This document discusses fungicide resistance in plant pathogens. It notes that fungicides have been used for over 200 years, but resistance has increased with repeated use of systemic fungicides. Resistance arises from genetic variability and selection pressure from fungicide use. Mechanisms of resistance include altered target sites, detoxification, removal of the fungicide from cells, and reduced uptake. Examples are given of resistance to different classes of fungicides like benzimidazoles, carboxamides, phenylamides, and demethylation inhibitors. Managing resistance involves integrating different control methods and fungicide classes in a program to reduce selection pressure for resistance.

1. FUNGICIDE
RESISTANCE IN
PLANT
PATHOGENS
NUSRATH BEEGUM C.H
2015-11-105
1

2. Introduction
 Fungicides have been used for over 200 years to protect
plants against disease
 With the introduction of the systemic fungicides, the
incidence of resistance increased greatly
 Repeated use of the fungicide
 Once it arises, resistance is heritable
 Mechanism of resistance may or may not related to
fungicidal action
 B. cinerea was one of the first fungi for which
resistance was described
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3. Stable , inheritable adjustment by a fungus to
a fungicide, resulting in a less than normal
sensitivity to that fungicide
(FAO)
3

4. Resistance risk
 Single site of action in the target fungus
 Cross-resistance with existing fungicides
 Facile generation of fit, resistant mutants
in the laboratory
 Use of repetitive or sustained treatments
in practice
 Extensive areas of use
 Large populations and rapid multiplication
of target pathogen
 No complementary use of other types of
fungicide
 Lack of non-chemical control measures
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5. 5
Carboxanilide resistant Loose
smut (Ustilago)

6. Basic process of resistance
development
Resistance can only develop in spore populations
where there is the genetic potential to resist the
disease
Resistant spores occur at extremely low numbers
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7. When a fungicide spray is applied
some of the sensitive spores also
survived, because they “escaped”
the fungicide treatment
This can result from incomplete spray
coverage
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8. If environmental conditions favour continued
disease activity, the surviving spores grow and
produce a new crop of spores
This spores has a higher percentage of resistant
spores
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9. Mechanisms
Altered target site:
o A fungicide has a specific
target site where it acts
to disrupt a particular
biochemical process
o If this site altered
fungicide no longer binds
to site of action and
unable to exert its toxic
effect
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10. Detoxification or
metabolism:
o Metabolism within the
fungal cell
o Detoxify a foreign
compound such as
fungicide
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11. Removal:
o A fungal cell may rapidly
export the fungicide
before it can reach the
site of action
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12. Reduced uptake :
o The resistant pathogen
simply absorbs the fungicide
much more slowly than the
susceptible type
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13. 1. Genetic variability: The fungus has spores
with the genes necessary to resist the
toxin
2. Selection: The toxin is used repeatedly
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14. Benzimidazoles and
Thiophnates
Carbendazim
 It binds to tubulins
 Inhibit the assembly of microtubules and
formation of spindle
 Leads to general disturbance of cellular
function
 Eg: Benomyl resistance in cucumber
powdery mildew
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15.  Mutation - at loci ben A, ben B, ben C
 Changes in tubulin structure which enables
microtubule to function in the presence
of benzimidazoles
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16. Carboxamides
 Vitavax, plantvax, calirus, panorm, basizac
 Seed treatment- cereals
 Leaf rust
Site of action – mitochondria
 Interferes with respiration by specific inhibition of
succinate
Resistance –
 chrysanthemum rust
 Ustilago mydis
Mutation - change at the target site in the succinate
dehydrogenase complex
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17. Phenylamide
 Metalxyl, furalaxyl, benalaxyl
 systemic activity against oomycetes
Inhibition of the RNA polymerase enzyme
 Ribosomal RNA is selectively inhibited
 Metalaxyl resistance- Phytophothora infestans
 Mutation – uridine incorporation into RNA
 Chandge in target site
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18. Demethylation Inhibitors
(DMI)
 Triadimefon, propiconazol, flusilazol,
penconazol
 Powdery mildew, rust
Mode of action: Inhibit ergosterol
biosynthesis
 Site of action – sterol 14 ᶛ- demethylation
 Polygenic resistance
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19. Organophosphorus
 Pyrazophos, edefenphos, kitazin P
 Metabolite of pyzarophos is the fungitoxic
principle
 Resistance- inability of the strains to
convert pyrazophos to toxic compound
 Rice blast(Pyricularia oryzae) in japan
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20. Build up of resistant pathogen population
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21. The type of fungicide
1. Monogenic or polygenic resistance
 Monogenic- develops in one step
 Highest level of resistance
 More than one locus involved
 Polygenic- many mutant genes are
required
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22. 2.Fitness of resistant strains
 Genetic changes in sensitive cell influence
other characteristics of the cell
 Strains with lower fitness will be less
competitive
 Slow down the build up of a resistant
pathogen population
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23. Nature and life cycle of the pathogen
 Build up will be faster in heavily
sporulating pathogen on aerial parts
 Late blight (Phytophthora infestans) faster
than avocado root disease(P.cinnamomi)
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24. Selection pressure by the fungicide
 Continuous high selection pressure favour
build up of resistant population
 High doses of fungicide, frequency,
method of application , persistence of the
fungicide
Environmental factors
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25. Management
 Do not use the product exclusively
 Apply it as a mixture with one
 More fungicides of a different type
 As one component in a rotation or
alternation of different fungicide
treatments
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26.  Use other fungicides both beforehand and
subsequently
 Reduces the total number of applications
of the at-risk fungicide
 slow down selection to some extent
 It can favour decline of resistant strains
that have a fitness deficit
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27.  Restrict the number of treatments applied
per season, and apply only when strictly
necessary
 Maintain manufacturers’ recommended
dose
 Avoid eradicant use
 Integrated disease management
 Chemical diversity
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28. FARC
 In 1994 the Fungicide Resistance Action
Committee (FRAC)
 FRAC is a Specialist Technical Group of
CropLife International
 To provide fungicide resistance
management guidelines to prolong the
effectiveness of "at risk" fungicides and to
limit crop losses
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29. Reference
 Altman, J., 1993. Pesticide Interactions In
Crop Production- Beneficial And
Deleterious Effects. Boca raton ann arbor.
London
 Brent , K. J. and Holloman, W. D., 2007.
Fungicide Resistance In Crop Pathogens:
How Can It Be Managed?. FARC
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