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Here is a list of nine major diseases of Sunflower: 1. Sunflower Necrosis Disease 2. Alternaria Leaf Blight Disease 3. Downy Mildew Disease 4. Rust Disease 5. Sclerotium Wilt and Collar Rot Disease 6. Charcoal Rot Disease 7. Sclerotinia Wilt and Rot Disease 8. Powdery Mildew Disease 9. Head Rot Disease.
Diseases of Sunflower:
- Sunflower Necrosis Disease
- Alternaria Leaf Blight Disease
- Downy Mildew Disease
- Rust Disease
- Sclerotium Wilt and Collar Rot Disease
- Charcoal Rot Disease
- Sclerotinia Wilt and Rot Disease
- Powdery Mildew Disease
- Head Rot Disease
1. Sunflower Necrosis Disease (SND):
In India, sunflower necrosis disease (SND) was reported for the first time at Bagepally region of Kolar district and around Bangalore in Karnataka during 1997. This disease was later reported in Andhra Pradesh, Karnataka, Tamil Nadu and Maharashtra. Now, the disease has become a potential threat for sunflower cultivation in all traditional sunflower growing areas in India.
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The intensity of disease ranges from 2 to 100%. The disease greatly reduces the growth and seed yield. All the growth and yield parameters were significantly affected due to sunflower necrosis disease (SND) resulting in yield loss of 89% under severe conditions of 50-75% disease severity, 63% and 20% at 11-50% and 5-10% disease severity levels respectively.
In general, the disease occurrence has been erratic and its incidence varies from season to season and place to place.
Tobacco streak virus (TSV) of liar virus group causes necrosis disease. The virus is transmitted through sap, but failed to transmit through seed and grafting. However, it was observed that the virus might be present in the infected flower heads/immature seeds till the plant is alive and subsequently it did not carry along with seeds after harvest.
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The virus is transmitted by insect vector thrips. Scirtothrips dorsalis Hood, Frankliniella schultzei (Trybom), Megalurothrips usitatus (Bagnall), Karyothrips flavipes (Jones), Thrips hawaiiensis (Morgan) and Microcephalothrips abdominalis (Crawford) are commonly observed on sunflower.
Three thrips species (S. dorsalis, F. schultzei and M. usitatus) assist in transmission of TSV in groundnut, cowpea, sunflower plants by carrying the infected pollen not by acquiring the virus in their body.
The main source of inoculum was identified as the pollen grains of infected crop plants or weeds. The thrips could carry 20-200 pollen grains over their body externally thus helping in spreading the inoculum and causing the disease.
Parthenium weed plays a major role in spreading the disease as a symptom less carrier of the virus and also it produces several flushes during its life cycle, thus provides infective pollen throughout the year.
The disease incidence was higher in Kliarif and summer seasons whereas it was low in rabi season. Necrosis occurrence was more during July-September and January-March sowings, whereas it was low during October-December sown crops. Dry weather (July-August) with moderate temperature of 30-32°C and 55-75% relative humidity was conducive to thrips incidence.
Highest disease incidence was observed during the prolonged dry spells immediately after heavy rains. There was positive correlation between thrips population and the weather parameters viz., temperature, sunshine and dry spells whereas, negative correlation was observed with rainfall, and relative humidity.
Further, the thrips population and the incidence of the necrosis disease were positively correlated. Higher the thrips incidence more is the incidence of necrosis.
Number of genotypes comprising of CMS, R lines, germplasm accessions and derivatives of wild sunflower were evaluated and none of them are resistant. The disease produces different types of symptoms and sometimes it becomes difficult to identify the disease based on these symptoms alone.
Intercropping of sunflower with groundnut, urdbean or mungbean has no effect on disease incidence. As by the time sunflower is in flowering stage, the other crops complete the critical periods of infection and hence even if sunflower is infected with necrosis disease, other intercrops would remain free from the disease.
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Clean cultivation does not allow the vector to breed on collateral hosts in off-season and on alternate hosts in the main season. Removal of weeds particularly Parthenium from the field, growing wild in fallow lands, roadsides, field bunds and adjoining areas of crop is helpful in reducing the necrosis incidence as it serves as source of inoculum throughout the year.
Growing chrysanthemum and marigold close to sunflower has to be avoided. Rouging of infected plants before flowering helps to destroy the virus source and spread of the disease.
Border crop like sorghum/pearl millet /maize in 5-7 rows (30 cm apart) has to be grown around sunflower crop which attracts the thrips population and also obstructs the wind borne thrips and inoculum carrying pollen grains of Parthenium from landing on sunflower plants.
Seed treatment with imidacloprid at 5g /kg of seed found to protect the crop from insect vectors in the initial stages of crop growth. Spraying of imidacloprid 0.01% or oxydemeton methyl 0.025%, three times at 15 days interval starting from 15 days after sowing was effective in control of insect vectors.
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Use of insecticides for the control of insect vectors proves to be less effective in management of necrosis disease; hence efforts on use of biotechnological tools for development of transgenic sunflower plants against necrosis disease are in progress.
2. Alternaria Leaf Blight Disease:
In India, Alternaria leaf blight is the major disease since the introduction of sunflower crop. It appears in the entire sunflower growing areas of India in low to severe form. The disease has been reported to reduce the seed yield by 27 to 80% and oil yield by 17 to 33%.
The correlation between increase in disease intensity (25-96%) and reduction in yield components and oil content is negative. The disease also affects the seed germination and vigor of seedlings. The loss in germination varies from 23 to 32%. In Northern Karnataka, Hiremath (1990) reported 95 to 100 % incidence of disease.
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Variation among the isolates of A. helianthi collected from Kurnool, Hyderabad, Akola, Latur, Raichur, Coimbatore was observed with respect to mycelial growth, sporulation and disease reaction. Mesta (2006) reported three distinct groups from 17 isolates of A. helianthi based on isozyme patterns for peroxidase and catalase.
Two groups were detected from eight isolates of A. helianthi based on pathogenicity of lesion size on sunflower leaves. Presence of six genetically distinct groups was observed among 21 isolates of A. helianthi by random amplified polymorphic DNA (RAPD) analysis.
Pathotoxins extracted from A. helianthi culture filtrates proved to be host specific to sunflower and produced typical leaf spot symptoms at concentrations as low as 20 mg/ kg. The toxin from A. helianthi was isolated and identified as 3- propyl,4 hydroxy,2- oxo-2, 3 dihydro furone.
This is host specific and inhibited seed germination, root and shoot length at 50 ppm and above concentration. Shaik and Ravikumar (2003) reported that detached leaf evaluation under in vitro did not show definite trend of association with field disease score in case of Alternaria leaf blight of sunflower.
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They used culture filtrate of A. helianthi for in vitro evaluation studies, which had inhibitory effect on seed germination and seedling traits under in vitro conditions. An artificial inoculation technique has been standardized for screening number of sunflower germplasm lines against Alternaria leaf blight under pot culture conditions.
The fungus over winters as mycelium in infected plant residues and in dry conditions, survives for 20 weeks in soil. The fungus is seed borne with 22.9% seed transmissible nature. Seedling blight caused by Alternaria may develop when sunflower plants emerge in rainy season on Alternaria infested land. Seedlings were more susceptible than adult plants.
The disease incidence was low in young crop and increased with increasing age. The disease is favoured by 25-27°C temperature and 12 h of wet foliage. Extended leaf wetness periods of three to four days can cause serious losses as the spots will become much larger and coalesce with each other. The disease appears in winter crop also.
The disease spreads rapidly in rainy season and the conidia spread by wind and splashing water. Hot weather and frequent rains during the milk and wax stages of plant development favour infection. The role of stalk mulch incorporated from previous sunflower crop in inducing higher disease incidence of Alternaria leaf spot was well established.
In India, the winter growing season with lower temperatures and high rainfall is more favourable for A. helianthi infection than the spring growing season, while incidence of A. alternata was almost same in both seasons.
Epidemiological studies revealed that percent disease index was negatively correlated with minimum temperature, while positively correlated with relative humidity. Borkar and Patil (1995) reported that a temperature of 25.9 to 33.7°C with a relative humidity of 85 to 95% favoured development of Alternaria leaf blight in Maharashtra.
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Rajivkumar and Singh (1996) correlated the leaf blight intensity and weather parameters and revealed that the important weather conditions were temperature of 27-29°C and relative humidity of 78-80% and disease was highest in last week of August.
Different genotypes evaluated for sources of resistance under both field and artificial conditions revealed none of the genotypes were immune to the disease.
Screening of thirty two Helianthus species against A. helianthi revealed resistant reaction in nine species viz., H. maximiliani, H. mollis, H. divaricatus, H. simulans, H. occidentalis, H. pauciflorus, H. decapetalus, H. resinosus and II. tuberosus, while the diploid annuals were susceptible.
Efforts are being made to develop interspecific Alternaria resistant cultivars from these wild Helianthus sources.
In North America, Abbas (1995) suggested that weeds like musk thistle and cocklebur serves as source of inoculum to infect cultivated sunflower, however the role of weeds serving as source of inoculum reservoir was discontinued in India.
Mohammad (1983) reported that the disease intensity was least severe at the highest plant densities and more severe at plant spacing of 30 by 20 cm. The disease severity increased with each increment of added nitrogen up to 120 kg/h.
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Occurrence and severity of the disease depends on the season and planting dates. The spring crop sown in late February will have higher incidence than the crop sown in first week of January. Mid September planting of sunflower in Nainital and Tarai region of Uttaranchal keeps the crop free from major diseases particularly with low infection of leaf spot.
Early planting of sunflower during kharif season results in low occurrence of leaf spot. Intercropping sunflower with groundnut in the ratio of 6 : 2 reduces the disease incidence. Closer spacing induces more disease build up. Spacing of 60 x 30 cm or 45 x 30 cm is optimum in reducing the build up of Alternaria leaf blight.
Seed treatment with thiram or captan at 2.5 g or carbendazim at 1.0 g /kg protects the seed from seed borne infection. Spraying mancozeb (0.3%) four times at an interval of 7-10 days was found effective in controlling the disease with an increase in yield by about 43 to 65%.
Spraying of carbendazim + mancozeb (1:1) three times at 15 days interval after disease appearance improves seed yield and reduces the leaf spot disease.
Fungicides viz., zineb, ziram and captafol were also effective. Iprodione and propiconazole 0.1% are very effective and economical in controlling the disease. Spraying of propiconazole 0.1% three times at 30, 45 and 60 days after sowing effectively reduced the leaf blight incidence.
3. Downy Mildew Disease:
(Plasmopara Halstedii (Farl.) Berl. and De Toni)
The disease was recorded for the first time in 1984 in Latur and Beed districts of Marathwada region of Maharashtra in India with an intensity ranging from 5 to 60%. Later the disease has spread to other areas of Maharashtra, Andhra Pradesh and Karnataka.
The disease was reported from Madhya Pradesh and Punjab also. The losses in yield were reported to be 2-25%. Under favourable weather conditions, 95% destruction of the plants was recorded. Seeds produced by affected plants show significantly smaller and higher seeds with a high hull percentage and lower oil content.
The susceptibility of the seedlings decreases as the age advances. Rain in the early phases of growth and age of seedlings at the time of infection are important factors for disease incidence. Three day old seedlings were more susceptible to systemic infection. Cool weather with 16-18°C temperatures, cloudy weather with winds and light drizzle or high relative humidity favours infection and disease development.
Heavy soils with poor drainage favours the disease development. Heavy showers following sowing increase the disease intensity to the extent of 58%. Sunflower plants suffering from boron deficiency become more susceptible to downy mildew.
Downy mildew disease was noticed in India in 1984 and presently race 1 is present. North American race of P. halstedii is highly virulent than Indian race. Quarantine measures should be strictly followed to prevent the entry of other races of the pathogen into India.
Some sunflower growing areas in India are still free from the disease, so it is necessary to adopt local quarantine measures strictly to restrict the spread of the disease to disease free areas.
Growing resistant cultivars is the most effective and economically practical for control of downy mildew. Two downy mildew resistant hybrids LSH-1 and LSH-3 for endemic pockets of Maharashtra were released. High yielding hybrids such as BSH-1, KBSH-1, ICI-302, PKVSH- 27, DSH-1, NSH-22, ITC-601, MSFH-17, SPIC-105, Jwalamukhi, NARF- 114 and varieties viz., PKVSF-9, Sidheswar are resistant to downy mildew.
Most of the recently released hybrids are resistant to downy mildew, while, many varieties are susceptible.
Healthy seed obtained from disease-free areas should be sown in well-drainea lields. Early planting during rainy season generally escapes from disease. Late rainy season planting particularly July-August should be avoided. Shallow sowing (3 cm) is desirable to minimize the disease incidence. Optimum spacing has to be followed for sowing.
Spacing of 60 x 30 cm or 45 x 30 cm recorded least disease incidence compared to 60 x 15 cm or 45x 15 cm. Pre sowing irrigation followed by one irrigation at 10 or more days after sowing reduces disease considerably in endemic areas. Frequent irrigation upto 25 days after sowing or water stagnation due to unseasonal rains induces higher disease incidence in susceptible cultivars /hybrids.
Water stagnation should be avoided as it favours quick development of pathogen. Rouging of mildew infected seedlings during thinning, removal and destruction of infected plants as and when they appear before flowering reduces spread of the disease.
It also reduces oospore build up for the following season and the inoculum is destroyed before the seed is infected. Elimination of volunteer downy mildew infected plants at the onset of the monsoon is advisable to avoid the spread of the disease. Infected plant debris of the previous crop season should be removed and destroyed from the field.
This practice helps in reducing the spread of the disease. Six-year crop rotation in sunflower with groundnut and pigeon-pea is advisable in endemic areas. Cropping sequence of sunflower followed by groundnut reduces the disease incidence compared to sunflower after sunflower.
Metalaxyl fungicide i.e., APRON 35 ES was found to be highly effective in reducing the incidence of downy mildew disease, even in sick plot conditions, when seeds were treated with the chemical at 105 g a.i./100 kg (3 ml / kg of seed). Seed treatment with Apron 35 SD 6 g/kg followed by foliar sprays of ridomyl MZ 72 at 0.2% two times at 15 days interval provides effective control.
4. Rust Disease:
(Puccinia Helianthi Schwein)
This disease is prevalent throughout the sunflower growing areas in India. It is more severe in the rabi season and causes a considerable yield reduction whenever it appears in early stages of crop growth. In kharif season, the appearance is usually late. Under severe rust conditions, the seed yield loss of 11-33% has been reported, it becomes unnoticeable if rust occurs in later stages of the crop.
The fungus mainly survives through teliospores on leaves left in the field or on the soil surface. They can live longer and normally exhibit dormancy for a period of variable length in soil, seed and plant debris.
Uredia, sporidia, pycnia and aecia may appear on volunteer seedlings among plant debris of the previous years crops and thus the fungus survives on such volunteer plants. The primary infection is from sporidia or germinating teliospores or aeciospores or uredospores from volunteer plants at high altitudes, which carried through air currents.
Secondary infection occurs through uredospores, which are repeatedly produced in a crop season. Spore production and infection continue to occur. This “repeating stage” is the most damaging with spores being spread by wind to other fields.
Temperature of 25.5 to 30.5°C with 86-92% relative humidity favoures high rust intensity and the disease is positively related with relative humidity. Excessive nitrogen fertilization and abnormally high seeding rates promote excessive foliage, this, in turn, favours rust development. The incidence of rust increases with plant age.
A differential excretion of coumarins to the leaf surface was also observed among genotypes, with the highest levels corresponding to the most resistant genotype and the lowest to the most susceptible. Amzalek and Cohen (2007) reported that DL-3-amino-n- butanoic acid (DL-b-aminobutyric acid [BABA]) was the most effective and sodium salicylate (NaSA) was the least effective in protecting against rust.
BABA did not affect urediospores germination, germ tube growth, appresorial formation or initial ingress of P. helianthi, but strongly suppressed mycelial colonization in the mesophyll and consequently pustule and urediospore formation.
Growing of resistant varieties offers the best means of control. Majority of the hybrids released for cultivation are tolerant or highly resistant to rust. Wild species of sunflower viz., Helianthus tuberosus, H. praecox ssp. praecox, H. praecox ssp. runvonii, H. petiolaris ssp. petiolaris are resistance to this disease. Removal and burning of infected crop residues minimizes initial inoculum.
Clean cultivation and removal of volunteer sunflower plants carrying infection reduces the primary inoculum. Deep ploughing in summer exposes the inoculum present in the soil to high summer temperatures and kills the fungus. Crop rotation with non-host crops for 3 years reduces the inoculum load in the soil. Avoid high nitrogen rates and high plant populations.
Spraying of mancozeb or zineb at 0.25% two to three times at 10 days interval is very effective in control of the disease. Application of sulphur fungicides, sulphur dust (15 kg/ ha) or wettable sulphur 0.2% or mixture of sulphur + zineb also gives good control of the disease.
Spraying of oxycarboxin 20 EC and benodanil 50WP at 0.4% two times at 30 days interval also effectively control the disease. Application of boron to soil reduces the rust incidence.
5. Sclerotium Wilt and Collar Rot Disease:
(Sclerotium Rolfsii Sacc)
The disease causes 10-11% yield loss with 10-11% disease incidence in sunflower crop planted in July or August or in February or March in Nainital and Tarai region of Uttaranchal. The major reduction in yield occurs when plants infected by the disease is due to rapid wilting and loss of leaf tissue.
The disease appears generally 40 days after sowing. This fungus can cause collar rot in the seedling stage. The fungus survives as sclerotia or mycelium in infected plant residue and soil. Aerobic conditions, high temperatures, and high humidity favour the germination of sclerotia and mycelial growth.
The mycelium colonizes on organic debris and produces the characteristic fan-like mats of hyphae that infect the plant. Large amounts of organic debris in combination with high humidity and temperature in fields, with a high population of the fungus are the main factors favourable for disease development.
The fungus becomes active during rainy season or when the plant is weakened due to physiological conditions or due to insect attack. The incidental or other types of wounds in the roots, favour the entry of the fungus. Once inside the host, the organism becomes virulent, causing severe damage to the plant.
Crop rotation of 3-4 years helps to reduce disease. Removal of weeds and elimination of infected plant residue minimizes the disease incidence. Deep ploughing of soil exposes the sclerotia and infested crop debris to sunlight and lowers the amount of the pathogen. Mid-September sowing of sunflower escapes the disease in Uttaranchal. Moisture stress and water logging conditions should be avoided in the field.
Addition of amendments like oat straw and finely grounded castor and neem oilcakes in the infested soil reduce the inoculum in the soil and disease incidence. Such reduction in incidence has been attributed to inhibition of the growth of S. rolfsii due to water or ether- soluble toxic substances as released in the decomposition process and also due to enhanced antagonistic activity of increased microflora.
The growth of plants also enhances in amended soil, so the plants become less susceptible to the disease.
Biocontrol agent Trichoderma harzianum Rifai grown on finger millet seeds or on straw pieces incorporated into soil reduces the soil pathogen. Seed dressing with thiram + carboxin (2:1) at 3-6 g/kg of seed is found to be effective control of the seedling phase of the plant.
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. Charcoal Rot Disease:
(Macrophomina Phaseolina (Tassi) Goid)
The disease is more prevalent and economically important in regions with hot, dry growing seasons. It can cause 30-46% reduction in seed weight. The disease also causes lodging that incurs indirect loss.
Additionally, oil from infected plants has a higher free fatty acid content and is darker in colour. Flowers from affected plants do not attain full size and yield few seeds. Sometimes the disease causes seedling blight, damping off, root rot or basal stem rot.
Pathogen survives as sclerotia and pycnidia in soil and crop residue. The fungus is seed borne. Plants at seed development stage are stressed and most vulnerable to infection. The disease is favoured by higher salt concentration in irrigation water, higher temperature (25-35°C) and moisture stress.
Removal and destruction of diseased plants reduces the disease intensity in the following season. Deep ploughing in summer and crop rotation are effective in reducing the disease. As the charcoal rot is associated with moisture stress and high temperature, any practice that may reduce exposure of plants to these conditions will reduce yield loss.
Early season planting or choosing an early maturing variety to escape mid-summer heat and drought are practices, which could reduce loss from the disease.
Use cultural practices that conserve soil moisture such as irrigation, weed control, reduced plant populations, and reduced tillage or no-till. Application of balanced dose of NPK fertilizers reduces the infection, as the high incidence of the disease may be due to high nitrogen and low phosphorus and potassium.
Nitrogen applied as ammonium sulphate or calcium nitrate and phosphorus as single super phosphate is reported to be effective in decreasing the incidence of the disease. Seed treatment with thiram 3-4 g/kg seed reduces the seed borne inoculum.
7. Sclerotinia Wilt and Rot Disease:
(Sclerotiniasclerotiorum (Lib.) Se Bary)
The disease was reported from all major sunflower-growing areas. The sunflower field with 60% Sclerotinia wilt infected plants reduces the seed yield by more than 70%. The major reduction in yield occurs when plants infected by the disease is due to rapid wilting and loss of leaf tissue. In northern parts of India, 10 % of the plants are killed due to Sclerotinia wilt causing a direct loss of 10% in yield.
The fungus also causes root rot and wilt, stem or stalk rot and head rot. Sclerotinia wilt generally appears during anthesis and seed development stage. Myceliogenic phase of sclerotial germination causes root-rot, stem-rot while leaf blight, stalk rot and head rot by carpogenic phase of sclerotia.
Under Indian conditions, myceliogenic phase is more active while under European conditions, carpogenic phase plays role and thus in India seed treatment with carbendazim is more effective than spray.
The fungus survives through sclerotia and mycelial strands in soil and seed. The mycelium grows saprophytically and over winters on sunflower stalks. When it comes in contact with the host plant, the fungus is indiscriminate and can invade roots at any site.
The wilt can spread through root contacts between adjacent plants. Wet soil conditions and temperature > 27°C were detrimental for survival of sclerotia, however dry soil at 5°C are favourable for sclerotial survival and viability and they can survive for 2-3 years in soil.
Generally, high soil moisture and long periods of rainfall favours the carpogenic germination of sclerotia. Sclerotia buried at 2-5 cm in the soil are capable of producing apothecia, with highest frequency of apothecial formation close to the soil surface.
Considering the soil borne and polyphagous nature of the pathogen, management of disease is still far from satisfaction. Inter specific hybrids of H. tuberosus xH. annuus and H. tuberosus x H. strumosus are reported to be resistant to stalk rot. The most promising lines were from crosses including H. Praecox ssp.runyonii, H. annuus, H. resinosus, and H. paradoxus.
Crop rotation for 3 to 5 years with non host crops reduce the sclerotia in the soil. Wide plant spacing allows air movement within crop canopy thus hastening drying of the soil and reduces the chances of infections to sunflower stalks and flower heads by ascospores. Burning of the disease infected crop debris reduces the build-up of inoculum.
Seed treatment with carbendazim at 0.1% or thiophanate-methyl 0.1% or thiram 0.25% are found to be effective for the control of the disease. Spraying of benomyl at 0.1% two times at the budding and at early flowering stage give better control of the disease.
Pre sowing flooding for 30 days, seed treatment with carbendazim at 0.2% followed by addition of Trichoderma harzianum at 2 g/kg soil and spraying of carbendazim at 0.2% after appearance of wilt proved highly effective for management of Sclerotinia wilt.
8. Powdery Mildew Disease:
(Erysiphe cichoracearum f.sp. Helianthi DC ex Meret and Sphaerotheca Fuliginea (Schlecht. ex Fr) Pollaci)
The disease occurs in great intensity in tropical areas. Pathogen survives through cleistothecia containing ascospores in the off-season and when suitable host plants are grown, the ascospores germinate to cause fresh infection.
The fungus produces conidia, which are wind disseminated causing secondary spread. The conidia are capable of germinating even under dry conditions with low humidity and hence the secondary infection takes place very rapidly.
Hyperparasite Cicinnobolus cesatii is often found to parasitize the conidial stage of the mildew. The development of cleistothecial stage of the fungus on sunflower under Indian conditions appears to be governed by the presence or absence of the hyperparasite.
During the monsoon season in the vicinity of Pune area, the mildew was parasitized by Cicinnobolus sp., preventing the formation of cleistothecia, whereas in winter season, the mildew remain free from any infection of hyperparasite and it grows rapidly leading to the formation of cleistothecia.
Powdery mildew generally occurs late enough in the crop season, hence control measures are not needed. Wild species of sunflower i.e., Helianthus debilis, H. californicus DC, H.ciliaris DC, H. decapetatus L., H. lacinatus Gray and if. rigidus (Cass.) Desf. show resistance to powdery mildew.
Application of wettable sulphur 0.2% or karathane 0.2% or propiconazole 0.1% or difenoconazole 0.05% three times at 15 days interval effectively controls the disease.
9. Head Rot Disease:
(Rhizopus Arrhizus fischer (R. Oryzar Went, R. Nodosus Man))
The disease is of importance in wet weather and causes loss in yield. Susceptibility of the flower head is increased as its age advances. Maximum rotting is noticed at the soft dough stage. Injury to the flower head is necessary for infection. Larvae of Heliothis armigera have been reported to predispose heads to infection. Rhizopus enters the head through wounds caused by hail, birds and insects.
The susceptibility of heads increases from the bud stage up to the full bloom and ripening stages. Oil from Rhizopus head rot infected seed has very much higher free fatty acid content. Disease development is most rapid in warm humid weather. In severe cases, the seeds are transformed into a black powdery mass. The spores of the fungus are carried away by the wind and infect the new host.
Injury to the head due to mechanical operation should be avoided as far as possible. Spraying of endosulphan 0.05% or diazinon 0.03% three times at 15 days interval at the onset of bloom stage is found efficient control of larvae, which causes damage to the head.
Spraying fenthion 0.1% plus thiovit 0.2% at the time of head initiation will be effective in controlling the disease. Spraying of copper-oxychloride 0.4% or mancozeb 0.3% or dichloran at completion of flowering stage reported to protect the flower head from head rot.
