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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.

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

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. Some fungicides are dangerous to human health, such as vinclozolin, which has now been removed from use.

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)


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.

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. 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.

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.

In addition 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, a phenylamide fungicide. When used as the sole product in Irelandmarker to control potato blight (Phytophthora infestans) resistance developed within one growing season. However in countries like the UKmarker where it was only ever marketed as a mixture resistance problems developed more slowly .

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





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. 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
  5. 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
  6. 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.
  7. 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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