Sheath blight of rice caused by Rhizoctonia solani and its management

1. ANNAMALAI UNIVERSITY
FACULTY OF AGRICULTURE
DEPARTMENT OF PLANT PATHOLOGY
Sheath blight of rice caused by Rhizoctonia
solani(kuhn)
M.Yuvaraj,
Msc.Agri (Plant Pathology) I year

2. INTRODUCTION
Rhizoctonia is derived from the two greek word
(rhiza=root,ktonos=murder/killing).
It has a wide host range of about 250 plant species
belonging to Poaceae, Malvaceae etc.,
In India it is reported on 62 economically important
plant and 20 families of weed.

3. Important crops affected by Rhizoctonia sp
Black scurf of potato Web blight of soyabean Root rot of sugar beet
Belly rot of cucumber Stem rot of crossandra Brown patch of truf
grasses

4. Sheath blight of Rice- Rhizoctonia
solani(kuhn)
J.G.Kuhn 1st reported R.solani in potato causing Black
scurf in 1898.
The disease was 1st reported in Rice from Japan in 1910
by Miyake.
In India the disease was 1st reported in Gurdaspur
district of Punjab by Paracer and chahal in 1963

5. INTRODUCTION
It is soil borne necrotrophic pathogen which causes yield
loss upto 50%.
R.solani is assigned into 14 anastomosis group(AG1-AG13
and AGB1)
Anastomosis – Fusion of hyphae
R.solani causing Sheath blight belong to AG1 group of
which subgroup AG1-IA.

6. They live in soil as dormant structure called Sclerotia
Sclerotia are nothing but aggregation of hyphae
Dark on outside and dull white inside made up of
prosenchyma and pseudoparenchyma cells.
Melanin – protect from UVrays
R.solani sclerotia are irregular and dark brown in
colour.
Pathogen entry though stomata by infection cushion

8. Causal organism:
Anamorphic stage – Rhizcotonia solani(Kuhn)
Telomorphic stage – Thanatephorus cucumeris(Frank)
Systmatic position:
Domain: Eukaryota
Kingdom: Fungi
Division: Basidiomycota
Class: Agaricomycetes
Order: Cantharellales
Family: Ceratobasidiaceae
Genus: Rhizoctonia
Species: R. solani

9. Symptoms

10. Disease cycle

11. Cultural and morphological Characteristics
of R.solani
Hyphae of R.solani have right – angled branches.
Stained with 0.05% lactophenol blue and examine for the
morphological characters.
The nuclei of the R.solani is stained by DAPI(4’,6
diamidino-2-phenylindole) stain.
Sclerotia are develop from middle to edges of the plate,
initially light to dark brown later black in colour

12. 0.05% Lactophenol blue DAPI Stain
Typical right angles branches

13. Mode of spread and epidemiology
 Primary spread – Crop debris, Sclerotia.
 Secondary spread –Irrigation water, Basidiospores
Temperature – 25 to 30 degree celcius.
Relative humidity – 80 to 100%.
The disease is more in sandy than clay soils.
PH – 6 to 7 for mycelial and sclerotial formation.

14. Pathogenecity factors
1.Effector proteins
2.Secondary metabolites
3.Carbohydrate active enzymes
1.Effector proteins
AG1 IA 09161- Glycosyl transferase, cytochrome oxidase
and pepdidase can cause cell death in rice.
Some of the effectors which inhibit the chitin triggered
immunity (Effector protein interfere with PAMP)

15. 2.Secondary metabolites
Host specific toxin
Biologically active molecules
a) Oxalic acid-Inhibits the synthesis of various phenolic
substances and cell wall degradation.
b) PAA-inactivates traumatin while inhibit the precursor
of jasmonic acid.
c) MTPA(3-methyl thiopropionic acid) – Mycelial
production and promotes disease progession.

16. 3. Carbohydrate Active Enzymes
CAZymes- degrade cellulose,hemicellulose and pectin
in host cell wall and break down physical barrier of
plant immune system.
Cellulose -cellulase and polysaccharide lyases.
Pectin – Polygalacturonase .
Hemicellulose – endo-1,4 beta-xylanase.

17. Countermeasures from host
1.PAMP PRR PTI
2.ETI
Reactive Oxygen species
 Initiate plant defense response like Phytoalexin
biosynthesis, activation of defense related genes and
callose dopsition in cell wall.
 H2O2 activates Phenyl Ammonia lyase biosynthesis
of lignin and result in thickening of cell wall.

18. Phytohormones
 SA - Biotrophs
 JA and Ethylene – Necrotrophs
 The overexpression of ethylene response factor which
resistant to RSB.
 Auxins applications enhance rice resistance to sheath
blight.
Transcription factors
 NAC,WRKY and bZIP regulates expression of various
defense genes.

19. MANAGEMENT
Cultural practices
 Wider spacing reducing disease severity
 Avoid excess doses of nitrogenous fertilizers
 Potassium and silicon application helps in reduces
disease severity.
 Avoid the flow of irrigation water from infected to
healthy fields.
 Summer ploughing.

20. Chemical control
 Apply fungicides at initiation of booting stage.
 Timely application of fungicides between panicle
differentiation and heading stage.

21. Chemical
Group
Active
Ingredients
Trade name Target site Dosage(g/ha)
Strobilurin Azoxystrobin23
%EC
Amistar Respiration –
Inhibition of
cytochrome
125
Kresoxy-methyl Sovran 250
Trifloxystrobin Flint 150
Triazole Difenoconazole
25%EC
Score Sterol
biosynthesis in
cell membrane
50
Hexaconazole
5%EC
Cursor 120
Tebuconazole2
5.9%EC
Folicure 187.5
Benzimidazoles Carbendazim50
%EC
Bavistin Cytoskeleton-
assembling of
beta-tubulin
during mitosis
250

22. Biological control
Actinomycetes
 Streptomyces spp. is reported to reduce the growth of
R.solani upto 50% and disease suppression upto53.3%.
 Ethyl acetate extracted from Streptomyces
diastatochromogenes, which inhibit mycelial growth
and sclerotia formation.

23. Fungi BCA
 The genera such as Trichoderma, Aspergillus,
Gliocladium, Chaetomium were used as BCA.
 Trichoderma and Gliocladium are widely used to
manage RSB.
 Trichoderma harzianum gives high yield and grain
weight with recommended dose of 4-8g/l.
 Trichoderma have been reported to inhibit R.solani
growth by 71% and reduce sheath blight infestation
upto 59%.

24. Bacterial BCA
 PGPR – root growth, phosphate solubilization,
nitrogen uptake, iron chelating seiderophores and
phytohormones.
 Pseudomonas fluorescence help to increase chitinase
activity for suppression of pathogen.
 Bacillus produce the antibiotics such as bacillomyxin
L and fengycin A compunds from Bacillus velezensis
inhibit mycelial growth of R.solani.

25. Resistance
1.Silencing essential pathogenicity genes via RNA
interference in fight against R.solani.
2.Targeting the essential pathogenicity factors in R.solani
via transgenic technology.
3.Quantitative trait loci.

29. THANK YOU