Fungicides for Vegetable Crops - Part 1

The mode of action (MOA) of a fungicide indicates how the fungicide works to eliminate or inhibit pathogens. From a biological perspective, most fungicides work by inhibiting the germination of fungal spores or inhibiting the growth of fungal hyphae (strands that make up the body of the fungus). The Fungicide Resistance Action Committee (FRAC) classifies fungicides into MOA classes, and it assigns FRAC codes to classes or class subgroups based on the physiological mechanisms by which they affect fungi, including interfering with respiration and energy production, inhibiting nucleic acid and protein synthesis, and inhibiting enzyme functions. A fungicide’s specific MOA determines which pathogens will be affected by that fungicide.^1,2

The FRAC code 3 fungicides are the demethylation inhibitors (DMIs), which are a subgroup of the sterol biosynthesis inhibitor (SBI) fungicides. The DMIs were first introduced in the 1970s and now include fungicides with a broad spectrum of activity against a wide range of fungal pathogens, including powdery mildew, rust, and leaf spot pathogens. They work by inhibiting the production of the sterol compound ergosterol, a molecule used in fungal cells, which results in abnormal fungal growth. Some DMIs can also inhibit spore germination to some extent.^3,4 They are locally systemic, absorbed into leaves, but may not move from leaf to leaf and do not move downward in the plant. DMI fungicides can have both preventative (protectant) and curative activities. The risk of pathogens developing resistance to DMIs is moderately high.^5,6 Fungicide active ingredients in this group include cyproconazole, difenconazole, flutriafol, propiconazole, metconazole, tebuconazole, and tetraconazole.

The succinate dehydrogenase inhibitor (SDHI) fungicides (FRAC code 7) are a diverse group with varying ranges (spectra) of activity. The group includes fungicides with relatively narrow spectra of activity, such as carboxin, which is effective against some basidiomycete fungi. Other fungicides in the group are effective against a broad range of pathogens, such as boscalid, which is effective against both ascomycete and basidiomycete pathogens. SDHI fungicides work by inhibiting respiration (energy production) in fungal cells. They are usually locally systemic with translaminar movement and some upward mobility in the plant.^4,5,7 SDHI fungicides are mostly preventative (protectant) and inhibit spore germination, but some also have curative activity. There is a moderate to high risk of pathogens developing resistance to SDHI fungicides.^5,6,7 There are a large number of active ingredients in this group, including carboxin, boscalid, fluopyram, and penflufen.^6,7

The quinone outside inhibitor (QoI) fungicides (FRAC code 11) are broad spectrum, effective against ascomycete, basidiomycete, and oomycete pathogens. The MOA of the QoI fungicides inhibits fungal mitochondrial respiration, stopping energy production. This results in the inhibition of spore germination and early hyphal growth.^4,7,8 The QoI fungicides are locally systemic to upwardly systemic. They can accumulate in the waxy cuticle layer on leaf surfaces and have preventative activity but limited to no curative activity. There is a moderate to high risk of pathogens developing resistance to QoI fungicides. This group includes the strobilurin fungicides, such as azoxystrobin, fluoxastrobin, picoxystrobin, pyraclostrobin, and trifloxystrobin.^5,6,8

The phenylpyrrole (PP) fungicides (FRAC code 12) have activity against ascomycete and basidiomycete pathogens. This group includes the fungicide fludioxonil, used primarily in seed treatments and in some foliar applications. These fungicides are thought to affect the osmotic regulation of fungal cells, but the specific mode of action is not well understood. Phenylpyrroles can inhibit spore germination and mycelial growth. There is no systemic movement of these fungicides within the plant. The risk of pathogens developing resistance to phenylpyrroles is low to medium.^4,6,7

The benzamide and thiazole carboxamide fungicides (FRAC code 22) primarily target oomycete pathogens. They work by disrupting the process of cell division, and they inhibit the growth of spore germ tubes and mycelium. They have preventative activity against pathogens and have no systemic movement within the plant. The risk of pathogens developing resistance to this group is low to medium. Zoxamide and ethaboxam are members of this group.^4,6

Cymoxanil is the only fungicide in the cyanoacetamide group (FRAC code 27) that is currently registered for use on agricultural crops. This fungicide is active against oomycete pathogens, including the downy mildews, Phytophthora infestans (the cause of late blight of potatoes and tomatoes), and Albugo candida (the white rust pathogen). The MOA for this group is currently unknown, but the fungicide has preventative activity and some early infection activity. There is a low to medium risk of pathogens developing resistance to this group of fungicides.^4,6

Propamocarb is currently the only fungicide in the carbamate group (FRAC code 28) available for use on agricultural crops. Propamocarb is active against oomycete pathogens, including species of Pythium causing root rots and seedling diseases, Phytophthora capsici and Phytophthora infestans, and the downy mildew pathogens. It also is used to help manage early blight, caused by Alternaria solani (an ascomycete fungus) on potato and tomato. This group of fungicides work by interfering with the production of phospholipids and fatty acids used in cell membrane formation. This action results in the disruption of mycelial growth, spore production, and spore germination. Propamocarb is taken up by the roots and the leaves and is upwardly mobile in the plant. There is a low to medium risk of pathogens developing resistance to carbamate fungicides.^4,6

The carboxylic acid amide (CAA) fungicides (FRAC code 40) are active against Phytophthora species (including P. infestans and P. capsici) and downy mildew pathogens. However, they are not effective against other oomycete pathogens such as species of Pythium. They have preventative activity and are most effective when applied before infection takes place. However, they have some curative activity as well. These fungicides inhibit cellulose synthesis, which disrupts cell wall formation. They inhibit mycelial growth and the germination of cystospores and sporangia but not zoospores. They are locally systemic with translaminar movement and upward mobility. The risk of pathogens developing resistance to CAA fungicides is low to medium. The group includes the active ingredients dimethomorph and mandipropamid.^4,6,7