery mildew is greater at mild
temperatures (15-22°C) and in lush crops. Rain suppresses development for up to five
days. Hence, the disease usually occurs during drier winters in most areas.
 Favourable Conditions:
• Temperature of 20-21°C.

31.  Disease cycle Powdery mildew

32.  Management:
 Controlling the disease involves eliminating conducive conditions as muchas possible by altering
planting density and carefully timing applications & rates of N2.
 Milk has long been popular with home gardeners and small-scale organic growers as a treatment for
powdery mildew. Milk is diluted with water (typically 1:10) and sprayed on susceptible plants at the first
sign of infection, or as a preventative measure, with repeated weekly application often controlling or
eliminating the disease.
 Another way to control wheat powdery mildew is breeding in genetic resistance, using "R genes"
(resistance genes) to prevent infection. Eg. KAMAL, LAL Bahadur, MP 1142, NP 852, NP 792, NP 818, NW
2036, NI 5439, NIAW 301, PBW 226, PBN 51, PV 18, Raj 4037, RAJ 2184, Sonaora 64,Sagarika, UP
215, UP 368, UP 1109, UP 2382,VL 829,VL 401,VL 616, WL 2265,WH 291,WG 377,WH 542,
NARMADA 195.
 Spray Wettable Sulphur 0.2% or Carbendazim @ 500 g/ha One spray of propiconazole (Tilt 25 EC) @
0.1 % at ear head emergence or appearance of disease (whichever is earlier) is recommended for the
powdery mildew prone areas.

33. 5. Alternaria blight : (Alternaria triticina /Bipolaris sorokiniana)
 Symptoms:
 The disease appears when wheat plants are 7-8 weeks old and becomes severe when the crop is
mature.
 Small, chlorotic, oval shaped lesions appear. These lesions become irregular in shape.
 The chlorotic borders of the lesions may become diffuse and turn light to dark brown in color. Lesions
are difficult to distinguish from spot.
 Infection usually starts on the lower leaves, but symptoms can be found on all plant parts.
 As the disease progresses, several lesions coalesce to cover large areas, resulting in the death of the
entire leaf. In some cases the leaf starts drying up from the tip, prematurely, when lesions appear.
 Black powdery conidia may cover the lesions at this stage under moist conditions.
 The lowermost leaves are the first to show the signs of infection; the fungus gradually spreads to the
upper leaves. In severe cases, similar symptoms are produced on the leaf sheath and stem, as well as
the awns and umes if spikes are infected at the pre-anthesis stage. If the spike is infected this early,
seeds do not form.
 Infection at the dough stage of seed development results in glumeinfection, ear infection and seed
infection. Heavily infected fields present aburnt appearance and can be identified from a distance
(Prasada and Prabhu, 1962; Prabhu and Prasada, 1966; Singh, 1990)

34.  Etiology:
Mycelium initially hyaline, becoming olive-buff to deep olivebuff, branched, septate, 2-7 um wide.
Conidiophores similar to mycelium in colour, septate, unbranched or occasionally branched, erect, broader towards
the distal end, on the host single or fasciculate, emerging through stomata, amphigenous, geniculate or straight,
length variable, between septa 17-28 x 3-6 um.
Conidia acrogenous, borne singly or in chains of 2-4, smooth, irregularly ovoid, both ends rounded, or ellipsoid, or
conical-ellipsoid, gradually tapering into a beak; beak (a secondary conidiophore) concolorous with the main
conidial body, straight, 20-37 x 3-7 um. Spore body pale brown to dark olive-buff, becoming darker with age,
verrucose, transverse septa 1-10, longitudinal septa o -5, constricted at septa, varying in size; length including beak
15-89 um, width 7-30 um.

35.  Management of alternaria blight of wheat:
 Seed borne infection can be controlled by treating seed with Vitavax @ 2.5 g/kg of
seed.
 Apply adequate fertilizers and irrigation.
 Alternaria leaf blight can also be controlled by Zineb or Dithane M-45. The
 fungicides may be sprayed as described for rust but mix the urea at 2-3 % with Zineb
for first and second sprays.
 Disease cycle
Primary spread is by externally seed-borne and soil borne conidia. Secondary spread by air-borne
conidia.
 Favourable Conditions
Temperature of 25°C and high relative humidity.

36. 6. Ear cockle: (Anguina tritici)
 Symptoms
 On Plant
 Affects all growing stages.
 Growth of the plant reduces.
 The ears of diseased plants do not emerge properly.
 The awns are twisted and the ear is also very much twisted.
 Infected seedlings are more or less severely stunted and show characteristics rolling and twisting of the
leaves.
 A rolled leaves often traps the next emerging leaf and inflorescence within it and causes it to become bent or
badly distorted
 Base of the stem are enlarged, bent and generally stunted.
 Plants show spreading nature and tents towards more tillering.
 “On Infected ears/kernels
 The affected ears are shorter and broader with very short or no awns on the glumes.
 The affected ears are greener than the healthy ones, and galls shed off the ear more readily than kernels.
 Diseased head may have one, few or all of its kernel turned into nematode galls.
 Galls are shiny at first but turn brown or black as the head matures.
 Mature galls are hard, dark, rounded and shorter than normal wheat kernels.

38.  Etiology:
 Pathogen is large nematode about 3.2 mm long and 120micrometer in diameter.
 Host: specific to wheat
 Nematode lays eggs and produces all its juvenile stages and adults in seed galls.
 Disease cycle:
 Seed gall nematode contains 1000 to 3000 larvae in a seed.
 Galls fallen to ground softens during warm, moist weather and release infective second stage juveniles.
 The juveniles swim upward on the leaves through film of water and feed ectoparasitically on leaves.
 When the inflorescence begins to form, the juveniles enter the flower primordia and produce the third and fourth
stage juvenile and adults.
 Each infected flower primodium becomes a seed gall and may contain 80 or more adults.

39.  Management:
 Use only healthy seed from healthy crop.
 Cleaning of contaminated seeds by sieving or floating in water.
 Crop rotation for 2.3 yrs such as barley or oat.
 Hot water treatment of seed, first soaking seed in cold water for 4-5 hours and treating at 54°C.
 Soil application of nematicides such as Nemaphos, Aldicap@ 10 kg a.i/ha.