With environmental concerns becoming increasingly commonplace and pressures increasing on turf managers to produce the best possible surface with minimal usage of pesticides such as fungicides. ‘Hard’ Chemistry is increasingly being replaced when possible with softer, what are perceived more environmentally safe options.
Turf diseases are best managed by integrating a number of control practices that may include: selection of disease-tolerant or disease-resistant turf varieties, time of planting, level of fertilisation, micro-climate modification, sanitation, and application of fungicides.
Fungicides are often a vital part of disease management as (a) they control many diseases satisfactorily, (b) cultural practices often do not provide adequate disease control, and (c) resistant varieties may not be available within Australia.
A fungicide is a chemical substance that destroys or inhibits the growth of fungi. In contrast with most human medicines, most fungicides need to be applied before disease occurs or at the first appearance of symptoms to be effective. Unlike many diseases of humans and animals, the damage caused by diseases on turf plants often does not go away, even if the pathogen is killed. Fungicides can only protect new uninfected growth from disease. Also, few fungicides are effective against pathogens after they have infected a plant.
Another way to describe a fungicide's mode of action is to say that it is used for protection, as a curative, or as an eradicant.
Protectants are applied to healthy plants to prevent fungal spores from germinating or penetrating host tissue. They must be applied before the fungal spore has a chance to infect the plant. New plant tissue that develops after application generally is unprotected. Protectants generally are not effective once the fungus is within plant tissues. Examples of protectants include mancozeb, coppers, and chlorothalonil.
Fungicides that have "curative" properties, which means they are active against pathogens that have already infected the plant, tend to have a higher risk of pathogens developing resistance to the fungicide. A resistant pathogen is less sensitive to the action of the fungicide, which results in the fungicide being less effective or even ineffective. Since these curative fungicides must be able to penetrate into plants and selectively kill the invading fungi, they are designed to target specific enzymes or proteins made by fungi. Since the mode of action of these fungicides is so specific, small genetic changes in fungi can overcome the effectiveness of these fungicides and pathogen populations can become resistant to future applications.
Disease management strategies that rely heavily upon the curative application of fungicides often lead to more resistance problems as (a) the size of the population from which resistant individuals are being selected
from is larger and (b) it is difficult to eradicate all of the fungi inside the plant and often, some pathogens escape the fungicide.
Fungicides can be classified by chemical class, general mode of action, specific mode of action, or by physical properties once in the plant. Many fungicides within a family, such as the benzimidazoles, have the same mode of action against fungi. Often, it is recommended to tank-mix or to alternate fungicides with different modes of action to prevent or delay the build up of resistant fungi. In general, fungi resistant to one chemical-family member, such as iprodione, also are resistant to all other chemicals in the family - in this example, to vinclozolin.
Fungicides kill by:
• Damaging cell membranes
• Inactivating critical enzymes or proteins
• Interfering with key metabolic processes, e.g. respiration
It is important to know mode of action of fungicide because it helps one • know which diseases can be controlled by the fungicide and enables the use of different MOA in a disease management program to delay fungicide resistance development.
A fungicide's mode of action can be described in general or specific terms. A fungicide with broad-spectrum activity is effective against a large variety of pathogenic fungi. Examples of broad-spectrum fungicides include captan, sulphur, and mancozeb. Some fungicides have a very narrow spectrum of activity; for example, metalaxyl is effective only against oomycetes like Phytophthora. Alternatively, a fungicide may affect a broad range of fungi but by only a specific mode of action. For example, Benlate® is useful to control many fungal diseases; it acts by binding to tubulin, thereby blocking mitosis.
Fungicidal action can be expressed in one of two physically visible ways, as either the inhibition of spore germination or as the inhibition of fungus growth and it is important to be familiar with the physiological mode of action of a fungicide for resistance management and preservation of fungicide effectiveness.
The physiological mode of action
Fungicides are termed as metabolic inhibitors and their modes of action can be classified into four broad groups.
o Inhibitors of electron transport chain.
o Inhibitors of enzymes.
o Inhibitors of nucleic acid metabolism and protein synthesis.
o Inhibitors of sterol synthesis.
Inhibition of electron transport chain (Respiration in mitochondria)
These include:
• Sulphur which disrupts electron transport along the cytochromes, is the oldest effective fungicide known and is still very effective for some diseases. In horticulture it is available as a sulphur dust for control of powdery mildew; a wettable powder for control of foliar fruit diseases; and lime sulphur which is frequently used as an eradicant. Sulphur can cause damage to some plants and cannot be used when temperatures exceed 26-32°C.
• Strobilurins (azoxystrobin, kresoxim-methyl, pyraclostrobin, trifloxystrobin) which inhibit mitochondrial respiration, blocking the cytochrome bc1 complex.
These have a common mode of action but but definite practical differences
azoxystrobin
pyraclostrobin
trifloxystrobin
Uptake into leaf
Low
Very Low
Very Low
Metabolic stability within leaf
Yes
Yes
Yes
Translaminar movement
Yes
Low
Low
Xylem systemic
Yes
No
No
Phloem mobile
No
No
No
Each of these two major fungicide groups works in distinctly different ways. Strobilurins injure fungi by disrupting the electron transport chain at work within the cells. Strobilurins are locally systemic (mesosystemic) with translaminar activity whose activity is favoured by long drying times and warmer temperatures after application. The best time to apply these is prior to infection or in early stages of disease development.
Fungicides in this class affect the electron transport chain in fungi mitochondria, causing energy production necessary for fungal metabolism to cease and as a result of their fairly narrow site of action have some real resistance concerns.
Inhibition of enzymes
These include:
• Copper which causes nonspecific denaturation of proteins and enzymes. This includes inorganic copper compounds which are practically insoluble in water. The copper ion provides the fungicidal as well as the phytotoxic properties of these compounds. The insolubility of these compounds allows for release of only low levels of copper, adequate for fungicidal activity but not enough to affect the plant. Because of their insolubility, they are not easily washed off by rain. They are relatively safe to use because of their low toxicity to animals and humans. With the exception of Bordeaux mixture and copper sulphate, they are often called fixed coppers. Some of the fungicides are also used to control bacterial diseases and as algaecides in waterways and ponds.
• Dithiocarbamates (mancozeb, penncozeb, dithane, etc) which inactivate –SH groups in amino acids, proteins and enzymes. This group of fungicides has been the most important, most versatile, and most widely used of the fungicides. Most contain a metal ion attached to an organic molecule derived from dithiocarbamic acid. They are chiefly used as foliar protectants, although thiram is a seed treatment.
• Substituted aromatics (chlorothalonil, PCNB) which inactivate amino acids, proteins and enzymes by combining with amino and thiol groups. Chlorothalonil also disrupts respiration, but the method by which it does so is very different from the strobilurins. Basically fungal tissues dies due to energy depletion or starvation and as a consequence of possessing a fairly broad site of action rsistance concerns are generally less.
Inhibition of nucleic acid metabolism and protein synthesis
• Benzimidazoles (benlate) inhibit DNA synthesis (nuclear division).
• Phenylamides (mefenoxam) inhibit RNA synthesis and dicarboximides (iprodione which inhibit DNA and RNA synthesis, cell division and cellular metabolism.
Captan for example is an extremely useful, wide-spectrum fungicide with low toxicity to plants and animals. The newer dicarboximides, such as iprodione are loosely related to captan but do not have as broad an action spectrum and are much more prone to the development of resistance by target fungi.
Inhibition of sterol synthesis (Inhibit demethylation of ergosterol)
Ergosterol is the major sterol in most fungi and is essential for membrane structure and function.
Sterol inhibiting fungicides
• Imidazoles
• Triazoles (propiconazole) Sterol inhibitors or triazoles also have a fairly narrow site of action causing some resistance concerns.
• Morpholines inhibits sterol production at different site than imidazoles and triazoles. Affect cell wall production.
It is important to know the physiological mode of action of fungicides for resistance management and preservation of fungicide effectiveness. This in turn means that fungicides with different modes of action can be incorporated into a disease management program by using them in alternation or as a mixture.
The triazoles such as propiconazole are broad spectrum but do not prevent spore germination and early germ tube growth because reserves are in the spore. They rapidly penetrates young leaf and stem tissue with warmer temperatures favouring this. They are xylem systemic – i.e. upward movement and have a T½ inside plant of 14 days. In order to be effective they must be inside plant tissue to be absorbed by fungus.
Keys To Successful Use of Bio-Fungicides
• Must be used in conjunction with good cultural practices.
• Must be applied before the onset of disease.
• Often need to be reapplied during the growing season.
• Growth- Will gain a little in optimum soils but will improve results in suboptimum conditions
• How Do Biological Fungicides Work?
• Direct Competition
• Antibiosis
• Predation or parasitism
• Plant activators
Direct Competition
Most associated with soil borne pathogens
• If the good guys live in the rhizosphere, the bad guys won’t find a room
• Inoculate before infection by pathogen occurs
• “Biological Control Organism” must become associated with roots or rhizosphere
• This area is nutrient rich, a food source
• Generally BCO must be present in large numbers to compete.
Predation or Parasitism
• Predation or parasitism is when the BCO attacks and feeds on the pathogen.
• Again the BCO must be present before the pathogen invades
• Mycorrhizal inoculants usually last the season however Bacterial inoculants should be reapplied every 2-3 weeks.
• Trichoderma moves vertically more than horizontally.
Plant activators
Plants use a vast array of signals originating from micro-organisms and the environment to recognise pathogens and elicit plant defence responses. Non-specific elicitors of biotic and abiotic origin induce host defences in a broad range of host species. Abiotic elicitors such as UV light can induce stress responses in exposed tissues, which may provide an additional barrier to invading pathogens or alternatively, increase the plant's susceptibility to infection. Biotic elicitors include cell wall fragments released from fungi and bacteria, hydrolytic enzymes of plant or pathogen origin, some peptides, glycoproteins and polyunsaturated fatty acids. These elicitors induce defence responses in a range of host species. Often, non-specific elicitors act as a general indication that the cell has been damaged in some way (for example, the release of fragments of the host's own cell wall can elicit defence responses).
Systemic acquired resistance, or induced resistance, is characterised by the increased resistance of a plant to a wide range of pathogens following infection by one pathogen. Rather than providing immunity per se, systemic acquired resistance reduces the severity of later diseases. The development of systemic acquired resistance usually requires the development of a localised response to infection, the release of a phloem-translocated signal originating from the infection site, and the subsequent priming of the plant against further attacks, allowing a more rapid response in the case of future infections. The nature of the signal that triggers systemic acquired resistance is as yet unknown, and is likely to be a complex signal transduction pathway mediated by a number of stress signals. Salicylic acid plays a key role, via interaction with salicylic acid-binding proteins that can cause build-up of reactive oxygen species or activate gene expression.
In contrast to conventional fungicides, plant activators have no direct effect on pathogens. Instead these induce plants to produce natural disease-fighting compounds.
Various chemicals have been discovered that seem to act at various points in these defence activating networks and mimic all or parts of the biological activation of resistance.
The best studied resistance activator is acibenzolar. At low rates it activates resistance in many crops against a broad spectrum of diseases, including fungi, bacteria and viruses. In monocots, activated resistance is very long lasting, while the lasting effect is less pronounced in dicots. Acibenzolar is translocated systemically in plants and can take the place of SA in the natural SAR signal pathway, inducing the same spectrum of resistance and the same set of molecular markers.
Resistance inducing chemicals that are able to induce broad disease resistance offer an additional option to the use of fungicides. If integrated properly in plant health management programs, they can prolong the useful life of both the resistance genes and the fungicides presently used.
Natural Plant Defence Mechanisms
• Salicylic acid pathway – Induces SAR (systemic acquired resistance), a natural biological defence response to pathogen attack.
• Jasmonic Acid Pathway - Induces the production of disease and insect defence compounds.
Salicylic Acid Pathway
• Production of active oxygen (hydrogen peroxide, peroxidase)
o Peroxidases have been associated with fungal cell wall degradation and pathogen defence signaling
• Thickening plant cell wall
o Increasing lignification
o Production of phenolic esters that strengthen cross linking
Chitinases such as ‘Softguard®’
The simple version of it's function is that chitosan (poly-D-glucosamine) is found in the shells of almost all insects and crustaceans, as well as in most fungi, algae and yeasts. Chitin is the second most abundant polymer in nature after cellulose, and it is a structural component of some fungi, insects, various crustaceans, and nematode eggs. Chitin is insoluble in water, organic or inorganic acids.
• Chitin is the major component of all fungal cell walls except for the Oomycetes
• Chitinases break down fungal cell walls
• Chitinases can break down insect exo-skeletons
• Activity is greatly enhanced by Glucanase.
• Chitosan is deacetylated chitin, and referred to as poly β-(1-4)-D glucosamine. Chitosan occurs naturally as a component of the chitin matrix. Chitinases are a class of enzymes capable of degrading chitin, the N-acetyl glucosamine polymer that makes up fungal cell walls. Chitinases are expressed at low levels in healthy plants but increased when under pathogen attack being located primarily in the cell wall and vacuole. Extracts containing chitinases will directly inhibit the growth of fungi by degrading their cell walls and also indirectly promote the release of oligosaccharides that act as elicitors of defence reactions
When acetylated chitosan (SoftGard®) is sprayed onto the leaves of plants the chitosan content triggers the plants natural defence mechanisms into thinking the plant is under attack by fungi, and the plant defends itself.
If treatment is carried out regularly during hot, wet or humid weather, and BEFORE the outbreak of fungal activity, it can prevent many forms of fungal outbreaks.
Addition of chitin to soil stimulates growth of bacteria actinomycetes, and a limited number of fungal species with chitinolytic properties. A beneficial function of these microorganisms is that they may attack and reduce parasitic nematode colonies, whereby more soil macronutrients and micronutrients become available to the plant through its healthy root system.
Jasmonic Acid Pathway
Insect predation also causes the synthesis of jasmonic acid and its ester methyl jasmonate. Jasmonate is highly volatile and can be detected by surrounding plants to warn them of potential insect predation by the inducing the production of systemin and the synthesis of proteinase inhibitors.
* Farmer and Ryan (1990) discovered that jasmonic acid volatilized from sagebrush could trigger defense gene expression in adjacent tomatoes
* Jasmonic acid volatiles act as attractants for beneficial insects
* Jasmonic acid induces the production of disease and insect defense compounds.
* Defence Proteins
* Phytochemicals
Phytochemicals
* Different from phytoalexins in that phytochemicals are induced by wounding.
* Phenolics such as furanocoumarins, Coumarins, Tannins, Lignin, other phenolics
* Terpenoids
* Alkaloids
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With environmental concerns becoming increasingly commonplace and pressures increasing on turf managers to produce the best possible surface with minimal usage of pesticides such as fungicides. ‘Hard’ Chemistry is increasingly being replaced when possible with softer, what are perceived more environmentally safe options.
ides need to be applied before disease occurs or at the first appearance of symptoms to be effective. Unlike many diseases of humans and animals, the damage caused by diseases on turf plants often does not go away, even if the pathogen is killed. Fungicides can only protect new uninfected growth from disease. Also, few fungicides are effective against pathogens after they have infected a plant.
Fungicides kill by:
Each of these two major fungicide groups works in distinctly different ways. Strobilurins injure fungi by disrupting the electron transport chain at work within the cells. Strobilurins are locally systemic (mesosystemic) with translaminar activity whose activity is favoured by long drying times and warmer temperatures after application. The best time to apply these is prior to infection or in early stages of disease development.
action-plant activators such as Alexin
