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Fungicides are chemical compounds or biological organisms used to kill or inhibit fungi or fungal spores. 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. Chemicals used to control oomycetes, which are not fungi, are also referred to as fungicides as oomycetes use the same mechanisms as fungi to infect plants.1

Fungicides can either be contact or systemic. A contact fungicide kills fungi by direct contact; a systemic fungicide has to be absorbed by the plant.

Most fungicides that can be bought retail are sold in a liquid form. The most common active ingredient is sulfur, 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, and the bacterium Bacillus subtilis.

Fungicide residues have been found on food for human consumption, mostly from post-harvest treatments.2 Some fungicides are dangerous to human health, such as vinclozolin, which has now been removed from use.3

Contents

Natural fungicides

Plants and other organisms have chemical defenses that give them an advantage against microorganisms such as fungi. Some of these compounds can be used as fungicides:

Whole live or dead organisms that are efficient at killing or inhibiting fungi can sometimes be used as fungicides:

  • The bacterium Bacillus subtilis
  • Kelp (powdered dried kelp is fed to cattle to protect them from fungi in grass)

History

Early development

The development of fungicides for planted crops began in earnest in the 1800s after a period of extensive crop damage caused by fungal infections in grapes and potatoes. Powdery mildew on grapes was first described in eastern North America, but it gained notoriety when it was introduced into European vineyards in 1845 and spread rapidly throughout the continent. At that time there were at least 15 million acres of grapevines in Europe.7 In the 1840s, the annual per capita consumption of wine in France was 76 liters.8 By 1851, powdery mildew had reached every grape-growing country of Europe, causing its maximum damage in France in 1854. In that year it reduced the French crop of grapes by 80%.9 Prior to powdery mildew infection, the annual production of wine in France averaged about one billion gallons. By 1854 output had dropped to 200 million gallons.10 The wine shortage produced by powdery mildew led to a doubling of wine prices in France. Moreover, the quality of the wine from the mildewed grapes was poor. The granting of subsidies for powdery mildew research led to the discovery that sulfur treatments controlled the disease. The use of sulfur as a fungicide became generally widespread in vineyards and by 1858 French wine grape production returned to its 1847 level.11 This use of sulfur as a treatment for powdery mildew is still in widespread use today.

In the U.S., California was largely spared the destructive impact of the mid-19th century powdery mildew epidemics because the state’s grape industry had not yet developed. The development of the massive California grape industry was largely a result of the discovery of sulfur's effectiveness as a fungicide. Once farmers in California saw the effectiveness of sulfur on grape cultivation it rapidly became one of the most popular crops in the state and marked the first major use of fungicides in the United States. Agricultural bulletins in California dating to the 1890s describe the powdery mildew treatment schedule still in use today: regular applications of sulfur at 7 to 14 day intervals during the period of vine susceptibility. A 1907 University of California Bulletin reported that powdery mildew was capable of destroying the entire crop in most vineyards during bad infection seasons if it was not controlled.12

Late blight on potatoes was first reported in the United States in Philadelphia in 1843, and subsequently spread throughout the country.13 Late blight was reported in Europe in 1845 where it had spread to Belgium, England, and Ireland. Ireland was especially dependent upon the potato crop as the climate and soils were ideal for potato cultivation and allowed abundant production. Because of plentiful potato crops, the population of Ireland had increased to about 8 million by 1845. Irish peasants subsisted almost entirely on potatoes. 40% of the Irish potato crop was destroyed by late blight in 1845 and almost 100% destruction occurred in 1846.14 An estimated 1.5 million Irish died of famine and disease during the late blight epidemic, and a similar number of people emigrated, mainly to North America.15

Late blight epidemics in Europe stimulated intense investigations into the nature of plant diseases and are generally regarded as initiating the development of plant pathology as a discrete discipline.16 Late blight continued to be a devastating disease until the 1880s when an effective fungicide was discovered. A mixture of copper sulphate and slaked lime (Bordeaux mixture) was found to prevent late blight infections if applied to the potato plant before fungal spores arrived. Bordeaux mixture became widely-used in Europe for control of late blight in the early 1900s. During World War I all the copper that Germany had was used for shell casings and electric wire and therefore there was none to spare for making copper sulphate to spray potatoes.17 This demonstrated the newfound importance of this fungicide as a a severe late blight outbreak in Germany’s potatoes in 1916 went untreated and much of the potato crop rotted in the fields. The resulting scarcity of potatoes led to the deaths of 700,000 German civilians from starvation during the winter of 1916–17.18

In the U.S. the losses of the potato crop to late blight in 1844 were estimated by state: New Hampshire (25%), Vermont (25%), Massachusetts (25–30%), Rhode Island (10%), Connecticut (25-30%), New York (50%), New Jersey (15%), Pennsylvania (20–25%), Maine (90%) and Delaware (25–30%).1920 Periodic epidemics occurred throughout the late 1800s. Experiments with Bordeaux mixture for control of late blight began in the U.S. in the late 1880s. A summary of twenty years of experimental data in Vermont (1890-1910) showed an average increase in potato yield of 64% with the use of Bordeaux.21 Increased use of Bordeaux mixture is credited with reducing potato losses due to late blight to an average of 2.8% during the 1930s.22 Growers who sprayed 10-12 times with Bordeaux had minimal late blight in their fields or in storage.2324

Most of the U.S. acres of fruit and vegetable crops were routinely treated with a fungicide (sulfur, lime sulfur, copper, Bordeaux mixture) for control of one or more plant diseases beginning in the early 1900s. The use of copper and sulfur as fungicides totaled 300 million pounds per year in the 1940s.25

Synthetic fungicide development and fungicide use today

Research with synthetic chemical fungicides began in the 1940s and demonstrated that crop yields were higher as a result of improved disease control efficacy and/or reduced damage to the crop. Although precise use estimates are not available, it is believed that growers of apples, potatoes and most other crops rapidly switched from older fungicides to new synthetic fungicides in the 1950s. For example, it was reported that the synthetic fungicides were used 75% of U.S. potato acreage in 195326. Experiments with zineb and nabam resulted in potato yields that were 23-35% higher than with Bordeaux mixture.

These synthetic fungicides were quickly seen as critical to crop production as seen in a 1950 report to Congress where the American Phytopathological Society reported that many fruit and vegetable crops could not be produced in reliable volume without chemical protection from diseases.27

As a result of the adoption of synthetic chemical fungicides the total volume of fungicides used in U.S. agriculture has decreased. Synthetic chemical fungicides are used at a significantly lower rate per acre than copper and sulfur. As newer fungicides with even lower use rates have been introduced the aggregate volume of fungicides has declined. Currently total fungicide use totals 108 million pounds per year in comparison to 300 million pounds per year in the 1940s.

Today more than 80% of fruit and vegetable crop acres in the U.S. are treated with fungicides every year.

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 often 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 mutation 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 back 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 decreased the selection pressure.28

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 are normally of the same chemical family or have the same mode of action, or can be detoxified by the same mechanism. Sometimes negative cross resistance occurs, where resistance to one chemical class of fungicides leads to an increase in sensitivity to a different chemical class of fungicides. This has been seen with carbendazim and diethofencarb.

There are also recorded incidences of pathogens evolving multiple drug resistance – 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, particular as a defence against 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 one amino acid (glycine) being replaced by another (alanine) in the target protein of the QoI fungicides, cytochrome b.29 This presumably 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.30

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 5 ABC type transporters with overlapping substrate specificities that together work to effectively pump toxic chemicals out of the cell.31

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

Fungicide resistance management

The fungicide resistance action committee (FRAC) has several recommended practices to try to avoid the development of fungicide resistance, especially in at-risk fungicides including Strobilurins such as azoxystrobin.

Products should not 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 developing resistance is greatly decreased by the fact that any resistant isolates to one fungicide will hopefully 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. 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 only ever marketed as a mixture resistance problems were not seen.

Fungicides should only be applied 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. 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 also recommended that where possible fungicides are only used in a protective manner, rather than to try to cure already infected crops. Far fewer fungicides have curative/eradicative ability than protectant. Thus fungicide preparations advertised as having curative action may only have one active chemical; a single fungicide acting in isolation increases the risk of fungicide resistance.

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 practises, 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

External links

References

  1. ^ Latijnhouwers M, de Wit PJ, Govers F. Oomycetes and fungi: similar weaponry to attack plants. Trends in Microbiology Volume 11 462-469
  2. ^ Pesticide Chemistry and Bioscience edited by G.T Brooks and T.R Roberts. 1999. Published by the Royal Society of Chemistry
  3. ^ Hrelia et al. 1996 - The genetic and non-genetic toxicity of the fungicide Vinclozolin. Mutagenesis Volume 11 445-453
  4. ^ "Cinnamaldehyde Use". PAN Pesticides Database. Retrieved on 2007-10-23.
  5. ^ López P, Sánchez C, Batlle R, Nerín C (August 2005). "Solid- and vapor-phase antimicrobial activities of six essential oils: susceptibility of selected foodborne bacterial and fungal strains". J. Agric. Food Chem. 53 (17): 6939–46. doi:10.1021/jf050709v. PMID 16104824. 
  6. ^ US patent 6174920 Method of controlling powdery mildew infections of plants using jojoba wax
  7. ^ Carefoot, G.L. and E.R. Sprott, "Famine on the Wind: Man's Battle Against Plant Disease", Rand McNally & Company, 1967
  8. ^ Simpson, James, Phylloxera, "Price Volatility and Institutional Innovation in France's Domestic Wine Markets 1870-1911", Universidad Carlos III de Madrid, Economic History and Institution Series 02, Working Paper 04-46, October 2004
  9. ^ Bioletti, frederic T., Oidium or Powdery Wildew of the Vine, University of California, Agricultural Experiment station, Bulletin No. 186, February 1907
  10. ^ G.L. and E.R. Sprott, "Famine on the Wind: Man's Battle Against Plant Disease", Rand McNally & Company, 1967
  11. ^ Spencer, D.M., Ed, "The Powdery Mildews", New York, Academic Press, 1978
  12. ^ Bioletti, Frederic T., "Oidium or Powdery Wildew of the Vine", University of California, Agricultural Experiment station, Bulletin No. 186, February 1907
  13. ^ Fry, William e., et al., "Historical and Recent Migrations of Phytophthora Infestans: Chronology, Pathways, and Implications," Plant Disease, Vol. 77, No. 7, P. 653, July, 1993
  14. ^ Austin Bourke, P.M., "Emergence of Potato blight, 1843-1846," Nature, Vol 203, No, 4948, P. 805, August 1964
  15. ^ Fry, William E., and Stephen B. Goodwin, "Resurgance of the Irish Potato Famine Fungus," Bioscience, Vol. 47, No. 6, June, 1967
  16. ^ Fry, William E., and Stephen B. Goodwin, "Resurgance of the Irish Potato Famine Fungus," Bioscience, Vol. 47, No. 6, June, 1967
  17. ^ Carefoot, G.L. and E.R. Sprott, "Famine on the Wind: Man's Battle Against Plant Disease", Rand McNally & Company, 1967
  18. ^ Carefoot, G.L. and E.R. Sprott, "Famine on the Wind: Man's Battle Against Plant Disease", Rand McNally & Company, 1967
  19. ^ Campbel, c. Lee, Paul d. Peterson, and Clay S. Griffith, "The Formative years of Plant Pathology in the United States, APS Press, 1999
  20. ^ Stevens, Neil E., "Phytopathology - The Dark Ages in Plant Pathology in America: 1830-1970," Journal of the Washington Academy of Sciences, vol. 23, no. 9, P. 435, Setpember 15, 1933
  21. ^ Jones, L.R., N.J. Giddings, and B.F. Lutman, "Investigations of hte Potato Fungus Phytophthora Infestans, Vermont Garicultural Experiment Station, Bulletin No. 168, August, 1912
  22. ^ McCallan, S.E.A., "Outstanding diseases of Agricultural Crops and Uses of Fungicides in the United States," Contributions of the Boyce Thompson Institute,' vol. 14, No. 3, PP. 105-116, January-March, 1946.
  23. ^ Dickey, J.B.R., "Methods and Trends in 400 Bushel Potato Production in Pennsylvania," American Potato Journal, P. 82, 1935.
  24. ^ Dean, Daniel, "Some Observations on Late Blight Development in 1928," American Potato Journal, Vol 6., P. 288, 1929
  25. ^ Groggins, Phillip H., "Chemicals in Food Production," United States War Food Administration, Nineteenth Annual Priestly Lectures, 1945
  26. ^ Brandes, Gordon A., "The History and Development of the Ethylene Bisdithiocarbamate," American Potato Journal, Vol. 30, P. 137, 1953
  27. ^ APS, "The Present Status of Chemicals Used to Control Diseases of Edible Fruits and Vegetable in the United States (Fungicides, Bactericides, Nematocides)," submitted to the Federal Security Agency, 'Docker No. FDC-57, January 24, 1950
  28. ^ Metcalfe, R.J. et al. (2000) The effect of dose and mobility on the strength of selection for DMI fungicide resistance in inoculated field experiments. Plant Pathology 49: 546-557
  29. ^ 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
  30. ^ 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.
  31. ^ 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
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