1. Chapter 3: Major economically important Plant diseases in
Ethiopia and their management
Definition of some important terminology
Plant Disease?
A physiological disorder or structural abnormality that is harmful to the plant or only it’s parts or products that reduced
the economic value.
• A plant disease is an abnormality in the structure and/or function of the host plant cells and/or tissue as a result of a
continuous irritation caused by a pathogenic agent or an environmental factor.
• A disease is not static; it is a series of changes in the plant.
• Plant disease is the result of an infectious, or biotic (a living component of an ecosystem) agent or a noninfectious, or
abiotic (nonliving, physical and/or chemical component) factor.
Plant injury is an abrupt alteration of form or function caused by a discontinuous irritant. Plant injury includes insect,
animal, physical, chemical or environmental agents.
2. A causal agent is a general term used to describe an animate or inanimate factor which incites and governs disease and
injury.
A causal organism is a pathogen of biotic origin.
The signs and symptoms
Signs are the appearance and/or physical evidence of the causal factor of the plants abnormality.
Signs are the physical evidence of damage caused by biotic or abiotic agents such as the pathogen itself, pests,
spores, fruiting bodies, chemical residue, bacterial ooze and so forth.
Symptoms are the visible response of a plant to biotic and/or abiotic factors that result in a change or abnormality in the
plant.
Symptoms can take form as galls, chlorosis, ring-spots, wilt, rotand so on.
The life cycle of an infectious disease is the sequence of distinct events, such as sexual reproduction, that occur between
the appearance and reappearance of the causal organism.
The stages of the disease cycle are the appearance, development and perpetuation of a pathogen and the effect of the
disease on the host.
Definition of some important terminology….
3. 3
Principles of Plant Disease Management
Principles of Plant Disease Management
i) Avoidance: It is preventing the contact between the host and the pathogen. It is done by identifying geographical area,
selection of a proper field, planting time, disease escaping varieties and avoidance of insect vectors and weed hosts.
ii) Exclusion: It means preventing the entrance and establishment of pathogens in uninfected crops in a particular area.
• It can be achieved by
quarantine,
inspection and certification,
seed treatment and
also by using certified seed or plants,
sorting bulbs before planting,
discarding any that are doubtful, possibly treating seeds, tubers or corms before they are planted and
most importantly refusing obviously diseased specimens from dealers.
4. 4
iii) Eradication: It involves elimination of a pathogen once it is established on a plant or in a field.
• It can be done by crop rotation, sanitation, rouging, soil treatment, use of antagonists and heat and chemical
treatment to diseased plant material.
iv) Protection: It is the use of some protective barrier between the susceptible host and the pathogen.
• In most cases, a protective spray or dust is applied to the plant in advance of the occurrence of pathogen.
• Sometimes, it is achieved by killing insects or other inoculating agents.
v) Host resistance/Immunization: It utilizes in-built mechanism to resist various activities of pathogen.
• The infection or subsequent damage by pathogen can be rendered ineffective through genetic manipulation
or by chemotherapy.
vi) Therapy: It is achieved by treating the plant with that will inactivate the pathogen. Chemotherapy,
thermotherapy are effective.
5. 5
Integrated Disease Management
• Integrated plant disease management (IDM) can be defined as a
• decision-based process involving coordinated use of multiple tactics for optimizing the control of
pathogen ecologically and economically.
• In most cases IDM consists of scouting with timely application of combination of strategies and tactics.
The basic objectives of any IDM program should be to achieve at least the following:
• Reduce the possibility of introducing diseases into the crop.
• Avoid creating conditions suitable for disease establishment and spread
• Simultaneous management of multiple pathogens
• Regular monitoring of pathogen effects, and their natural enemies and antagonists.
• Use of economic or treatment thresholds when applying chemicals.
• Integrated use of multiple, suppressive tactics.
Integrated Disease Management
6. 3.1.1. Major Potato Diseases, and Their Management
: Alternaria solani
: Phytopthora infestans
: Rhizoctonia solani
: Potato leaf roll virus
1. Early blight
2. Late blight
3. Black scurf
4. Leaf roll
5. Mosaic
a. Mild mosaic/Interveinal mosaic
b. Severe mosaic
c. Rugose mosaic of potato
:(Potatovirus X) PV X
:Potato virus Y (PV Y)
:Potato virus X &Y
Disease Causative agent
3.1. Major potato and tomato diseases and their management
7. Symptoms:
This is a common disease of potato occurring on the foliage at any stage of the growth and causes
characteristic leaf spots and blight.
Normally the disease symptoms become apparent during tuber bulking stage and develop leading to
the harvest.
The early blight is first observed on the plants as small, black lesions mostly on the older
foliage.
Spots enlarge, and by the time they are one-fourth inch in diameter or larger, concentric rings in a bull's
eye pattern can be seen in the center of the diseased area.
Tissue surrounding the spots may turn yellow.
If high temperature and humidity occur at this time, much of the foliage is killed.
1. Early blight: Alternaria solani
8. spread
Etiology:
The mycelium is septate, branched, light brown colour, inter and intracelluar in the host tissue.
The conodiophore are short, light brown, septate arise from disease tissue and emerge through stomata.
The conidia are borne in chain at tip of conidiophores.
Conidia are obclavate, muriform with 5-10transverse septa.
Lesions on the stems are similar to those on leaves, sometimes girdling the plant if they occur near the soil line.
Symptoms……
9. Disease Cycle/perpetuation of Early blight of disease:
Primary Infection: Mycelium or conidia in infected plant debris
Secondary Infection: C onidia dispersed by wind, water or rain splashes
Management of early blight disease
Use of disease free seed
Practicing crop rotation helps to minimize the disease incidence.
Removal and burning of diseased crop debris
Nursery spraying after 2 weeks after sowing with CO C 50WP
Mancozeb@0.25% or chlorothalonil@0.2% or Zineb@ 0.25%spray at weekly intervals.
Spray Mancozeb + urea solution i.e. at the rate of 2 g Mancozeb 75 WP + 10 g urea per litre of water at
15 days interval when symptoms start.
10. 2. LATE BLIGHT : PHYTOPTHORA INFESTANS
Symptoms:
A. Symptoms on leaf
• The first symptoms of late blight in the field are small, light to dark
green, circular to irregular -shaped water-soaked spots.
• These lesions usually appear first on the lower leaves. Lesions often
begin to develop near the leaf tips or edges, where dew is retained
the longest.
• During cool, moist weather, these lesions expand rapidly into large,
dark brown or black lesions, often appearing greasy.
• Leaf lesions also frequently are surrounded by a yellow chlorotic
halo.
11. The lesions are not limited by leaf veins, and as new infections occur and
existing infections coalesce, entire leaves can become blighted and killed
within just a few days.
The lesions also may be present on petioles and stems of the plant.
The lesions are not limited by leaf veins, and as new infections occur and
existing infections coalesce, entire leaves can become blighted and killed
within just a few days.
The lesions also may be present on petioles and stems of the plant.
A. Symptoms on leaf
2. LATE BLIGHT : PHYTOPTHORA INFESTANS….
12. Late blight infection of tubers is characterized by:
irregularly shaped, slightly depressed areas that can vary considerably from brown to purplish of
variable size on the skin.
A tan to reddish-brown, dry, granular rot is found under the skin in the discolored areas and extending
into the tuber usually less than ½inch
B. Symptoms on tubers:
2. LATE BLIGHT : PHYTOPTHORA INFESTANS….
13. Etiology of P. infestans :
Mycelium is coenocytic, hyaline, branched and both inter and intracelluar
The conidiophores are aerial and arise from the internal mycelium through stomata and lenticel on the tubes.
They are slender hyaline, branched and indeterminate.
The sporangia are thin walled, hyaline, oval or pear shaped with a definite papilla at the apex germinating
by zoospore. Oospore are thick walled and yellowish.
Disease cycle:
The infected tubers and the infected soil may serve as a source of primary infection.
The diseased tubers are mainly responsible for persistence of the disease from crop to crop.
The air borne infection is caused by the sporangia.
14. Disease spread and Development
Appearance and build-up of late blight depend solely on weather conditions.
There are specific requirements of temperature and humidity for initiation and further build up of disease.
1. Temperature
Pathogen growth - 16-20oC
Spore production - 18-22oC
Spore germination - 10-20oC
Infection and disease development 7.2-26.7oC(18+1oC)
2. Humidity
Spores are formed in moisture saturated atmosphere.
Spore germination and infection requires 100 per cent humidity.
Spores get killed under low humidity (less than 75% humidity)
3. Light
Spores are produced during the night and are
sensitive to light.
Cloudiness favours disease development.
15. • In Ethiopia the disease caused 100% crop loss on unimproved local cultivar, and 67.1% on a susceptible
variety (Bekele and Yaynu 1996).
• Late blight is a major limitation to potato production in high humid elevations; with estimate average
yield losses of about 30–75% on susceptible varieties (Olanya et al. 2001).
• Research centers have made estimates of losses ranging from 6.5 to 61.7%, depending on the level of
susceptibility of the varieties (GILB and CIP 2004a).
• According to Fekede et al. (2013); Binyam et al. (2014b), reports, in Ethiopia late blight of potato causes
tuber yield losses of 21.71– 45.8% and 29-57% depending on the resistance level of the cultivars,
respectively.
• Late blight can occur at any time during the growing season, it is more likely to be seen in late summer
and early autumn (Bevacqua 2000).
ECONOMIC IMPORTANCE OF LATE BLIGHT OF POTATO
16. Use of disease free seed.
Selection of well drained soils.
Destruction of plant debris.
High ridging.
Scouting of the field.
Stop irrigation when conditions become congenial.
Haulm cutting at 75% disease severity.
Harvesting should be done 15-20 days after haulms cutting.
Treat seed tubers with boric acid (30g per litre of water) before storage.
Integrated Disease Management
17. Management by Host resistance
Host resistance to late blight is of significance in integrated late blight management due to its long-term
economic benefits for farmers.
It also minimizes changes in the population structure of P. infestans, decreasing the likelihood of
fungicide resistance (Hakiza 1999; Mukalazi et al. 2001).
The use of resistant varieties is among the most effective and environmentally safe means of managing
the disease.
The resistant varities recommended for cultivation in Ethiopia are:
18. Chemical Management
Prophylactic spray with contact fungicides like mancozeb (0.2%) or chlorothalonil (0.2%) or propineb
(0.2%) before the closure of canopy.
On appearance of the disease, spray the crop with fungicides like dimethomorph -based or cymoxanil -
based or fenamidone - based @0.3%.
Depending upon disease severity and weather conditions, number of spray may be increased or decreased.
Ensure thorough coverage of plants top to bottom with fungicides.
Special attention should be given to lower leaves which need to be covered with fungicides.
Do not wait or allow late blight to appear and establish in the field.
Always use a sticker @0.1% for proper sticking and uniform spread of fungicides on leaf surface.
19. Symptoms can be observed on above and below ground plant parts.
Symptoms observed above ground early in the season include necrosis at the tips of the sprouts and
sunken lesions on stolons, roots, and stems.
Later in the season, sclerotia are produced in the tubers creating a sign called black scurf which is simply,
sclerotized mycelium.
Stems with cankers can become girdled, resulting in stunted plants.
Leaves of infected plants develop a purplish and chlorotic coloration.
In severe infections, green tubers develop above the ground.
Affected tubers are deformed and can produce sclerotia on the surface.
3. BLACK SCURF : RHIZOCTONIA SOLANI
Symptoms
20. Tuber russet
Sunken leisons on stem
Etiology:
Rhizoctonia solani is a basidiomycete fungus that does not produce any asexual spores (called conidia) and only
occasionally will the fungus produce sexual spores (basidiospores).
In nature, R. solani reproduces asexually and exists primarily as vegetative mycelium and/or sclerotia
Young mycelium of R Solani is silvery and become yellow to brown at maturity 8- 12µm in dia.
Having frequent septation and branched. Sclerotia are dark brown to black.
They are roughly spherical or somewhat flattened or irregular, shape of micro scleortia is oval to irregular
21. Disease Cycle
P.I: Oospores (Pythium) or Sclerotia (Rhizoctonia) in soil
S.I: Seedlings raised in infected soil carry the disease to field
Management:
Disease free seed tubers alone should be planted.
If there is a slight infection of black scurf that can be controlled by treating seed tubers with mercuric
chloride solution for 1.5 hr with acidulated mercuric chloride solution for 5 min.
Treating the soil with pentachloroni trobenzene at the rate of 70 kg/ ha lowers the incidence of the disease,
but it is too expensive and cumbersome.
Well sprouted tubers may be planted shallow to control disease.
The disease severity is reduced in the land is left fallow for 2 years.
22. 4. Leaf roll : Potato leaf roll virus
Symptoms:
The symptoms appear early and young leaves show an upward roll.
Leaves become dry, leathery and thick.
They turn brittle and give their distinctive rattle when shaken.
Plants may also be severely stunted, erect and light green.
Tubers are reduced in size and number. With some varieties, a net necrosis develops inside the tuber.
23. Transmission
Infected tubers (Sap inoculation)
Spread by aphids, Myzus persicae and Aphis gossypii
Management:
Disease free seed tubers for planting.
Use of disease free certified seed.
Rouging of diseased plants and burying them deep in soil.
Aphid control.(Phorate 10G ,10Kg/ha or monochrotophos).
24. : (Potato virus X) PV X
5.Mosaic :
a. Mild mosaic/Interveinal mosaic
Symptoms:
Often referred as latent potato mosaic
Light yellow mottling with slight crinkling on potato plants
Interveinal necrosis of top foliage
Stunting of diseases plants
Leaves may appear slightly rugose where strains of PV Y combines
25. Also called potato leaf drop streak
B) SEVERE MOSAIC – POTATO VIRUS Y (PV Y)
Symptoms
Chlorotic streaks on leaves which become necrotic
Necrosis of leaf veins and leaf drop streak
Interveinal necrosis and stem/petiole necrosis
Plant remain stunted in growth
Rugosity and twisting of the leaves occurs in combination
with PV X and PV A
26. Symptoms
Black streaks appear in leaf veins and on stems.
Early-season infection shows shriveled leaves that hang from the stem by a
thread of dead tissue.
Later in season, the plants become bare with a few leaves on top. Late- season
infection does not show any symptoms.
Plants from infected seed tubers have mottled and wrinkled leaves that are
distorted ("rough") and reduced.
Stems are brittle and dwarfing is common. Harvested tuber size is greatly
reduced.
The primary pathogen is Potato Virus Y (PVY) which may act alone or in
conjunction with PVX.
There are many strains of PVY with differing characteristics and behaviour.
PVY is spread by both seed and aphids.
C. Rogose and Common Mosaic : Potato virus X &Y
27. Transmission
a.)Mild mosaic/Interveinal mosaic
Spreads mechanically through rubbing of leaves, contact of infected plants (Sap inoculation), seed, cutting
knives, farm implements.
Root clubbing of healthy and diseased plants in field
b) Severe mosaic – Potato virus Y (PV Y)
Infected tubers (Sap inoculation)
Spread by aphids, Myzus persicaeandAphis gossypii
Management:
Disease free seed tubers for planting.
Resistant varieties (like chippewa & Irish cobs).
Use of disease free certified seed.
Rouging of diseased plants and burying them deep in soil.
Insect control in case of Mild and Rugose mosaic.(Phorate 10G ,10Kg/ha)
Avoid working of labour and animals from diseased to health crop in case of latent mosaic virus.
28. 6. Bacterial wilt (Ralstonia/Pseudomonas solanacearum)
Bacterial wilt also known as Brown rot, and southern bacterial wilt, is a bacterial disease of the potato
that is extremely destructive in tropical and subtropical regions.
The causal organism for this disease is a gram-negative, short-rod bacterium with one polar flagellum.
In Ethiopia, Bacterial wilt of potato was first recorded in 1956 on potato and egg plant in the Keffa
region.
Apart from solanaceous crops like chilli, potato, tomato, and eggplant the pathogen has been known to
attack a large number of other plants including castor, groundnut, banana and ginger.
It is very often associated with the root knot nematodes which affect potatoes and tomatoes.
29. Bacterial Wilt
of Potato
Inoculum Source
Diseased potato Infested soil Tubers &
plants
Seed tubers
Irrigation water
Soil in tools, hooves, shoes
Nematodes & insects in soil
Host crops & weeds
Harvest left over
Volunteers
Soil
Mode of spread and survival
30. Symptoms
Bacterial wilt of potatoes appears as sudden wilting of one or more stems of the potato plant.
This symptom can be mistaken for water stress.
Plants may also look stunted and begin to yellow.
Brown discolouration is visible in the vascular tissues of the stem and tubers.
When stems or tubers are cut and slight pressure applied, creamy bacterial slime comes from the infected
vascular elements.
Bacterial slime oozes from the eyes of tubers and soil sticks to the tubers where the slime has emerged.
Secondary infection can cause decay of the whole tuber.
External symptoms and internal browning are not always visible in infected plants, and potato tubers can
be infected without any visible symptoms.
31. Symptom of Bacterial wilt (Ralstonia solanacearum)…
when cut and oozing of milky fluid from the vascular ring of cross-sectioned tubers were the most
commonly encountered disease symptoms.
Symptoms of potato brown rot with bacteria oozing from cut vascular tissues (a) and eyes (b) (and wilted plant in the field
(c) .
32. Management methods of R. solanacearum
• Use of healthy seed
• Do not cut seed tubers. Cutting spreads pathogen even to healthy tubers.
• Apply stable bleaching powder @12kg/ha mixed with fertilizer in furrows while planting. It reduces
wilt incidence by 80%.
• 2-3 years crop rotation with n o n h o s t c r o p s s u c h a s maize, cereals, millet, garlic,onion,
cabbage, etc .
• Full earthing up. Deep ploughing twice at 20-30 days interval after harvest during summer in plains and
in winter in hills.
• Biological control: The use of rhizosphere resident microbial antagonist specifically the fluorescent
pseudomonas is noted as a promising control method.
33. Favourable condition
Disease development is favoured by warm temperatures (25° – 35°C) and is limited by temperatures below
10°C.
RH above 50 % and PH 6.2-6.6 is also favours for the development of disease.
Acid soil is not favourable.
Soil moisture is important as the bacterium cannot tolerate dry soil conditions.
34. 3.1.2. MAJOR TOMATO DISEASES AND THEIR MANAGEMENT
Common Disease of tomato
Tomato Diseases can be:
Fungal disease
Bacterial disease
Viral disease
Nematode disease
Bacterial disease includes
• Bacterial canker
• Bacterial spot
• Bacterial wilt
• Bacterial speck
Fungal disease includes
• Early bligh
• Fusarium wilt
• Anthroconose
• Late blight
35. 1.Early blight
Caused by Alternaria solani
SYMPTOMS
Early blight shows up as small, irregular, brown, dead spots on lower, older leaves.
The spots then grow to ½-inch in "bulls-eye" patterns.
The whole leaf then may go yellow.
As fruit begins to occur, when suffering from blight, the older fruits may show dark leathery sunken spots.
36. Leaf spots and blight on the foliage.
The disease first becomes visible as small, isolated,
scattered pale brown spots on the leaf.
Spots are irregular, brown to dark brown in colour, and with
concentric rings inside the spot.
Often several spots coalesce to form large patches resulting
in the leaf blight.
Lowest leaves are attacked first and the disease
progresses upwards.
Symptoms of tomato early blight
37.
38. DISEASECYCLEANDEPIDEMIOLOGY
Infection by the fungus is most rapid under warm (28-30°C) wet conditions.
Survives between crops in plant debris and on seed.
It can also survive on volunteer tomato plants (warm climates) and on other cultivated and wild solanaceous
plants (potato, eggplant, horse nettle and black nightshade).
Early blight symptoms (leaf spot and defoliation) are most pronounced in the lower canopy.
Disease severity and prevalence are highest when plants are loaded with fruit
FAVOURABLE CONDITION :
Disease develops at moderate to warm 15 to 27 degree celsius;
Rainy weather or heavy dew, 90% humidity ,
June-July sowing - weak and old plants prone to infection high soil moisture.
Mode of spread: Seed borne and air borne conidia
39. Management
CULTURAL CONTROLS
Use pathogen-free seed and transplants.
Maintain plant vigor through adequate irrigation and
fertilization to increase disease resistance.
Use long rotations away from tomato and other solanaceous crops,
avoid planting tomato near related
crops that are more mature and eliminate weed hosts.
Avoid plant injury which allows entry of the pathogen and spread
of the fungus through adequate insect management.
CHEMICALCONTROL
Contact fungicides such as
chlorothalonil and mancozeb provide moderate
levels of control when applied preventively.
Newer chemistries including;
strobilurin fungicides (azoxystrobin,
pyraclostrobin, etc.) have provided
excellent control in university trials.
Mancozeb (0.175%), chlorothalonil or copper
fungicides (0.125 %).
Hot water Treatment of seeds for 25 mints at 50°C.
Resistant variety
No resistant varieties avaliable
40. 2.LATEBLIGHTOFTOMATO(Phytophthora infestance)
• Late blight is a potentially devastating disease of tomato and potato, infecting leaves, stems, and fruits
of tomato plants.
• Worldwide distribution, but most severe epidemics occur in areas with frequent cool, moist weather.
• The host range is mainly limited to solanaceous crops, including tomato, nightshade (Solanum nigrum) and
potato.
• Sweet potato (Ipomea batatas) is not a host for late blight.
• The disease spreads quickly in fields and can result in total crop failure if untreated.
• phytophthora in Latin means "plant destroyer." Infected plant tissue dies.
41. Signs and symptoms of Tomato late blight
On Leaves :
⚫ Leaves have large, dark brown blotches with a green gray edge; not confined by major leaf veins
⚫ Infections progress through leaflets and petioles, resulting in large sections of dry brown foliage.
42. On Stem :
⚫ Stem infections are firm and dark brown with a rounded edge.
43. On tomato fruit:
Such infected fruits are not fit for human consumption.
They should be removed from affected gardens and destroyed.
The fruit damage that appears in this photograph can occur in a
few days or less under the right weather conditions.
Infected tomato fruits turn greasy, olivaceous-brown, decay, and can shrivel up and fall off the plant and never ripen.
44. Management Tomato late blight
Select a tomato variety that reaches maturity quickly.
Stake up tomato plants, especially indeterminate types.
Keep tomato stems and branches away from the ground.
Plant blight-resistant tomato varieties when they become available.
Intercrop tomato with non-susceptible host plants, preferably non-solanaceous plants.
Practice good crop sanitation; inspect the plants regularly and remove diseased material from the
plot .
Destroy volunteer tomato plants.
Avoid moving through the tomato garden or field when plant foliage is wet.
Control solanaceous weeds around the tomato garden. Prophylactic sprays with copper fungicides or
dithiocarbomates 0.25% .
Metalxyl / amiston 0.2%.
45.
46. FAVOURABLE CONDITIONS:
High relative humidity >90 %
Low temperature 10 – 25 degree celsius
Cloudy weather and rainfall with splashing rains.
DISEASE CYCLE :
PSI : Oospores in the infected debris and soil.
SSI : Sporangia or zoospores dispersed by wind or rainwater
Mode of spread:
Soil borne-spread through sporangia or zoospores dispersed by wind or rainwater.
48. Fusarium wilt on tomatoes is caused by Fusarium oxysporum f sp. lycopersici.
It is a soil born fungus that is found throughout the world, especially in warm regions.
The organism is specific for tomato .
The diseases develop more quickly in soils that are high in nitrogen and low in potassium.
3. Tomato Fusarium wilt
ECONOMIC LOSSES:
Due to high temperature and humidity Fusarium oxysporum f sp. lycopersici can cause damage.
It is a soil borne pathogen in the class Hyphomycetes that cause wilt of tomato as the only host of pathogen
and they reported 10- 90% loss in yield of tomato in temperate region due to this disease.
49. Symptom Fusarium wilt on tomatoes
The first symptom of the disease is clearing of the veinlets and
chlorosis of the leaf.
Soon the petiole and leaves droop and wilt.
The younger leaves may die
Dark brown or black discoloration of the vascular tissues.
Fungus survives saprophytically in soil.
Growth is typically stunted and little or no fruit develops.
Brown, vascular tissue can be found when the infected stem is cut at
its base.
Infected plants often die before maturing.
50. Use resistant Variety
pH 6.5 to 7.0
Keeping tomato plants weed-free.
Avoid activity in wet plantings
Prevention and Treatment
Use nitrate-based nitrogen fertilizer, such as calcium nitrate, rather than an ammonia-based nitrogen
fertilizer.
Seed treatment with 4 g Trichoderma viride formulation or 2.5 g Carbendazim per kg seed is effective.
51. 4. VERTICILLIUM WILT OF TOMATO
• Caused by:Verticillium dahliae, V. albo-atrum, V. tricorpus
• Hosts: Over 400 plant species includes eggplant, potato, strawberry, cucumber, pepper, radish, corn,
other cereals and grasses
Economic significance
It reduces the quality and quantity of a crop by causing discoloration in tissues, stunting, and
premature defoliation and death.
Once a plant is infected, there is no way to cure it.
Most severe losses are from early infections and can be as high as 30-50%.
52. Symptoms of Verticillium wilt on Tomato
The initial symptoms of Verticillium on tomato consist of characteristic V-shaped lesions on the lower
leaves, with yellowing that narrows down from the leaf margins.
The leaf progressively turns from yellow to brown and eventually dies.
Older and lower leaves are the most affected.
Sun-related fruit damage is increased because of the loss of foliage which decreases the quality of fruits.
Pinkish color discoloration in stem extends up to 10-12 inches.
53. Symptoms of Verticillium wilt on potato
Yellowing of leaves
Yellow blotches on the lower leaves
54. Favorable conditions
Verticillium wilt is a cool weather disease.
The fungus thrives in cool temperatures and when soil is moist and not too warm(15 - 20° C) .
Verticillium occurs primarily in neutral to alkaline soils.
It can attack at any stage in a tomato plant’s growth, but is most common in fruit formation stage.
Plants in poorly drained soil are more susceptible to infection than those in well-drained soil.
Wet soil allows the fungus to multiply and move up through the tomato plant’s water-conducting tissue.
Its wide host range permits Verticillium to persist in soils for long periods.
55. Management Verticillium wilt of tomato
Crop rotations with non related crops (4-5 years).
Cultivate the crop in well-drained soils.
Soil solarization heats up the soil which kills the fungus.
Tomato seedlings inoculated with arbuscular mycorrhizal fungi and Trichoderma harzianum show increased
resistance towards Verticillium wilt.
Applying optimal rates of nitrogen and phosphorus reduces the severity of Verticillium wilt symptom.
Soil moisture kept at the minimum for good growth. Limiting the amount of water applied to the field can
reduce severity of the disease.
Flaming crop residue at the end of a growing season reduces the amount of inoculum returned to the soil.
There is no fungicide available that can be used to control Verticillium Wilt once the plants have been
infected.
Choose disease resistant tomato varieties (letter “V” is mentioned after the variety name)
56. symptom
Fruit may be infected when green and small, but symptoms do not
appear until it begins
to ripen.
Symptoms first appear on ripe fruits as small, slightly depressed
circular lesions.
12 mm Lesions and become more sunken, with concentric ring
markings.
Centre is usually tan, and as the lesion matures becomes dotted
with small black specks.
Surface of the mature lesion remains smooth and intact.
Small, circular, brown lesions surrounded by yellow halos
characterize leaf infections.
5. Anthracnose disease in tomato
• Caused by Colletotrichum coccodes, Colletotrichum dematium, Colletotrichum gloeosporioides, Glomerella
cingulata
57. Use resistant plants, or buy healthy transplants.
Plant your plants in well-drained soil.
Water your plants with a drip sprinkler.
Don’t touch the plants when they are wet.
Keep ripening fruits from touching the soil.
Remember to rotate your plants every 2 to 3 years.
Spraying Mancozeb 2.5 g/l, chlorothalonil or Carbendazim 1 g/l
gives effective control.
Prevention and control
58. Bacterial spot is one of the most devastating diseases of pepper and tomato grown in warm, moist
environments.
It is almost impossible to control the disease and prevent major fruit loss when environmental conditions
remain favourable.
Caused by Xanthomonas species such as (X. campestris pv. vesicatoria or X. euvesicatoria) anthomonas
euvesicatoria (synonym = Xanthomonas campestris pv. vesicatoria race 1),Xanthomonas perforans (synonym
= Xanthomonas campestris pv. vesicatoria races 3 & 4), Xanthomonas gardneri
The spots usually brown and close to circular shape.
6.Tomato Bacterial spot
59. Small circular to irregular water-soaked areas showing as definite spots
on the lower leaf surface.
A narrow yellow halo may surround the spots.
When the spots are too many, the interveinal tissues become dry and
brown.
If the spots are at the edge, they may break away.
Annual production loss due to this disease is 10–20%, which my rise to
80% in some case.
Symptom of Tomato Bacterial spot
Bacterial spot stem lesions
60. Use of pathogen-free certified seeds
Treat seeds with dilute bleach, hydrochloric acid, or hot
water
Field sanitation and crop rotation reducesthe disease
incidence.
Minimize overwatering
Spraying the plants with a mixture of Streptocycline 200
ppm and Copper oxychloride 3g/l
Biological control , by using some of viruses
(Bacteriophages)
Xanthomonas campestris pv. Vesicatoria strains (75-3s
hrpG, hrpX, hrpF and hrpE1)
Bacterial spot on tomato fruit
Prevention and control of bacterial spot
61. 7.Tomato yellow leaf curl disease
• Tomato yellow leaf curl disease (TYLC) is a major constraint of tomato production worldwide.
• Caused by whitefly transmitted begomoviruses collectively called Tomato yellow leaf curl virus
(Aunpam and Malathi, 2003).
• The epidemic of TYLC in the affected areas is consistently associated with the high population of the
whitefly vector (Bemsia tabaci).
• It is indicated that the warmer environmental conditions together with more intensive monoculture
have provided favorable condition for population increase of its whitefly vector.
62. Symptom of Leaf Curl of Tomato
The leaf curl is characterised by severe stunting of the plants
with downward rolling and crinkling of the leaves.
Partial or complete sterility of the plant is also common.
Newly formed leaves show chlorosis.
The older, curled leaves become leathery and brittle.
Plants are stunted due to shortening of the internodes.
Diseased plants look pale and produce more lateral branches
resulting in bushy growth.
63. Total losses is in between 17.6% to 99.7%.
92.3% loss when infection occurred at 30 days after
transplanting.
The yield reductions were 94.9, 90.0, 78.0, and 10.8%
when plants got infected in 2, 4, 6, and 10 weeks after
planting
Economic loss
64. Use resistant variety Lycopersicon perurvianum, Akara
Ananya,Akara Rakshak, Akara Samrat.
Do not smoke near field.
Use of systemic insecticide such as Dimethoate (0.05 % )
as spray or Carbofuran or Phorate granules (50 kg / ha) as
soil application are useful in vector control and reducing
the disease
Prevention
65. They exist in soil in areas with hot climates or short winters.
About 2000 plants are susceptible to infection by root-knot nematodes and they cause approximately
5% of global crop loss
Symptoms of this disease is galls that can be diagnosed only in roots:
It caused by Meloidogyne species such as M. hapla, M. incognita, M. arenaria, M. javanica,
and M. naasi.
8. Root-not nematode of tomato
Some of tomato cultivars are used to resist this type of disease which contained Mi gene that is
responsible for this resistance.
The rotation is also applied to control this pest, by planting tomato plants with some type of
grasses such as (Pangola grass).
Managemet of Root-not nematode
68. 1.Turcicum leaf blight (TLB)
TLB is one of the major maize diseases having
wide distribution and high economic importance
in Ethiopia.
The disease is prevalent from low land humid
through highland humid agro-ecologies during
the wet rainy seasons.
Turcicum leaf blight (TLB) caused by Exserohilum turcicum (Pass.) is known to infect maize from the
seedling stage to maturity.
The disease has been reported throughout the world wherever maize is cultivated.
TLB can be severe in mid-altitude tropical regions where high humidity, low temperature and cloudy
weather prevail during the maize growing season.
69. 1. Long elliptical grayish green or tan lesions on leaves 2.5 to 25 cm in
length and 4 cm in width.
2. Lesions first appears slightly oval, water soaked, small spots on lower
leaves and increase in size and number.
Progress upwards until a complete burning of the foliage.
3. Under high humidity the whole leaf area becomes necrotic and plants
appear as dead.
4. Spores produced on the under surface are arranged in concentric zones
resembling a target like pattern.
Turcicumleaf blight symptoms
70. Turcicumleaf blightDisease management
1. Use of resistant cultivars For example BH541 and BH543 showed resistance to this disease
2. Two or three foliar sprays with 0.25 % mancozeb or zineb at 10-15 days intervals. First spray soon after
the disease appearance.
3. Application of urea followed by a light irrigation helps to minimize the disease as this disease becomes
serious under poor management,
i.e., under low nitrogen and water stress
71. 2. Common leaf rust (Puccinia sorghi)
Common leaf rust (CLR), caused by Puccinia sorghi is another important disease of maize in
Ethiopia that is
The disease is widely distributed throughout the major maize growing regions of the country.
It is more severe in the southern mid-altitude and the highland sub-humid maize growing agro-
ecologies of the country.
The first quality protein maize (QPM) hybrid variety registered in Ethiopia, BHQP542, was
short-lived in the commercial production and seed systems due to this disease.
72. Common leaf rust symptoms
It is most conspicuous when plants
approach tasseling.
It is recognized by small, oval to
elongate pustules.
Pustules are brown in early stages of
infection;
later, the epidermis is ruptured and the
lesions turn black as the plant
matures.
73. Disease management
1) Select resistant maize cultivars for planting in areas where rust becomes problem,
e.g., In maize, major race-specific resistance genes (Rpgenes) have been used to control
common rust in different parts of the world.
2) The severity of the disease can be reduced by spraying mancozeb or zineb @ 2.5 g/l, or
hexaconazole / propiconazole @ 1 ml/l.
The first spray should be given as soon as rust pustules appear on the foliage and then two or
three more sprays at 10-15 days intervals.
74. 3. Grey leaf spot (GLS) of maize
Grey leaf spots (GLS), caused by the fungus Cercospora zeae-maydis, is an important foliar disease of
maize worldwide.
In Ethiopia, the disease was first reported in 1999 (Tefferi, 1999) on a few maize farms.
Later, the disease was spread to all major maize producing mid altitude sub humid agro-ecology of the
country.
A major epidemic occurred in early 2000s which caused considerable maize grain yield losses
(Tilahun et al., 2012).
To date, the disease is one of the most important threats to maize production in the country, causing
yield losses as high as 29.1% (Wegary et al., 2004)
75. Symptoms of grey leaf spot
Early Lesions:
Early lesions of gray leaf spot are small, necrotic spots and may have a chlorotic halo (more visible when
leaf is backlit).
Lesions usually appear first on lower leaves before silking.
Lesions progress from lower to upper leaves.
The immature lesions are similar to lesions caused by other foliar maize pathogens, and first appear as
small tan spots about 1 to 3 mm in size and are irregular in shape.
Fully Developed Lesions:
Typical lesions of ray leaf spot are rectangular with straight edges (5 to 70 mm long and 2 to 4 mm wide), .
Lesion expansion is limited by parallel leaf veins.
Lesion appearance may differ somewhat on different genetic backgrounds.
76.
77. Gray Leaf Spot Impact on Crop
Depends on leaf area loss relative to grain fill:
If grain fill outpaces disease progression, yield loss may be minor.
If significant leaf area is lost before grain fill is complete, yield loss will be
greater.
Stalk rots may increase:
Loss of functional leaf area during grain fill may lead to stalk rots as carbohydrates are
taken from stalk to fill kernels.
Stalk lodging may increase harvest losses or slow harvest progress.
78. Management of Gray Leaf Spot
GLS-resistant hybrids:
Hybrids with genetic resistance can reduce yield loss due to GLS.
Hybrids and parent lines are rated and screened in "disease nurseries" as well as locations with high
levels of natural GLS occurrence’
For example, the hybrids and parents of recently released drought tolerant varieties, such as BH546,
BH547 and BH661, are resistant to this diseases
Crop rotation:
May reduce disease pressure, but rotation is only a partial solution.
Compared to other residue-borne pathogens, gray leaf spot survival time in debris.
Tillage: Encourages breakdown of crop residue.
Fungicide application: Foliar fungicide treatment is the only management option available
following planting.
79. 4. Maize streak disease
Maize streak disease is caused by Maize streak virus (MSV).
It is a major viral disease of maize in sub-Saharan Africa.
Eleven strains of MSV are known to exist; named from MSV-A to MSV-K (SMonjane et al.,2011).
In Ethiopia, this disease was formerly known only in Gambella (the western low land sub-humid plains
bordering South Sudan).
But in recent years, the disease is becoming very important in the mid-altitude agroecology of Ethiopia
and posing a significant threat to maize production in the country.
Most commercial varieties currently under production are found to be susceptible to the virus.
80. Symptom of Maize streak disease
Early disease symptoms begin within a week after infection and consist of very small, round, scattered
spots in the youngest leaves.
The number of spots increases with plant growth; they enlarge parallel to the leaf veins.
Soon spots become more profuse at leaf bases and are particularly conspicuous in the youngest leaves.
Fully elongated leaves develop a chlorosis with broken yellow streaks along the veins, contrasting with
the dark green color of normal foliage.
Severe infection causes stunting, and plants can die prematurely or are barren.
Many cereal crops and wild grasses serve as reservoirs of the virus and the vectors.
81. • A popular maize hybrid, BH540, highly infected by MSV on farmers‟ field in Benishangul Gumuz, Western
Ethiopia.
Symptom of Maize streak disease
82. Maize streak disease management
• A number of options have been recommended for management of maize streak disease including
cultural, chemical and host plant resistance.
• The most effective, environmentally friendly and economically viable method
of MSV management is by the use of host plant resistance.
• In Ethiopia two open pollinated maize cultivars were released for MSV prone areas (Gambella
Regional State);
namely, Gambella Composite and Abo–Bako are resistant to this disease.
83. 5. Maize lethal necrosis
• Maize lethal necrosis disease (MLND) is a result of a combination of two viruses, Maize Chlorotic Mottle Virus
(MCMV) and any of the cereal viruses in the Potyviridae group, such as:
Sugar Cane Mosaic Virus (SCMV),
Wheat Streak Mosaic Virus (WSMV)
Maize Dwarf Mosaic Virus (MDMV).
).No lethal necrosis will develop if only MDMV and WSMV occur together.
• The double infection of the two viruses gives rise to what is known as MLN.
• In Ethiopia, although its first epidemics was reported in the Central Rift Valley in 2014 main season (Mahuku et al.,
2015),
• MLN attack has now been confirmed in all major maize growing areas of the country at varying level of severity
(Demissie et al.,2016).
• In addition to threatening food security directly, MLN has the potential to negatively impact human health and
wellbeing via secondary fungal infections which lead to the production of mycotoxins.
84. Infected plants are short.
The leaves show chlorosis and die at about flowering time.
There is no ear development in plants infected during early stages of growth.
Symptom of Maize lethal necrosis
85. 6. Maize Ear Rots
• Gibberella ear rot, Fusarium ear rot, and Aspergillus ear rot are three predominant ear rot diseases of
maize in the world.
• Gibberella ear rot are caused by Fusarium graminearum.
• Fusarium ear rot is predominantly caused by Fusarium verticillioides and F. Proliferatum.
• Aspergillus ear rot caused by Aspergillus flavus
• Infection by this fungal species results not only in yield reduction but also in contamination with
mycotoxins.
• Aspergillus species produce a mycotoxin called aflatoxin.
• Aflatoxin affects grain quality and marketability and is primarily a threat to human health.
• Aflatoxin is extremely carcinogenic and most countries.
• The main mycotoxins produced by F. graminearum are deoxynivalenol (DON), nivalenol (NIV) and
zearalenone (ZEA),
• Whereas F. verticillioides produces mainly fumonisins (FUM) B1 and B2.
86. Signs and Symptoms of maize ear rots
• Aspergillus ear rot appears as an olive-green mold on the kernels
• The fungal spores appear powdery and may disperse like dust
when you pull back the husk.
• These signs are most commonly observed at the tip of the ear,
but can be scattered throughout the ear and all the way to the
base of the ear
The fungus that causes Aspergillus ear rot produces olive-green spores that
are scattered throughout the ear.
The tip of this corn cob shows signs of Aspergillus ear rot, which is
caused by the fungus Aspergillus flavus
87. Signs and Symptoms of maize ear rots…
Gibberella ear rot produces a pinkish mold that often begins at the ear tip.
On severely affected ears, the husks and silks may adhere tightly to the ear because of mold growth — such
ears are called “mummified ears”
• Corn ears with Gibberella ear rot.
Except in highly susceptible hybrids or under severe
conditions, the disease usually affects only part of the
ears.
It is relatively easy to identify Gibberella ear rot in the
field on intact ears,
But it is much more difficult to identify after the grain
has been shelled.
88. Signs and Symptoms of maize ear rots…
The signs and symptoms of Fusarium ear rot vary
fromother ear rots.
Diseased kernels are scattered or in patches on the ear,
especially on kernels damaged by European corn
borer, earworm, or bird feeding.
Fusarium-affected kernels appear purple, tan, or brown
When fungal growth is visible on the ear, infected
kernels will appear white to pink or salmon.
In some cases, kernels have white streaks (called a
“starburst” symptom), which is caused by the
pathogen
growing under the kernel pericarp (seed coat).
The starburst symptom on kernels is often seen on ears affected by
Fusarium ear rot.
Ears with Fusarium ear rot have white to purple mold visible on
kernels.
89. • Cultural practices to manage ear rot and aflatoxin contamination in maize includes early planting, crop
rotation, residue management, maintaining optimum fertility for corn production etc
• Managing insect damage that will inoculate the fungus during feeding.
Management of ear feeding insects using insecticide application and manipulation of sowing date
significantly reduce infection due to Fusarium and contamination with fumonisin.
• Breeding maize for genetic resistance is the most effective way to manage maize ear rot and mycotoxin
contamination.
• A biological product that contains a non-toxigenic strain of A. flavus (Afla-Guard) has been effective at
reducing aflatoxin contamination by 60 to 75% in the field.
Several Trichoderma spp, including Trichoderma viride and Trichoderma harzianum, are capable of
effectively reducing F. verticillioides (= F. moniliforme) growth and fumonisin production in vitro and
in planta (in vivo) (Yates et al., 1999).
Management of maize ear rots
90. Symptoms
The disease is confined to individual spikelets.
The first symptom is the secretion of honey dew (creamy sticky liquid) from infected florets.
The honey dew secretion attracts large number of insects and ants which help in spreading the
disease.
Often the honey dew is colonized by Cerebella sorghivulgaris which gives the head a blackened
appearance.
Under favourable conditions, grain is replaced by long (1-2cm), straight or curved, cream to light brown,
hard sclerotia.
At the base of the affected plants white spots can be seen on the soil surface, denoting the drops
of honey dew which had fallen on the soil.
3.3. Major sorghum diseases and their
management
1. ERGOT or SUGARY DISEASE (Claviceps sorghi or Sphacelia sorghi)
91.
92. Disease cycle
• Primary source of infection is through the germination of sclerotia which
produce ascospores, which infect the ovaries.
• The secondary spread takes place through air and insect borne conidia,
which settle in the spikelets.
• Rain splashes also help in spreading the disease.
Favourable Conditions
• Aperiod of high rainfall and high humidity during flowering season.
• Cool night temperature (20-25 ℃) and cloudy weather during anthesis
encourages disease spread rapidly causing severe losses in hybrid seed
production.
• Male sterile lines are highly susceptible.
93. Management
Adjust the date of sowing so that the crop does not flower during the periods of
high rainfall and high humidity.
Grow resistant varieties
Deep summer ploughing
Soaking seeds with 2% saline solution will aid to remove ergot infested seeds, as
ergot infested seeds will float in the salt solution.
Seed treatment with fungicides such as Captan or Thiram@4g/kg seed Spray
Ziram (or) Zineb (or) Captan (or) Mancozeb @0.2% at emergence of earhead (5-
10 per cent flowering stage) followed by a spray at 50 per cent flowering and
repeat the spray after a week, if necessary.
Control of ergot with fungicides such as Propiconazole or Tebuconazole has
proved to be cost effective in seed production plots.
94. 2.ANTHRACNOSE OR RED LEAF SPOT(Colletotrichum
graminicola)
Symptoms
The fungus causes both leaf spot (anthracnose) and stalk rot (red rot) in sorghum.
The disease appears as small red coloured spots on both surfaces of the leaf.
The centre of the spot is white in colour encircled by red, purple or brown margin.
Numerous small black dots are seen on the white surface of the lesions which are the fruiting
bodies (acervuli) of the fungus.
Many lesions coalesce and kill large leaf portions.
In midrib region, elongate elliptical, red or purple regions with black acervuli are formed.
Stalk and inflorescence infection can be characterized externally by the development of circular
cankers.
95.
96. Disease cycle
• Fungus has wide host range and survives
on Johnson grass, Sudan grass, maize,
barley and wheat.
• Also survives in seed and infected plant
debris.
• Primary infection is from the conidia
produced on the infected plant debris
and infected seed.
• Disease spread within the season is through
air borne conidia, which are produced on
first infected plants.
Favorable Conditions
• Continuous rain, temperature of 28-30℃ and
high humidity aggravates the disease.
Management:
• Destruction of infected plant debris and collateral
hosts.
• Crop rotation with non-host crops .Grow
resistant varieties like SPV 162, CSV 17, Texas
Milo and Tift sudan.
• Treat the seeds with Captan or Thiram @3 g/kg.
Spray the crop with Mancozeb @0.25% or
carbendazim@0.1% .
97. 3.RUST (Puccinia purpurea)
Symptoms
• Small reddish brown flecks on lower surface of the leaf.
• Reddish brown pustules on the both surfaces of the leaves.
• Initially pustules contain reddish powdery mass of uredospores.
• In later stages teliospores are developed which are darker & longer than the uredospores.
• Premature drying of leaves ,stunted growth of the plants is seen.
Rust on leaf Pustules on stalk Telio & Uredospores
98. Disease cycle
The fungus is long cycled rust with Oxalis corniculata as the alternate host with aecial and pycnial stages.
Presence of alternate host helps in perpetuation of the fungus.
The uredospores survive for a short time in soil and infected debris.
Air borne uredospores help in the secondary spread of the disease.
Favorable Conditions: Low temperature of 10 to 12℃ favors teliospore germination and a spell of
rainy weather favours the onset of the disease.
Management :
Grow resistant varieties
Remove and destroy the alternate host
Spray the crop with Mancozeb @0.25%.
Dusting of sulphur@25 kg/ha .
100. A. Grain smut/Kernel smut / Covered smut / Short smut -
Sphacelotheca sorghi
Symptoms
The individual grains are replaced by smut
sori.
The sori are oval or cyclindrical and are
covered with a tough creamy skin
(peridium) which often persists unbroken up
to thrashing.
Ratoon crops exhibit higher incidence of
disease.
101. Symptoms
The affected plants can be detected before the
ears come out.
They are shorter than the healthy plants with
thinner stalks and marked tillering.
The ears come out much earlier than the
healthy.
The glumes are hypertrophied and the earhead
gives a loose appearance than healthy.
The sorus is covered by a thin membrane
which ruptures very early, exposing the spores
even asthe head emerges from the sheath.
B. Loose smut/ kernel smut - Sphacelotheca cruenta
102. C. Long smut - Tolyposporium ehrenbergii
Symptoms
This disease is normally restricted to a relatively a small
proportion of the florets which are scattered on a head.
The sori are long, more or less cylindrical, elongated, slightly
curved with a relatively thick creamy-brown covering membrane
(peridium).
The peridium splits at the apex to release black mass of spores
(spore in groups of balls) among which are found several dark
brown filaments which represent the vascular bundles of the
infected ovary.
103. D. Head smut - Sphacelotheca reiliana
Symptoms
• The entire head is replaced by large sori.
• The sorus is covered by a whitish grey membrane of
fungal tissue, which ruptures, before the head emerges
from the boot leaf to expose a mass of brown smut spores.
• Spores are embedded in long, thin, dark colored filaments
which are the vascular bundles of the infected head.
104. Management for all smuts
• Treat the seed with Captan or Thiram at 4 g/kg.
• Use disease free seeds.
• Follow crop rotation.
• Collect the smutted ear heads in cloth bags and bury in soil.
105. Comparison of characteristics of Four smuts of Sorghum
Character Grain smut Loose smut Long smut Head smut
Organism S. sorghi S. cruenta T. ehrenbergii S. reiliana
Ear infection All or most grains
smutted
All or most grains
smutted
Only about 2% of
grains are infected
Entire head smutted
into a single sorus
Sori Small, 5-15 × 3-5mm Small,3-18 × 2-4mm Long, 40 × 6-8mm 7.5-10cm × 2.5-5cm
Columella Short columella
present
Long columella
present
Columella
absent,but 8-10
vascular strands
present
Columella absent,
but a network of
vascular tissues
present
Spores In single round to
oval,olive-brown
In single spherical or
elliptical,dark brown
Always in
balls,globose or
angular,brownish
green
Loosely bound into
balls,spherical or
angular,dull brown
Viability of spores Over 10 years About 4 years About 2 years Upto 2years
In culture Yeast like growth
with sporidia
In colonies with
sporidia
In colonies with
masses of sporidia
In colonies germ
tubes and sporidia
Spread Externally seed-
borne
Externally seed-
borne
Air-borne Soil-borne and
Seed-borne
106. 5. LEAF BLIGHT OR STRIPE
Symptoms:
Long elliptical necrotic lesions, straw coloured in the centre
with dark margins.
Straw coloured centre becomes darker with the sporulation of
the fungus.
The lesions can be several centimeters long and wide and
coalesce on the leaves, destroying large areas of leaf
tissue.
This gives the crop a distinctly burnt appearance leading to
premature drying of leaves.
The leaf blight pathogen also causes seed rot and seedling blight
of sorghum.
The disease appears in the form of small narrow elongated
spindle shaped spots in the initial stage.
Caused by Exserohilum turcicum or Trichometasphaeria
turcica (Syn : Helminthosporium turcicum or Drechslera
turcicum)
107. Disease cycle:
• The fungus is found to persist in seed, soil
and infected plant debris.
• Seed borne conidia are responsible for
seedling infection.
• The secondary spread of the disease is
through wind-borne conidia and seed.
Favourable Conditions :
• Cool moist weather, high humidity (90 per
cent) and high rainfall.
• Management
• Use disease free seeds.
• Rotation with non susceptible crops.
• Collect and destroy infected plant debris.
• Treat the seeds with Captan or Thiram at 4 g/kg.
• Spray the crop with Mancozeb@0.25% at the age of 40
days and the spraying have to be repeated twice at 15
days interval.
• Resistant variety
108. If rains occur during the flowering and grain filling stages, severe grain moulding can occur.
Infected grains are covered with pink or black mold and such grains disintegrate during threshing
process.
Fusarium semitectum and F.moniliforme develop a fluffy white or pinkish colouration.
C. lunata colours the grain black.
Moldy grains contain toxic mycotoxins and are unfit for human consumption and cattle feed.
Fungi from many genera have been isolated from the infected sorghum grains the most frequently
occurring genera are:
Symptoms
6. Head mold/grain mold/ head blight
Fusarium,
Curvularia,
Alternaria,
Aspergillus,
Cheatomium,
Rhizopus,
Helminthosporium and
Phoma.
109.
110. Disease cycle
• The fungi mainly spread through air-borne conidia.
• The fungi survive as parasites as well as
saprophytes in the infected plant debris.
Favorable Conditions
• Wet weather following the flowering favors grain
mold development and the longer the wet period
the greater the mold development.
• Compact ear heads are highly susceptible.
Management
Adjust the sowing time
Grow resistant varieties.
Seed disinfestation with Thiram@0.3% will
prevent seedling infection.
Spray Mancozeb (0.25%) or captan (0.2%) or
captan 2g + Aureofungin 200ppm per liter, in
case of intermittent rainfall during earhead
emergence, a week later and during milky stage.
111. 7. PARISITIC DISEASES
Phanerogamic parasite (Striga or Witch Weed) Striga asiatica and Striga
densiflor
Symptoms
• Infestation causes yellowing and wilting of the host
• Stunted in growth and may die prior to seed setting,
• The parasite grows faster and appears at the base of
the plant.
112.
113. Etiology
It is a partial root parasite and occurs mainly in the rainfed sorghum.
It is a small plant with bright green leaves, grows upto a height of 15-30 cm.
It always occurs in clusters of 10-20/host plant.
S. asiatica produces red to pink flowers while. S. densiflora produces white flowers .
Each fruit contains minute seeds in abundance which survives in the soil for several years.
Disease cycle:
The seeds remains for many years.
The seeds germinate with roots of host.
Seeds can germinate even one foot below soil.
Soil temperature of 35C and soil moisture of 30 per cent is favorable for Striga infection.
114. Management
Hand weeding of the parasites before flowering.
Crop rotation with cowpea, groundnut and sunflower.
Mixing of ethrel with soil , triggers germination of Striga in the absence of host.
After germination, Striga can be removed and destroyed.
Spray Fernoxone (sodium salt of 2, 4-D) or Agroxone (MCPA) at 450g/500 liters of water or
Praquat@1kg/ha.
1% Tetrachloro dimethyl phenoxy acetate can be used for instant killing of Striga.
