Deep270 (1)

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Welcome To The Seminar Series 2020-21
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Fungicidal resistance in plant pathogens and its
remedial measures
Speaker Deep Narayan Mishra M. Sc. (Agri.) Plant
Pathology, 3rd Semester Reg. No. 2010119024
Major Guide Dr. R. K. Gangwar Associate Research
Scientist Main Rice Research Station, AAU,
Nawagam-387540
Minor Guide Dr. S. D. Patel Training Associate
(Pl. Protection) Directorate of Extension
Education, AAU Anand-388110
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CONTENT
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Fungicides
Introduction
Fungicides are substances which kills the fungal
spore or mycelium and prevent the fungal growth.
They can be used to control fungi that damage
plants, including rusts, mildews and blights.
Why are Fungicides Needed?
To control a disease during establishment of crop.
To improve the storage life and quality of
harvested plants and produce.
https//www.google.com/url
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• Fungicidal resistance refers to an acquired,
  heritable reduction in sensitivity of a fungus to
  a specific anti-fungal agent or fungicide.

• The development of fungicide resistance is a
  population evolutionary process. Fungi like other
  organisms, are constantly changing. Occasionally,
  under certain conditions, these changes provide
  an advantage in terms of the progenys ability to
  survive and reproduce.

• Recently early blight fungus has been reported to
  be less sensitive to members of the QoI-group of
  fungicides which affect single biochemical
  processes of specific pathogens.

FRAC (2014)
http/www.frac.info/resistance-overview
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• Fungicides holds a large share in agrochemical
  market in India.
• Development of resistance is mainly due to
  insufficient dose, faulty application, heavy
  disease pressure, and poor disease management.
• Among various methods, chemical control with
  fungicides still remains focused and quick
  relievers against a large group of plant
  pathogens inspite availability of novel molecular
  tools.
• Resistance to fungicides has become a challenging
  problem in the management of plant diseases and
  has threatened the performance of some highly
  potent commercial fungicides.

Potato blight has shown resistance to
phenylamides. Photo potatomuseum.com
Carboxanilide resistant
Barley loose smut
Photo I. R. Evans
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How does resistance develop?

• Origin rare genetic mutations that alter the
  target site(s) in the fungus to block the action
  of the fungicides.
• Natural selection fungicide causes selection of
  the fitted (resistant) individuals.

Source CropLife Intenational
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Fungicide risk

1. Type (s) of fungicide
2. Frequency of fungicide
3. Whether applied alone
4. Time of application

Factors affecting resistance development

1. Life cycle
2. Spore production
3. Dispersal mechanism (Soil vs wind)
4. Growth stages affected
5. Sexual stages
6. Relative fitness after mutations
7. Acclimatization

1. Climatic factors favoring disease
2. No. of applications per year
3. No. of applications targeting the same pathogen
   year after year
4. Rates used
5. Resistant cultivars
6. Irrigation
7. Sanitation

Pathogen risk
Agronomic risk
https//www.cropscience.bayer.com/
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Fig 1 Development of fungicide resistance
Deising et al. (2008)
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History of fungicidal resistance
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Table 1 HISTORY OF FUNGICIDAL
RESISTANCE
Year First observed Fungicide Class Years of comm. Use before resistance obs. Diseases and pathogens affected
1960 Aromatic Hydrocarbons (Dichloran) 20 Citrus Storage rots Penicillium spp.
1964 Organomercurials (MEMC) 40 Cereal leaf spot and stripe Pyrenophora spp.
1969 Guanidines (Dodine) 10 Apple scab Venturia inaequalis
1970 Benzimidazoles (Benomyl) 2 Many pathogens
1971 2-Amino-Pyrimidines 2 Cucumber and Barley powdery mildews
1971 Kasugamycin 6 Rice Blast
1976 Phosphorothiolates 9 Rice Blast
Conti
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Year First observed Fungicide Class Years of comm. Use before resistance obs. Diseases and pathogens affected
1977 Triphenyltins 13 Sugar beet leaf spot
1980 Phenylamides (Metalaxyl) 2 Potato blight and grape downy mildew
1982 Dicarboxiamides (Iprodione) 5 Grape grey mould
1982 DMIs (Triadimefon) 7 Cucurbit and barley downy mildews
1998 Strobilurins (Azoxystrobin) 2 Many target pathogens
2002 Melanin biosynthesis inhiobitors (Cyprodinil) 2 Rice Blast
Kaku et al. (2003)
Kikugawa (Japan)
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Table 2 INDIAN EXPERIENCE OF FUNGICIDAL
RESISTANCE
Fungicide Pathogen Host Reference
Carbendazim Venturia inequalis Apple Chaudhary et al., 1984
Gloeosporium ampelophagum Grape Kumar et al., 1992
Aspergillus flavus Groundnut Gangawane et al., 1985
Edifenphos Dreschlera oryzae Rice Annamalai et al., 1990
Pyricularia oryzae Rice Lalithakumari et al., 1987
Metalaxyl Plasmapora viticola Grape Rao et al., 1988
Phytophthora infestans Potato Arora et al., 1992 Thind et al., 2001
Pseudoperenospora cubensis Cucumber Thind et al., 2011
Oxadixyl Phytophthora infestans Potato Singh et al., 1993
Triadimefon Uncinula necator Grapoe Thind et al., 1998
Thind et al. (2011)
Ludhiana (Punjab)
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Types of Fungicidal resistance
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QUALITATIVE RESISTANCE
MULTIPLE RESISTANCE
Types of resistance
QUANTITATIVE RESISTANCE
CROSS RESISTANCE
CROSS RESISTANCE MULTIPLE RESISTANCE
Any pathogen population that is resistant to one fungicide within a group will almost certainly be resistant to other members of that same group. H. solani populations had been exposed to thiophanate fungicide (Group 1)were found also to be resistant to thiabendazole and benzimidazole (also Group 1). Any pathogen populations develop resistance to fungicides from more than one chemical group. Cucurbit powdery mildew strains have been detected with resistance to three groups of fungicides, including the QoIs, benzimidazoles and DMIs just after 2 years of intensive use.
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QUALITATIVE RESISTANCE QUANTITATIVE RESISTANCE
A quick variation in sensitivity to a fungicide with in a pathogen population. Fungicides associated are generally single site in MOA. The pathogens are either resistant or sensitive to the fungicides but never intermediate type. After attending practical resistance even higher dosage of fungicides cant control pathogens. Also known as disruptive or discrete or extremely rapid resistance. A continuous variation in sensitivity to a fungicide within a pathogen population. Fungicides associated are generally Multi site in MOA. The pathogens are of increasingly intermediate and higher degree of resistance type. Higher dosage of fungicide may control the resistant pathogens. Also known shifting-type or multistep or continuous resistance.
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Monitoring of fungicidal resistance
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• It is crucial to understand what changes the
  pathogen population may be undergoing in the
  field for which a baseline should be established
  before launching of the new active ingredient

• A profile of the sensitivity of the target fungus
  to the fungicide constructed by using biological
  or molecular techniques to assess the response
  of previously unexposed fungal individuals or
  populations to the fungicides.

Fig. A. Hypothetical example of a fungicide
baseline shown as a frequency histogram. B.
Frequency histogram showing quantitative or
shifting-type resistance. C. Early detection of
qualitative resistance. In this example, a few
isolates, which are circled in red, were detected
that fell outside the baseline. D. Qualitative
resistance after significant selection pressure
has shifted the population to a much higher mean
EC50 value.
FRAC (2014)
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Protectant Active on plant surface where they
form barrier between the plant and fungus without
penetrating the plant system
Translaminar Move through the leaf from one side
to the another
Xylem mobile Move upward in plants and outward to
periphery of leaves with water through xylem
called as acropetal movement
Fungicide categories
Amphimobile/ truly systemic Move both upward
through the xylem and downward through the phloem

Beckerman, J. (2008)
Purdue (USA)
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Table 3 MAJOR CHEMICAL CLASSES OF FUNGICIDES
ALONG WITH THEIR ACTION MECHANISM
CHEMICAL CLASS INCLUSIVE FUNGICIDES FUNGI TARGETED ACTION MECHANISM RESULTANT PHYTOTOXICITY
Triazoles propiconazol, diniconazole, ciproconazole Fusarium, Cochliobolus, Erysiphe, Altemaria Inhibit sterol Biosynthesis There is a violation of the synthesis of gibberellins
Strobilurins Picoxystrobin, fluoxastrobin, azoxystrobin, trifloxystrobin, Fusarium, Rhizoctonia, Ustilago Inhibit mitochondrial respiration by blocking electron In the plant are rapidly hydrolyzed by ether linkage
Benzimidazoles benomyl, carbendazim Sclerotmia, Septoria, Uncinula Inhibit the synthesis of ergosterol in the fungal cell . induces a considerable reduction on the chlorophyll a,b
Phenylpyrroles Fluodioxonyl Tilletia, Fusarium, Ascochyta, Fusarium disrupt the function of cell membranes Decrease CO2 assimilation
Baibakova et al. (2019)
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Biochemical action
of fungicide
Syngentaturf.com.au
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Fungicide at risk

• Those fungicides which have single site
  inhibitory action and thus act as single gene
  mutants which helps in evolving the pathogen by
  developing resistance.

FRAC Class/Code Risk Common name Trade name
Benzimidazoles (1) High thiophanate-methyl Topsin-M
Phenylamides (4) High mefenoxam Ridomil
Strobilurins (QoI) (11) High azoxystrobin, kresoxim-methyl, pyraclostrobin, trifloxystrobin Abound, Sovran, Pristine (boscalid), Flint
Dicarboximides (2) Med High iprodione Rovral
Sterol biosynthesis inhibitors (SBI) (3) Med fenarimol, myclobutanil, tebuconazole, triflumizole Rubigan, Rally, Elite, Procure
Carboximides (7) Med boscalid Endura, Pristine ( pyraclostrobin)
Anilinopyrimidins (9) Med cyprodinil, pyrimethanil Vangard, Scala
Quinolines (13) Med quinoxyfen Quintec
Hydroxyanilid (17) Med fenhexamid Elevate, CaptEvate ( captan)
FRAC (2016)
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Mechanisms of Fungicidal resistance
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1. Altered target site
A fungicide has a specific target site where it
acts to disrupt a particular biochemical process
or function which gets altered, therefore
fungicide no longer binds to it and is unable to
exert its toxic effects.
This is the most common mechanism in fungi to
become resistant
i)
ii)
iii)
A part of site is altered preventing the
fungicide from binding and hence allows
carbohydrate metabolism.
Enzyme A is necessary for carbohydrate metabolism
in fungi.
Fungicide A interferes with carbohydrate
metabolism by filling the target site of enzyme A.
Cont
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2. Detoxification
A fungus metabolized/ quickly degrade the foreign
compounds (fungicides) in to a nontoxic/
inactivated compounds before reaching to its
target site of action.
Sclerotium rolfsii against Cycloheximide which is
detoxified in to Isocycloheximide
3. Removal
A fungal cell may able to export the fungicides
rapidly before it can reach the target site of
action.
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Cont
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4. Reduced uptake
Resistant fungi simply absorbs the fungicide much
more slowly than the susceptible type.
5. Efflux transporters
Two families of plasma membrane-localized efflux
transporter are known to be involved in secretion
of toxicants, i.e. ATP-Binding Cassette (ABC) and
Major Facilitator Superfamily (MFS) Transporters.
ABC transporter has two repeats of nucleotide
binding domains and 6 trans-membrane domains
utilize the energy from hydrolysis of ATP for
transporting different natural and artificial
toxins against a concentration gradient across
the plasma membrane.
Possess a highly conserved ABC module which
displays Walker motifs and also shows a short,
highly conserved LSGGQ consensus sequence known
as linker peptide or ATP signature.
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Eg. ABC1 gene in Rice blast fungus (Magneporthe
grisea) and MgAtr1 to MgAtr5 in Mycosphaerella
graminicola in wheat.
MFS transporter has 12 trans-membrane domains and
are unable to hydrolyze ATP, however can use the
proton motive force to facilitate the transport
of not only toxicants but also sugars, peptides
and ions.
Eg. Bcmfs1 a MFS gene from botrytis cinerea
showed resistance against several fungicides
belonging to different chemical groups.
Deising et al. (2008)
Fig 2 Diagram of a fungal ABC and an
MFS-transporter
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Fungicide or fungicidal class Mechanism of resistance
1. Aromatic hydrocarbon Unknown, but show cross-resistance with dicarboximides hydrocarbons and phenyl pyrroles
2. Organo-mercurial Detoxification by binding substances
3. Dodine Unknown
4. Benzimidazole Altered target site (ß-tubulin)
5. 2-Amino-pyrimidines Unknown
6. Kasugamycin Altered target site (ribosomes)
7. Phosphorothiolates Metabolic detoxification
8. Phenylamides Altered target site (RNA polymerase)
9. Dicarboximides and Phenylpyrroles Altered target site (protein kinase involved Phenylpyrroles in osmoregulation)
10. DMIs Increased efflux altered target site decreased demand for target-site product target-site over-production
11. Carboxamides Altered target sites (succinate-ubiquinone oxidoreductase)
12. QoIs (strobilurins) Altered target sites (ubiquinol-cytochrome c reductase)
13. Melanin Biosynthesis Inhibitors (Dehydratase) Altered target sites (scytalone dehydratase)
Brent and Hollomon (2007)
Bristol (UK)
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Fungicide Resistance Action Committee (FRAC)

• Fungicide resistance action committee formed by
  the Global Crop Protection Federation in 1981 at
  Brussels. It has been instrumental in promoting
  resistance management.
• Indian Crop Protection Association (Crop Life
  india) has also set up Fungicide Resistance
  Action Committee (FRAC India) in 1999 with the
  main aim to make people aware of the problem of
  fungicide resistance and management of this
  problem.
• The purpose of FRAC is to provide fungicide
  resistance management guidelines to prolong the
  effectiveness of "at risk" fungicides and to
  limit crop losses due to resistance.

https//www.frac.info/
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Case studies
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Table 4 Competitive fitness of metalaxyl
resistant and sensitive populations of P.
infestans.
Metalaxyl (µg/ml) Disease index () with different populations Disease index () with different populations Disease index () with different populations Disease index () with different populations Disease index () with different populations
Metalaxyl (µg/ml) R S R(50) S (50) R(25) S (75) R(75) S (25)
0 86.0 85.0 74.8 74.1 75.6
10 65.3 13.4 38.5 29.3 71.1
50 49.2 0.0 31.2 23.3 46.6
100 44.2 0.0 22.1 7.2 33.5
R Resistant strain PI-24 S susceptible
strain PI-31
Ludhiana (Punjab)
Kaur et al. (2010)
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First report of Strobilurin resistance in
Cercospora beticola in sugar beet (Beta vulgaris)
in Michigan and Nebraska, USA
Cercospora leaf spot (CLS) caused by Cercospora
beticola sacc. Is the most important foliar
disease of sugar beet world wide
CLS is controlled mainly with
fungicides including strobilurins
In 2011, fields infected with CLS in Michigan,
treated with strobilurins were noted diminished
control
Individual leafspot lesions were sampled from
leaves and grown on sugar beet leaf extract agar
(SBLEA) covered with water agar amended with
pyraclostrobin, azoxystrobin or trifloxystrobin
at 0, 0.001, 0.01, 0.1, 1, 10, and 100 µg/ml
After 24 h of incubation at 22C, under ambient
light, percentage of germination of conidia was
calculated from 3 replicates/treatment
The EC50 values was found to be 0.01 µg/ml
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However, 2 isolates each of Michigan and Nebraska
were able to grow on spiral gradient dilution
plates amended with 3 strobilurins for
illustrating resistance response
Pure culture of four resistant isolates grown
in PDA and DNA was isolated
A fragment of cytochrome b gene was amplified by
PCR to amplify the region of the CYTB gene likely
to contain resistant mutations
The fragment was sequenced which showed 99
identity with both the C. beticola cyt. b mRNA,
partial sequence and C. kikuchi mitochondrial
gene for cyt. b partial sequence
All 4 isolates with G143A mutation germinated at
100 µg/ml pyraclostrobin, while the isolates
lacked mutation failed to grow
Michigan (USA)
Kirk et al. (2012)
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In vitro sensitivity and resistant to SDHI
fungicides in Alternaria solani
For molecular characterization of the succinate
dehydrogenase (SDH) complex. DNA was extracted
from the subunits B, C and D were amplified by
PCR with three different primer sets.Products
were sequenced in both directions. The sequences
obtained for every SDH subunit were assembled
into a single contiguous sequence and analysed to
identify single-site mutations using
GENEIOUS. Primers were developed to amplify two
sequence fragments surrounding two predominant
single-site mutations (H277R in the SDH subunit
B, and H133R in the SDH subunit D) present in the
SDH complex of boscalid-resistant A. solani
isolates . Unique restriction sites were
identified, using GENEIOUS, to selectively
differentiate between wildtype (sensitive) and
mutant (resistant) genotypes in the PCR product.
Poisoned-agar technique to evaluate boscalid
sensitivity of four Alternaria solani isolates
from Idaho, USA potato fields in 2010. (ad) PDA
plates amended with 1000 mg L1 boscalid (eh)
non-amended PDA control plates. The observable
growth of isolates AS5 and AS4 on the
boscalid-amended plates demonstrates in vitro
resistance.
Miles et al. (2014)
Aberdeen (USA)
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First Report of QoI Resistance in Downey mildew
(Plasmopara viticola) from Vineyards of
Maharashtra, India
3-Pune
6- Sangli
1-Mizoram
5-Nashik
The sensitivity to QoI fungicides determined
using Leaf Disk Bioassay with 0, 1, 10, 50, 100
and 1000 µg/ml of azoxystrobilin inoculated with
10 µg/ml of spore suspension
The EC50 Value were calculated by using of
inhibition vs fungicide concentration and was
found lt0.13 µg/ml for untreated samples and gt110
µg/ml for fungicide treated samples
DNA was isolated from the resistant isolates from
pure culture and nested PCR-RFLP was conducted
The Nested PCR-RFLP revealed that there is
Guanine to Alanine substitution at 143 condon
which is responsible for the QoI resistance
(Furuya et al., 2009)
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Sawant et al. (2016)
Maharashtra
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Table 5 Average fungicide effective
concentration required to inhibit mycelial growth
by 50 (EC50) in Argentinian isolates of
Cercospora sensitive to DMI and carbendazim
(MBC), resistant to QoI and insensitive to SDHI
and mancozeb
Active ingredient Mode ofaction No. of isolates tested EC50(µg/ml)
Difenoconazole DMI 32 0.027 a
Carbendazim MBC 19 0.048 ab
Prothioconazole DMI 32 0.157 b
Epoxiconazole DMI 32 0.154 b
Tebuconazole DMI 32 0.602 c
Cyproconazole DMI 32 0.889c
Azoxystrobin QoI 62 gt100
Pyraclostrobin QoI 62 gt100
Trifloxystrobin QoI 62 gt100
Boscalid SDHI 62 gt100
Pydiflumetofen SDHI 62 gt100
Fluxapyroxad SDHI 62 gt100
Mancozeb Multisite 62 gt100
Note Means followed by the same letter do not
significantly differ as determined by
KruskalWallis one-way analysis of variance
followed by Dunn's multiple comparison test. All
62 Argentinian isolates were completely resistant
or insensitive to QoI and SDHI fungicides,
respectively.
Sautua et al. (2020)
Buenos Aires (Argentina)
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Framework for the assessment of risk of the
development of resistance during commercial use
of a new fungicide
Factor Positive indication of resistance risk
1. Fungicide associated 1. Fungicide associated
Fungicide class When the test fungicide is a member of a chemical class which has a record of resistance problems
Site of action in target pathogen If there is a single site of action or if the site is known to be capable of change to a form that is unaffected or less affected by other fungicides
Cross-resistance If there are target pathogen strains resistant to existing fungicides which also resist the test fungicide
Response to mutagenic agents If treatment with mutagenic agents causes the target pathogen to produce resistant
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Cont
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Factor Positive indication of resistance risk
2. Pathogen associated 2. Pathogen associated
Generation time If multiplication cycles of the target pathogen and fungicide applications are frequent
Amount of sporulation If sporulation of the pathogen is abundant
Spore dispersal If spores spread readily between plants, crops and regions
Cont
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Factor Positive indication of resistance risk
3. Conditions of use (locally determined) 3. Conditions of use (locally determined)
Application of the fungicide Fungicide applications will be repetitive
Complementary measures Integrated management methods e.g. crop rotation, resistant varieties are not used
Pathogen incidence Presence in large amounts or rapid multiplication
Pathogen isolation Confined preventing re-entry of sensitive forms
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Management of fungicidal resistance
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• LIMITATION
• Limiting the number of applications

• PREVENTION
• Spraying fungicide before infection can prevent
  the infection happening

• MIXTURE
• Using a combinations of types of chemicals helps
  to avoid resistant mutation multiplying

• MONITORING
• To determine fungicides efficacy and for signs of
  failure

Management of fungicidal resistance

• IDM
• Combining conventional chemical fungicides with
  bio-fungicides and host plant resistance by
  conventional plant breeding or GM technology

• ALTERNATION
• Alternating fungicides types provides more
  chances to kill the mutant strains

FRAC (2010)
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Fig 3 Dose response of famoxadone, azoxystrobin,
folpet, mancozeb and fosetyl-aluminium for the
control of Plasmopara viticola in a whole plant
bioassay.
Nambsheim (France)
Genet et al. (2006)
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Main principle for management
includes..
1. Integration with cultural practices

• Appropriate cultural practices along with optimum
  fungicide use patterns can effectively retard
  development of resistance in a pathogen
  population.
• The desired result is to minimize selection
  pressure through a reduced in time of exposure or
  the size of the population exposed to the at-risk
  fungicide.
• Cultural practices and fungicide use patterns
  that reduces disease pressure and selection for
  fungicide resistance.

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Table 7 Cultural practices and fungicide
use patterns
Strategy Result
Use resistant varieties Lower disease increase rate
Maintain proper soil fertility Reduces disease incidence
Avoid sites with high disease pressure Avoids high selection
Crop rotation Reduces pathogen population
Sanitation Reduces pathogen population
Fungicide use patterns Fungicide use patterns
Use only when justified Avoids unnecessary selection
Use protectively Hits small population
Alternate fungicides from different group Reduces selection time
No. soil application against foliar diseases Reduces selection time
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2. Avoiding sole use of at risk fungicides

• Combination of site specific at risk fungicide
  with multisite action compatible fungicide.
• E.g. Metalaxyl and Mancozeb, Cymoxanil and
  Mancozeb, Mancozeb and Carbendazim.
• Such combination products are widely used for
  disease control in fruits, vegetables and cereals
  and have helped in resistance development in
  pathogens.
• Alteration of at risk site specific fungicides
  with multisite fungicides or compounds with novel
  mode of action.

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Table 8 Resistance risk of spray programmes
Programme sequence Programme type Risk
H-H-H-H Repeat High
H-L-H-L Alternation Low
(HL)-(HL)-(HL)-(HL) Mixture Low
(HL)-H-(HL)-L Combination Low
L-L(HL)-L Combination Low
H- Fungicide at risk L- Partner fungicide
https//www.frac.info/docs/
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3. Reduction in number of applications

• The other non risky fungicides should be used
  subsequently to get desirable disease control.
• Number of applications restricted to minimum per
  season to avoid unnecessary selection.
• Multiple applications of fungicides with same
  mode of action should be avoided.

4. New fungicides with
novel target sites

• Effective at low dose rates.
• Eco-friendly.
• Less residue problem.
• Less chances of cross resistance because of novel
  modes of action.
• Less hazard to human and animals.

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5. Integrated disease management

• Integrated disease management (IDM) and reduction
  in the use of fungicides is the superior strategy
  to avoid resistance problem.
• The use of resistant varieties, alteration of
  cultural practices, water management,
  phytosanitory measures, biological control etc.
  have been included.
• Changes in spray programme, use of fungicides in
  combination, alteration of fungicides having no
  cross resistance.

6. Application of
recommended dose

• It is advisable to use the at risk fungicide as
  per manufacturers recommended dose rate.
• Many farmers have regularly used reduced rates of
  application of fungicides, mainly to reduce
  costs, particularly in circumstances where
  disease pressures are usually low, or where the
  risk of financial loss from reduced performance
  was not immense.

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7. Negative cross resistance

• Combination of fungicides with a different modes
  of action allows one compound to eliminate
  strains resistant to other compound (Hewitt,
  1998).
• Compounds showing negative cross resistance
  appears more toxic to resistant strains than wild
  type strains in the population.

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Conclusion
Fungicidal resistance in pathogen leads to
failure of disease control measures. Pathogens
develop different mechanism of fungicidal
resistance namely altered target site,
detoxification of the metabolism, removal,
reduced uptake, efflux transporters. Development
of resistance in P. infestans (strain PI-24)
against fungicide metalaxyl as compared to
sensitive (strain PI-31). Fungicides that act at
a single site are more prone to resistance
development. Single point mutation found at 143
codon of P. viticola developed resistance against
QoI fungicides.
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Future thrust
Need to

• rotate fungicide products with a different mode
  of action to prevent over-use
• develop disease forecasting models and need based
  fungicides application
• conduct molecular level studies to understand
  mechanism of resistance
• develop integrated disease management module

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Where there is power, there is resistance
Michel foucault
Thank you. . .
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