{"id":44264,"date":"2026-10-15T16:40:37","date_gmt":"2026-10-15T14:40:37","guid":{"rendered":"https:\/\/biocontroltechnologies.com\/2026\/10\/15\/mechanisms-of-action-resistance-evidence-and-criteria-for-evaluating-a-biological-control-solution\/"},"modified":"2026-10-20T13:32:44","modified_gmt":"2026-10-20T11:32:44","slug":"mechanisms-of-action-resistance-evidence-and-criteria-for-evaluating-a-biological-control-solution","status":"publish","type":"post","link":"https:\/\/biocontroltechnologies.com\/en\/2026\/10\/15\/mechanisms-of-action-resistance-evidence-and-criteria-for-evaluating-a-biological-control-solution\/","title":{"rendered":"Mechanisms of action: Resistance, evidence, and criteria for evaluating a biological control solution"},"content":{"rendered":"\t\t
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T34 Biocontrol\u00ae \u00b7 Modes of Action
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The mechanisms of action of biological control:<\/h1>

Resistance and the advantages of biological plant protection products<\/h4>
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PART 3\/3<\/p>

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Most synthetic fungicides currently in use act on a single target site: they block a specific enzyme or protein in the pathogen. Biocontrol agents, by contrast, can act through several mechanisms simultaneously. This difference has an important practical consequence: biological products with multiple modes of action have a markedly <\/span>low <\/span>risk of resistance development<\/span>. T<\/span>his is<\/span> also<\/span> reflected in their classification in FRAC group BM02 (<\/span><\/span>Fungicide<\/span> Resistance<\/span> Action<\/span> Committee<\/span><\/span><\/em>).<\/span><\/span> <\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t

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\n What is FRAC?\n <\/h3>\n\n
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\n FRAC<\/strong> (Fungicide Resistance Action Committee<\/em>) is a technical group within CropLife International,\nthe global trade association of the crop protection\nindustry. It was set up in the early 1980s to prevent\nand manage the emergence of fungicide resistance\nin crop pathogens. \n <\/p>\n\n

\n Its main tool is the FRAC Code List<\/strong>, a regularly updated list that classifies active ingredients by mode of action and resistance risk, assigning each group a code such as BM02<\/strong>.\n <\/p>\n\n

\n Building on that list, FRAC issues\nrecommendations to help products stay\neffective for as long as possible.\n <\/p>\n\n

\n It is not a regulatory body:<\/strong>\nit does not authorize products,\nnor does it endorse specific ones.\n <\/p>\n\n <\/div>\n <\/div>\n\n \n

\n \"Fungicide\n <\/div>\n\n <\/div>\n\n<\/div>\n\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t
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In this third and final module, we look at what multiple mechanisms mean for resistance, how to interpret the FRAC BM02 classification, and which criteria help separate agronomic evidence from a mere sales pitch.<\/span> <\/span><\/p>

FRAC groups fungicidal active ingredients by mode of action and resistance risk. Group BM02 is made up mainly of microbial biological control agents (living fungi or bacteria) that act through several mechanisms at once: parasitism, antibiosis, competition for space and nutrients, or activation of the plant\u2019s immune system. In practice, this means their efficacy does not hinge on a single target and no associated resistance risk is known. How each mechanism works was covered in the second module; here we focus on <\/span>how to evaluate them<\/span><\/b>.<\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t

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Download the PDF<\/a> by clicking on the image<\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t

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1. Mechanism, effect, and benefit: three things not to confuse <\/h3>\t\t\t\t<\/div>\n\t\t\t\t
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This distinction is worth reinforcing, because it is a critical-reading tool that applies to any technical data sheet that lands on an advisor\u2019s desk<\/span>, <\/span>whether for a synthetic or a biological product<\/span>:<\/span><\/span> <\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t

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\n\n\nMECHANISM OF ACTION\n<\/span>\n

The antagonist\nparasitizes the pathogen.<\/h4>\n
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\nOBSERVABLE EFFECT\n<\/span><\/div>\n
\n\nReduced germination of\npathogen spores<\/strong>\n\nLower incidence of\ndisease<\/strong>\n\n<\/div>\n<\/div>\n
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\n\n\nAGRONOMIC BENEFIT\n<\/span>\n

A healthier, more uniform,\nhigher-quality crop.<\/h4>\nWith fewer plant losses.\n\n<\/div>\n
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For a grower, however, the most important consequence of an agent acting through several mechanisms does not show up in any of those three lines: it becomes apparent over the seasons. A fungicide that acts on a single target tends to lose efficacy because the pathogen eventually develops resistance; with an agent that acts through several mechanisms, on the other hand, this rarely happens. Let\u2019s look at why. <\/span><\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t

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2. Why multiple mechanisms reduce resistance development <\/h3>\t\t\t\t<\/div>\n\t\t\t\t
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This is arguably the most strategically significant argument<\/span>, <\/span>so it is worth stating precisely.<\/span><\/span> <\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t

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How resistance emerges <\/h4>\t\t\t\t<\/div>\n\t\t\t\t
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In a pathogen population made up of millions of individuals, random mutations arise all the time. Most have no consequences, but some may alter precisely the target on which a synthetic fungicide acts. When that fungicide is applied, sensitive individuals die while those carrying the mutation survive and multiply. Season after season, the proportion of resistant individuals grows until the product no longer controls the disease. The fungicide does not create the mutation: it selects it. That is why we speak of <\/span>selection pressure.<\/span><\/i> <\/span><\/p>

It is the same phenomenon seen with antibiotics in medicine. Repeated use of an antibiotic favors bacteria that, through mutation or gene acquisition, are no longer susceptible, and over time that antibiotic loses its usefulness against them. Medicine has also learned how to slow the process down: tuberculosis, for example, is treated with several drugs at once, because it is highly unlikely that a single bacterium will be resistant to all of them simultaneously. The same principle explains the low resistance risk of biological control agents with multiple mechanisms of action. <\/span> <\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t

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One target versus many <\/h4>\t\t\t\t<\/div>\n\t\t\t\t
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Resistance is a serious problem with single-site fungicides: it shortens the useful life of active ingredients and calls for increasingly complex rotation strategies. That is why FRAC assigns many of them a medium or high resistance risk and recommends rotating them or combining them with other modes of action. Not all chemical fungicides are single site: multi-site fungicides (such as copper, sulfur, and others in FRAC\u2019s M groups) act on many targets at once and carry a low risk. The relevant dividing line, therefore, is not between chemical and biological, but between acting on one target or on many. <\/span> <\/span><\/p>

Generally speaking, a microbial antagonist does not exert pressure on a single target. It acts through combinations of processes, each of which in turn relies on multiple players: different lytic enzymes, different signaling molecules, different metabolites. To escape all of them, the pathogen would have to accumulate several independent adaptations at the same time \u2014 far less likely than altering a single target. On top of that, some mechanisms exert little or no selection pressure: according to K\u00f6hl et al. (2019), competition for nutrients resembles the stresses the pathogen already endures in the soil, and induced resistance acts not directly on the pathogen but on the plant. <\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t

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What the literature says (and what it doesn\u2019t)<\/h4>\t\t\t\t<\/div>\n\t\t\t\t
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The literature does not claim that resistance is impossible, only that it is considerably less likely. K\u00f6hl et al. (2019) document variability in the sensitivity of pathogen populations to specific metabolites (for example, <\/span>Botrytis cinerea<\/span><\/i> to pyrrolnitrin) and even cases of adaptation in <\/span>in vitro<\/span><\/i> assays with increasing concentrations. At the same time, they point out that no pathogen has been reported to develop resistance to hyperparasitism, and they pin the risk down to one very specific scenario: applying a purified antimicrobial metabolite, formulated at high rates, across the entire crop \u2014 a situation that is functionally close to that of a single-site fungicide.<\/span> <\/span><\/p>

The practical takeaway is that low resistance risk is not an automatic property of \u00abbiologicals\u00bb, but a consequence of multiple mechanisms acting <\/span>in situ<\/span><\/i>. And that multiplicity is precisely what defines Group BM02. For growers, it translates into a tool that can remain effective season after season and that, when built into a mode-of-action rotation, can also help protect the efficacy of synthetic fungicides.<\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t

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3. How a mechanism of action is demonstrated (and why the Petri dish can be misleading)<\/h3>\t\t\t\t<\/div>\n\t\t\t\t
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There is a methodological bias worth knowing about, because it shapes much of the available literature and many of the sales arguments in circulation.<\/span> <\/span><\/p>

The <\/span>in vitro<\/span><\/i> dual culture assay (two fungi facing off on a plate, with their inhibition zone) is fast, reproducible, inexpensive and visually very compelling. Its image has become the iconic representation of biological control. The problem is that it <\/span>systematically selects for a single mechanism<\/span><\/b>: the production of antimicrobial metabolites in an artificial, nutrient-rich medium.<\/span> <\/span><\/p>

K\u00f6hl et al. (2019) document just how much this skews the picture. Standard culture media are roughly one hundred times richer in nutrients than a plant\u2019s rhizosphere, and agar promotes the diffusion of compounds in a way that does not occur in soil or on leaf surfaces. The result is a self-fulfilling prophecy: <\/span>in vitro<\/span><\/i> assays confirm the importance of antibiosis because, by design, they rule out every other mechanism.<\/span> <\/span><\/p>

The most telling case they report is a screening of 256 isolates of <\/span>Trichoderma<\/span><\/i> against <\/span>Rhizoctonia solani<\/span><\/i>. In dual culture, 192 showed antagonism and 64 did not. In pot trials with corn salad in infested soil, mean efficacy in reducing damping-off<\/em> (pre- and post-emergence rot) was 61.2 % for the former and 59.7 % for the latter. Virtually identical. Antagonism on the plate did not predict efficacy on the plant (K\u00f6hl et al., 2019b).<\/span> <\/span><\/p>

The practical consequence for anyone evaluating products: <\/span>a plate image is not evidence of agronomic efficacy<\/span><\/b>. Robust proof requires trials that bring together antagonist, pathogen and plant under representative environmental conditions, as well as field trials across a range of experimental conditions.<\/span> <\/span><\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t

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256 Trichoderma<\/i> isolates<\/h4>\n

Each tested twice: on a plate against Rhizoctonia solani<\/i> and in pots with plants.<\/p>\n\n

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1<\/span>256 isolatesEach dot is one isolate<\/small><\/p>\n\n

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