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Fungicide

December 07, 2023

Fungicides are pesticides used to kill parasitic fungi or their spores.[1] They are most commonly chemical compounds, but may include biocontrols and fungistatics. Fungi can cause serious damage in agriculture, resulting in critical losses of yield, quality, and profit. Fungicides are used both in agriculture and to fight fungal infections in animals. Fungicides are also used to control oomycetes, which are not taxonomically/genetically fungi, although sharing similar methods of infecting plants.[2] Fungicides can either be contact, translaminar or systemic. Contact fungicides are not taken up into the plant tissue and protect only the plant where the spray is deposited. Translaminar fungicides redistribute the fungicide from the upper, sprayed leaf surface to the lower, unsprayed surface. Systemic fungicides are taken up and redistributed through the xylem vessels. Few fungicides move to all parts of a plant. Some are locally systemic, and some move upward.[3]

Most fungicides that can be bought retail are sold in liquid form. A very common active ingredient is sulfur,[4] present at 0.08% in weaker concentrates, and as high as 0.5% for more potent fungicides. Fungicides in powdered form are usually around 90% sulfur and are very toxic. Other active ingredients in fungicides include neem oil, rosemary oil, jojoba oil, the bacterium Bacillus subtilis, and the beneficial fungus Ulocladium oudemansii.

Fungicide residues have been found on food for human consumption, mostly from post-harvest treatments.[5] Some fungicides are dangerous to human health, such as vinclozolin, which has now been removed from use.[6] Ziram is also a fungicide that is toxic to humans with long-term exposure, and fatal if ingested.[7] A number of fungicides are also used in human health care.

Types edit

Further information: List of fungicides

Fungicides can be classified according to their mechanism of action (MOA), specifically the biological process or target site they block. The Fungicide Resistance Action Committee (FRAC) assigns chemicals into classes according to MOA and subdivides these according to similarities in their structure.[8] Examples of commercial fungicides within each class are given below.

Nucleic acid metabolism edit

Cytoskeleton and motor proteins edit

Respiration edit

Amino acid and protein synthesis edit

Signal transduction edit

Lipid synthesis / membrane integrity edit

Melanin synthesis in cell wall edit

  • tricyclazole

Sterol biosynthesis in membranes edit

Cell wall biosynthesis edit

Host plant defence induction edit

Chemicals with multi-site activity edit

Mycoviruses edit

Some of the most common fungal crop pathogens are known to suffer from mycoviruses, and it is likely that they are as common as for plant and animal viruses, although not as well studied. Given the obligately parasitic nature of mycoviruses, it is likely that all of these are detrimental to their hosts, and thus are potential biocontrols/biofungicides.[10]

Resistance edit

See also: Antimicrobial resistance

Pathogens respond to the use of fungicides by evolving resistance. In the field, several mechanisms of resistance have been identified. The evolution of fungicide resistance can be gradual or sudden. In qualitative or discrete resistance, a mutation (normally to a single gene) produces a race of a fungus with a high degree of resistance. Such resistant varieties also tend to show stability, persisting after the fungicide has been removed from the market. For example, sugar beet leaf blotch remains resistant to azoles years after they were no longer used for control of the disease. This is because such mutations have a high selection pressure when the fungicide is used, but there is low selection pressure to remove them in the absence of the fungicide.

In instances where resistance occurs more gradually, a shift in sensitivity in the pathogen to the fungicide can be seen. Such resistance is polygenic – an accumulation of many mutations in different genes, each having a small additive effect. This type of resistance is known as "quantitative" or "continuous" resistance. In this kind of resistance, the pathogen population will revert to a sensitive state if the fungicide is no longer applied.

Little is known about how variations in fungicide treatment affect the selection pressure to evolve resistance to that fungicide. Evidence shows that the doses that provide the most control of the disease also provide the largest selection pressure to acquire resistance, and that lower doses decrease the selection pressure.[11]

In some cases when a pathogen evolves resistance to one fungicide, it automatically obtains resistance to others – a phenomenon known as cross resistance. These additional fungicides typically belong to the same chemical family, act in the same way, or have a similar mechanism for detoxification. Sometimes negative cross-resistance occurs, where resistance to one chemical class of fungicides increases sensitivity to a different chemical class of fungicides. This has been seen with carbendazim and diethofencarb.

There are also recorded incidences of the evolution of multiple drug resistance by pathogens – resistance to two chemically different fungicides by separate mutation events. For example, Botrytis cinerea is resistant to both azoles and dicarboximide fungicides.

There are several routes by which pathogens can evolve fungicide resistance. The most common mechanism appears to be alteration of the target site, particularly as a defense against a single site of action fungicides. For example, Black Sigatoka, an economically important pathogen of banana, is resistant to the QoI fungicides, due to a single nucleotide change resulting in the replacement of one amino acid (glycine) by another (alanine) in the target protein of the QoI fungicides, cytochrome b.[12] It is presumed that this disrupts the binding of the fungicide to the protein, rendering the fungicide ineffective. Upregulation of target genes can also render the fungicide ineffective. This is seen in DMI-resistant strains of Venturia inaequalis.[13]

Resistance to fungicides can also be developed by efficient efflux of the fungicide out of the cell. Septoria tritici has developed multiple drug resistance using this mechanism. The pathogen had five ABC-type transporters with overlapping substrate specificities that together work to pump toxic chemicals out of the cell.[14]

In addition to the mechanisms outlined above, fungi may also develop metabolic pathways that circumvent the target protein, or acquire enzymes that enable the metabolism of the fungicide to a harmless substance.

Fungicide resistance management edit

The Fungicide Resistance Action Committee (FRAC)[15] has several recommended practices to try to avoid the development of fungicide resistance, especially in at-risk fungicides including Strobilurins such as azoxystrobin.[15] FRAC assigns groups of fungicides into classes where cross-resistance is likely, usually because the active ingredients share a common mode of action.[16] FRAC is organized by CropLife International.[17][15]

Products should not always be used in isolation, but rather as mixture, or alternate sprays, with another fungicide with a different mechanism of action. The likelihood of the pathogen's developing resistance is greatly decreased by the fact that any resistant isolates to one fungicide will be killed by the other; in other words, two mutations would be required rather than just one. The effectiveness of this technique can be demonstrated by Metalaxyl, a phenylamide fungicide. When used as the sole product in Ireland to control potato blight (Phytophthora infestans), resistance developed within one growing season. However, in countries like the UK where it was marketed only as a mixture, resistance problems developed more slowly.

Fungicides should be applied only when absolutely necessary, especially if they are in an at-risk group. Lowering the amount of fungicide in the environment lowers the selection pressure for resistance to develop.

Manufacturers’ doses should always be followed. These doses are normally designed to give the right balance between controlling the disease and limiting the risk of resistance development.[citation needed] Higher doses increase the selection pressure for single-site mutations that confer resistance, as all strains but those that carry the mutation will be eliminated, and thus the resistant strain will propagate. Lower doses greatly increase the risk of polygenic resistance, as strains that are slightly less sensitive to the fungicide may survive.

It is better to use an integrative pest management approach to disease control rather than relying on fungicides alone. This involves the use of resistant varieties and hygienic practices, such as the removal of potato discard piles and stubble on which the pathogen can overwinter, greatly reducing the titre of the pathogen and thus the risk of fungicide resistance development.

See also edit

References edit

  1. ^ Haverkate, F.; Tempel, A.; Held, A. J. (1969). "Interaction of 2,4,5-trichlorophenylsulphonylmethyl thiocyanate with fungal spores". Netherlands Journal of Plant Pathology. 75 (5): 308–315. doi:10.1007/BF02015493. S2CID 23304303.
  2. ^ Latijnhouwers, Maita; de Wit, Pierre; Govers, Francine (2003). "Oomycetes and fungi: similar weaponry to attack plants". Trends in Microbiology. Cell Press. 11 (10): 462–469. doi:10.1016/j.tim.2003.08.002. ISSN 0966-842X. PMID 14557029. S2CID 22200121.
  3. ^ Mueller, Daren. "Fungicides:Terminology". Iowa State University. Retrieved June 1, 2013.
  4. ^ C.Michael Hogan. 2011. Sulfur. Encyclopedia of Earth, eds. A.Jorgensen and C.J.Cleveland, National Council for Science and the environment, Washington DC October 28, 2012, at the Wayback Machine
  5. ^ Pesticide Chemistry and Bioscience edited by G.T Brooks and T.R Roberts. 1999. Published by the Royal Society of Chemistry
  6. ^ Hrelia et al. 1996 - The genetic and non-genetic toxicity of the fungicide Vinclozolin. Mutagenesis Volume 11 445-453
  7. ^ National Center for Biotechnology Information. PubChem Compound Database; CID=8722, https://pubchem.ncbi.nlm.nih.gov/compound/8722 (accessed Jan. 13, 2019)
  8. ^ "FRAC Classification of Fungicides" (PDF). CropLife International. 2022-04-21.
  9. ^ Thao, Hoang Thi Bich; Yamakawa, Takeo (April 2009). "Phosphite (phosphorous acid): Fungicide, fertilizer or bio-stimulator?". Soil Science and Plant Nutrition. 55 (2): 228–234. Bibcode:2009SSPN...55..228T. doi:10.1111/j.1747-0765.2009.00365.x.
  10. ^ PEARSON, MICHAEL N.; BEEVER, ROSS E.; BOINE, BARBARA; ARTHUR, KIEREN (2009). "Mycoviruses of filamentous fungi and their relevance to plant pathology (Review)". Molecular Plant Pathology. British Society for Plant Pathology (Wiley-Blackwell). 10 (1): 115–128. doi:10.1111/j.1364-3703.2008.00503.x. ISSN 1464-6722. PMC 6640375. PMID 19161358. S2CID 34331588.
  11. ^ Metcalfe, R.J. et al. (2000) The effect of dose and mobility on the strength of selection for DMI (sterol demethylation inhibitors) fungicide resistance in inoculated field experiments. Plant Pathology 49: 546–557
  12. ^ Sierotzki, Helge (2000) Mode of resistance to respiration inhibitors at the cytochrome bc1 enzyme complex of Mycosphaerella fijiensis field isolates Pest Management Science 56:833–841
  13. ^ Schnabel, G., and Jones, A. L. 2001. The 14a-demethylase (CYP51A1) gene is overexpressed in V. inaequalis strains resistant to myclobutanil. Phytopathology 91:102–110.
  14. ^ Zwiers, L. H. et al. (2003) ABC transporters of the wheat pathogen Mycosphaerella graminicola function as protectants against biotic and xenobiotic toxic compounds. Molecular Genetics and Genomics 269:499–507
  15. ^ a b c "Fungicides Resistance Action Committee website".
  16. ^ (PDF). 2020. Archived from the original (PDF) on 2021-08-16. Retrieved 2020-09-04.
  17. ^ "Resistance Management". CropLife International. 2018-02-28. Retrieved 2020-11-22.

External links edit

  • Fungicide Resistance Action Committee
  • , United Kingdom
  • General Pesticide Information 2007-12-29 at the Wayback Machine - National Pesticide Information Center, Oregon State University, United States

December 07, 2023
fungicide, pesticides, used, kill, parasitic, fungi, their, spores, they, most, commonly, chemical, compounds, include, biocontrols, fungistatics, fungi, cause, serious, damage, agriculture, resulting, critical, losses, yield, quality, profit, used, both, agri. Fungicides are pesticides used to kill parasitic fungi or their spores 1 They are most commonly chemical compounds but may include biocontrols and fungistatics Fungi can cause serious damage in agriculture resulting in critical losses of yield quality and profit Fungicides are used both in agriculture and to fight fungal infections in animals Fungicides are also used to control oomycetes which are not taxonomically genetically fungi although sharing similar methods of infecting plants 2 Fungicides can either be contact translaminar or systemic Contact fungicides are not taken up into the plant tissue and protect only the plant where the spray is deposited Translaminar fungicides redistribute the fungicide from the upper sprayed leaf surface to the lower unsprayed surface Systemic fungicides are taken up and redistributed through the xylem vessels Few fungicides move to all parts of a plant Some are locally systemic and some move upward 3 Most fungicides that can be bought retail are sold in liquid form A very common active ingredient is sulfur 4 present at 0 08 in weaker concentrates and as high as 0 5 for more potent fungicides Fungicides in powdered form are usually around 90 sulfur and are very toxic Other active ingredients in fungicides include neem oil rosemary oil jojoba oil the bacterium Bacillus subtilis and the beneficial fungus Ulocladium oudemansii Fungicide residues have been found on food for human consumption mostly from post harvest treatments 5 Some fungicides are dangerous to human health such as vinclozolin which has now been removed from use 6 Ziram is also a fungicide that is toxic to humans with long term exposure and fatal if ingested 7 A number of fungicides are also used in human health care Contents 1 Types 1 1 Nucleic acid metabolism 1 2 Cytoskeleton and motor proteins 1 3 Respiration 1 4 Amino acid and protein synthesis 1 5 Signal transduction 1 6 Lipid synthesis membrane integrity 1 7 Melanin synthesis in cell wall 1 8 Sterol biosynthesis in membranes 1 9 Cell wall biosynthesis 1 10 Host plant defence induction 1 11 Chemicals with multi site activity 1 12 Mycoviruses 2 Resistance 2 1 Fungicide resistance management 3 See also 4 References 5 External linksTypes editFurther information List of fungicides Fungicides can be classified according to their mechanism of action MOA specifically the biological process or target site they block The Fungicide Resistance Action Committee FRAC assigns chemicals into classes according to MOA and subdivides these according to similarities in their structure 8 Examples of commercial fungicides within each class are given below Nucleic acid metabolism edit bupirimate metalaxylCytoskeleton and motor proteins edit carbendazim pencycuronRespiration edit azoxystrobin binapacryl boscalid carboxin cyazofamid pydiflumetofenAmino acid and protein synthesis edit blasticidin S kasugamycin pyrimethanilSignal transduction edit fludioxonil procymidoneLipid synthesis membrane integrity edit propamocarb pyrazophos tecnazeneMelanin synthesis in cell wall edit tricyclazoleSterol biosynthesis in membranes edit fenpropimorph hexaconazole imazalil myclobutanil propiconazoleCell wall biosynthesis edit dimethomorph polyoxinsHost plant defence induction edit acibenzolar fosetyl Al phosphorous acid 9 Chemicals with multi site activity edit chlorothalonil copper mancozeb sulfur zinebMycoviruses edit Some of the most common fungal crop pathogens are known to suffer from mycoviruses and it is likely that they are as common as for plant and animal viruses although not as well studied Given the obligately parasitic nature of mycoviruses it is likely that all of these are detrimental to their hosts and thus are potential biocontrols biofungicides 10 Resistance editSee also Antimicrobial resistance Pathogens respond to the use of fungicides by evolving resistance In the field several mechanisms of resistance have been identified The evolution of fungicide resistance can be gradual or sudden In qualitative or discrete resistance a mutation normally to a single gene produces a race of a fungus with a high degree of resistance Such resistant varieties also tend to show stability persisting after the fungicide has been removed from the market For example sugar beet leaf blotch remains resistant to azoles years after they were no longer used for control of the disease This is because such mutations have a high selection pressure when the fungicide is used but there is low selection pressure to remove them in the absence of the fungicide In instances where resistance occurs more gradually a shift in sensitivity in the pathogen to the fungicide can be seen Such resistance is polygenic an accumulation of many mutations in different genes each having a small additive effect This type of resistance is known as quantitative or continuous resistance In this kind of resistance the pathogen population will revert to a sensitive state if the fungicide is no longer applied Little is known about how variations in fungicide treatment affect the selection pressure to evolve resistance to that fungicide Evidence shows that the doses that provide the most control of the disease also provide the largest selection pressure to acquire resistance and that lower doses decrease the selection pressure 11 In some cases when a pathogen evolves resistance to one fungicide it automatically obtains resistance to others a phenomenon known as cross resistance These additional fungicides typically belong to the same chemical family act in the same way or have a similar mechanism for detoxification Sometimes negative cross resistance occurs where resistance to one chemical class of fungicides increases sensitivity to a different chemical class of fungicides This has been seen with carbendazim and diethofencarb There are also recorded incidences of the evolution of multiple drug resistance by pathogens resistance to two chemically different fungicides by separate mutation events For example Botrytis cinerea is resistant to both azoles and dicarboximide fungicides There are several routes by which pathogens can evolve fungicide resistance The most common mechanism appears to be alteration of the target site particularly as a defense against a single site of action fungicides For example Black Sigatoka an economically important pathogen of banana is resistant to the QoI fungicides due to a single nucleotide change resulting in the replacement of one amino acid glycine by another alanine in the target protein of the QoI fungicides cytochrome b 12 It is presumed that this disrupts the binding of the fungicide to the protein rendering the fungicide ineffective Upregulation of target genes can also render the fungicide ineffective This is seen in DMI resistant strains of Venturia inaequalis 13 Resistance to fungicides can also be developed by efficient efflux of the fungicide out of the cell Septoria tritici has developed multiple drug resistance using this mechanism The pathogen had five ABC type transporters with overlapping substrate specificities that together work to pump toxic chemicals out of the cell 14 In addition to the mechanisms outlined above fungi may also develop metabolic pathways that circumvent the target protein or acquire enzymes that enable the metabolism of the fungicide to a harmless substance Fungicide resistance management edit The Fungicide Resistance Action Committee FRAC 15 has several recommended practices to try to avoid the development of fungicide resistance especially in at risk fungicides including Strobilurins such as azoxystrobin 15 FRAC assigns groups of fungicides into classes where cross resistance is likely usually because the active ingredients share a common mode of action 16 FRAC is organized by CropLife International 17 15 Products should not always be used in isolation but rather as mixture or alternate sprays with another fungicide with a different mechanism of action The likelihood of the pathogen s developing resistance is greatly decreased by the fact that any resistant isolates to one fungicide will be killed by the other in other words two mutations would be required rather than just one The effectiveness of this technique can be demonstrated by Metalaxyl a phenylamide fungicide When used as the sole product in Ireland to control potato blight Phytophthora infestans resistance developed within one growing season However in countries like the UK where it was marketed only as a mixture resistance problems developed more slowly Fungicides should be applied only when absolutely necessary especially if they are in an at risk group Lowering the amount of fungicide in the environment lowers the selection pressure for resistance to develop Manufacturers doses should always be followed These doses are normally designed to give the right balance between controlling the disease and limiting the risk of resistance development citation needed Higher doses increase the selection pressure for single site mutations that confer resistance as all strains but those that carry the mutation will be eliminated and thus the resistant strain will propagate Lower doses greatly increase the risk of polygenic resistance as strains that are slightly less sensitive to the fungicide may survive It is better to use an integrative pest management approach to disease control rather than relying on fungicides alone This involves the use of resistant varieties and hygienic practices such as the removal of potato discard piles and stubble on which the pathogen can overwinter greatly reducing the titre of the pathogen and thus the risk of fungicide resistance development See also editAntifungal drug Index of pesticide articles PHI base Pathogen Host Interaction database Phytopathology Plant disease forecastingReferences edit Haverkate F Tempel A Held A J 1969 Interaction of 2 4 5 trichlorophenylsulphonylmethyl thiocyanate with fungal spores Netherlands Journal of Plant Pathology 75 5 308 315 doi 10 1007 BF02015493 S2CID 23304303 Latijnhouwers Maita de Wit Pierre Govers Francine 2003 Oomycetes and fungi similar weaponry to attack plants Trends in Microbiology Cell Press 11 10 462 469 doi 10 1016 j tim 2003 08 002 ISSN 0966 842X PMID 14557029 S2CID 22200121 Mueller Daren Fungicides Terminology Iowa State University Retrieved June 1 2013 C Michael Hogan 2011 Sulfur Encyclopedia of Earth eds A Jorgensen and C J Cleveland National Council for Science and the environment Washington DC Archived October 28 2012 at the Wayback Machine Pesticide Chemistry and Bioscience edited by G T Brooks and T R Roberts 1999 Published by the Royal Society of Chemistry Hrelia et al 1996 The genetic and non genetic toxicity of the fungicide Vinclozolin Mutagenesis Volume 11 445 453 National Center for Biotechnology Information PubChem Compound Database CID 8722 https pubchem ncbi nlm nih gov compound 8722 accessed Jan 13 2019 FRAC Classification of Fungicides PDF CropLife International 2022 04 21 Thao Hoang Thi Bich Yamakawa Takeo April 2009 Phosphite phosphorous acid Fungicide fertilizer or bio stimulator Soil Science and Plant Nutrition 55 2 228 234 Bibcode 2009SSPN 55 228T doi 10 1111 j 1747 0765 2009 00365 x PEARSON MICHAEL N BEEVER ROSS E BOINE BARBARA ARTHUR KIEREN 2009 Mycoviruses of filamentous fungi and their relevance to plant pathology Review Molecular Plant Pathology British Society for Plant Pathology Wiley Blackwell 10 1 115 128 doi 10 1111 j 1364 3703 2008 00503 x ISSN 1464 6722 PMC 6640375 PMID 19161358 S2CID 34331588 Metcalfe R J et al 2000 The effect of dose and mobility on the strength of selection for DMI sterol demethylation inhibitors fungicide resistance in inoculated field experiments Plant Pathology 49 546 557 Sierotzki Helge 2000 Mode of resistance to respiration inhibitors at the cytochrome bc1 enzyme complex of Mycosphaerella fijiensis field isolates Pest Management Science 56 833 841 Schnabel G and Jones A L 2001 The 14a demethylase CYP51A1 gene is overexpressed in V inaequalis strains resistant to myclobutanil Phytopathology 91 102 110 Zwiers L H et al 2003 ABC transporters of the wheat pathogen Mycosphaerella graminicola function as protectants against biotic and xenobiotic toxic compounds Molecular Genetics and Genomics 269 499 507 a b c Fungicides Resistance Action Committee website Fungal control agents sorted by cross resistance pattern and mode of action PDF 2020 Archived from the original PDF on 2021 08 16 Retrieved 2020 09 04 Resistance Management CropLife International 2018 02 28 Retrieved 2020 11 22 External links editFungicide Resistance Action Committee Fungicide Resistance Action Group United Kingdom General Pesticide Information Archived 2007 12 29 at the Wayback Machine National Pesticide Information Center Oregon State University United States Retrieved from https en wikipedia org w index php title Fungicide amp oldid 1179643565, wikipedia, wiki, book, books, library,

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