Fungicides arepesticides used to killparasitic fungi or theirspores.[1][2] Fungi can cause serious damage inagriculture, resulting in losses of yield and quality. Fungicides are used both in agriculture and to fightfungal infections in animals. Fungicides are also used to controloomycetes, which are nottaxonomically/genetically fungi, although sharing similar methods of infecting plants. 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][4]
Most fungicides that can be bought retail are sold in liquid form, the active ingredient being present at 0.08% in weaker concentrates, and as high as 0.5% for less potent fungicides. Fungicides in powdered form are usually around 90% sulfur.
Some major fungal threats to agriculture (and the associated diseases) areAscomycetes ("potato late blight"),basidiomycetes ("powdery mildew"),deuteromycetes (various rusts), andoomycetes ("downy mildew").[1]
Like otherpesticides, fungicides are numerous and diverse. This complexity has led to diverse schemes for classifying fungicides. Classifications are based oninorganic (elemental sulfur and copper salts) vsorganic, chemical structures (dithiocarbamates vs phthalimides), and, most successfully, mechanism of action (MOA). These respective classifications reflect the evolution of the underlyingscience.
Traditional fungicides are simple inorganic compounds likesulfur,[5] and copper salts. While cheap, they must be applied repeatedly and are relatively ineffective.[2] Other active ingredients in fungicides includeneem oil,rosemary oil,jojoba oil, the bacteriumBacillus subtilis, and the beneficial fungusUlocladium oudemansii.
In the 1930sdithiocarbamate-based fungicides, the first organic compounds used for this purpose, became available. These includeferbam,ziram,zineb,maneb, andmancozeb. These compounds are non-specific and are thought to inhibit cysteine-based protease enzymes. Similarly nonspecific are N-substitutedphthalimides. Members includecaptafol,captan, andfolpet.Chlorothalonil is also non-specific.[2]
Specific fungicides target a particular biological process in the fungus.
Some fungicides targetsuccinate dehydrogenase, a metabolically central enzyme. Fungi of the classBasidiomycetes were the initial focus of these fungicides. These fungi are active against cereals.
Some of the most commonfungal crop pathogens are known to suffer frommycoviruses, and it is likely that they are as common as for plant and animal viruses, although not as well studied. Given theobligately parasitic nature of mycoviruses, it is likely that all of these are detrimental to their hosts, and thus are potentialbiocontrols/biofungicides.[7]
Doses that provide the most control of the disease also provide the largest selection pressure to acquire resistance.[8]
In some cases, the pathogen evolves resistance to multiple fungicides, a phenomenon known ascross resistance. These additional fungicides typically belong to the same chemical family, act in the same way, or have a similar mechanism for detoxification. Sometimes negativecross-resistance occurs, where resistance to one chemical class of fungicides increases sensitivity to a different chemical class of fungicides. This has been seen withcarbendazim anddiethofencarb. Also possible is resistance to two chemically different fungicides by separate mutation events. For example,Botrytis cinerea is resistant to both azoles anddicarboximide fungicides.
A common mechanism for acquiring resistance is alteration of the target enzyme. For example,Black Sigatoka, an economically important pathogen of banana, is resistant to theQoI fungicides, due to a singlenucleotide change resulting in the replacement of oneamino acid (glycine) by another (alanine) in the target protein of the QoI fungicides,cytochrome b.[9] 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 ofVenturia inaequalis.[10]
Resistance to fungicides can also be developed by efficientefflux of the fungicide out of the cell.Septoria tritici has developed multiple drug resistance using this mechanism. The pathogen had fiveABC-type transporters with overlappingsubstrate specificities that together work to pump toxic chemicals out of the cell.[11]
In addition to the mechanisms outlined above, fungi may also developmetabolic pathways that circumvent the target protein, or acquireenzymes that enable the metabolism of the fungicide to a harmless substance.
Fungicides that are at risk of losing their potency due to resistance includeStrobilurins such asazoxystrobin.[12] Cross-resistance can occur because the active ingredients share a common mode of action.[13] FRAC is organized byCropLife International.[14][12]
Fungicides pose risks for humans.[15]
Fungicideresidues have been found on food for human consumption, mostly from post-harvest treatments.[16] Some fungicides are dangerous to humanhealth, such asvinclozolin, which has now been removed from use.[17]Ziram is also a fungicide that is toxic to humans with long-term exposure, and fatal if ingested.[18] A number of fungicides are also used in human health care.
