7.1 Types of Pesticides, Modes of Action & Resistance Management
Key Takeaways
- Pesticide names ending in -cide identify the target: insecticide, herbicide, fungicide, rodenticide, acaricide, nematicide, molluscicide, bactericide, and avicide.
- Contact materials kill on contact, while systemic materials are absorbed and translocated within the plant or animal.
- Selective pesticides control a narrow group of organisms; broad-spectrum materials affect many and are more likely to harm natural enemies and pollinators.
- IRAC, FRAC, and HRAC group numbers printed on the label identify the mode of action, and rotation must be between group numbers, not between brand names.
- Resistance develops when repeated use of one mode of action selects for individuals that survive; it is managed by rotation, mixtures, refuges, threshold-based treatment, and non-chemical tactics.
7.1 Types of Pesticides, Modes of Action & Resistance Management
Pes 304.09(b)(5) lists as examination subjects "the types of pesticides," "the compatibility, synergism, persistence and toxicity of the formulation," "the hazards and residues associated with use," and "factors which influence effectiveness or lead to problems such as resistance to pesticides." This section covers the first and the last.
Naming by target
The suffix -cide means killer, and the prefix names the target.
| Pesticide | Target | Pesticide | Target |
|---|---|---|---|
| Insecticide | Insects | Acaricide / miticide | Mites and ticks |
| Herbicide | Weeds and unwanted plants | Nematicide | Nematodes |
| Fungicide | Fungi | Molluscicide | Slugs and snails |
| Bactericide | Bacteria | Rodenticide | Rodents |
| Avicide | Birds | Piscicide | Fish |
| Algicide | Algae | Predacide | Predatory vertebrates |
| Larvicide | Larvae | Ovicide | Eggs |
Some pesticides do not kill at all. Repellents drive pests away; attractants lure them to a trap; growth regulators disrupt development; defoliants cause leaf drop; desiccants dry plant tissue; plant regulators alter growth rate or maturity. RSA 430:29 defines defoliant, desiccant, and plant regulator by statute, and all are regulated as pesticides.
Contact versus systemic; selective versus broad-spectrum
+------------------------------------------------------------------+
| CONTACT | Kills what it touches. Coverage is |
| | everything. No redistribution. Protects |
| | only tissue present at application. |
+--------------------+----------------------------------------------+
| SYSTEMIC | Absorbed and translocated in the plant or |
| | animal. Reaches sheltered pests, new |
| | growth, and roots. Slower. Longer residue. |
+--------------------+----------------------------------------------+
| SELECTIVE | Controls a narrow group. Spares beneficials.|
| | Example: a grass herbicide in a broadleaf |
| | crop; Bt for caterpillars. |
+--------------------+----------------------------------------------+
| BROAD-SPECTRUM | Affects many organisms. Higher risk to |
| | natural enemies and pollinators; higher |
| | risk of secondary pest outbreak. |
+------------------------------------------------------------------+
These distinctions decide product choice. A contact fungicide on the upper leaf surface will not protect the underside or the leaves that unfold next week; a systemic will. A contact insecticide cannot reach an aphid inside a curled leaf; a systemic can. Conversely, a selective material lets the parasitoid wasps in the block survive to keep working after the spray dries.
Other functional distinctions worth knowing: preemergence versus postemergence herbicides (relative to weed emergence, not crop emergence); protectant versus curative fungicides (a protectant must be on the surface before infection, a curative acts after); anticoagulant versus acute rodenticides.
Major chemical families and how they work
| Family | Examples | Mode of action | Notes |
|---|---|---|---|
| Organophosphates | malathion, chlorpyrifos, phosmet | Inhibit acetylcholinesterase; the bond ages and becomes irreversible | High acute mammalian toxicity; cholinesterase monitoring available |
| N-methyl carbamates | carbaryl, methomyl, oxamyl | Inhibit acetylcholinesterase reversibly | Poisoning tends to be self-limiting but can still be fatal |
| Pyrethroids | permethrin, bifenthrin, lambda-cyhalothrin | Hold voltage-gated sodium channels open | Low mammalian toxicity; skin paresthesia; very high toxicity to fish and bees |
| Neonicotinoids | imidacloprid, thiamethoxam, clothianidin | Agonists at insect nicotinic acetylcholine receptors | Highly systemic; significant pollinator concern |
| Bt and biologicals | Bacillus thuringiensis, spinosad | Midgut disruption; nicotinic/GABA site activation | Narrow spectrum; must be ingested |
| Insect growth regulators | methoprene, diflubenzuron | Disrupt molting or chitin synthesis | Slow; affect immature stages only |
| Synthetic auxin herbicides | 2,4-D, dicamba, triclopyr | Mimic natural auxin, causing uncontrolled growth | Selective for broadleaves; vapor and drift risk to sensitive crops |
| ALS inhibitors | sulfonylureas, imazapyr | Block branched-chain amino acid synthesis | Very low use rates; resistance develops readily |
| EPSP synthase inhibitors | glyphosate | Block aromatic amino acid synthesis | Non-selective, translocated |
| Anticoagulant rodenticides | first generation: warfarin, chlorophacinone; second generation: brodifacoum, bromadiolone | Block vitamin K recycling, causing fatal hemorrhage | Second-generation products are lethal after a single feeding, persist in liver tissue, and pose secondary poisoning risk to predators |
Mode of action groups: the numbers that matter
Rotating brand names accomplishes nothing if both brands share a mode of action. The industry solved this with numbered group codes printed on the label, usually in a box on the front panel:
- IRAC - Insecticide Resistance Action Committee - insecticide and miticide groups
- FRAC - Fungicide Resistance Action Committee - fungicide groups
- HRAC / WSSA - herbicide site-of-action groups
The rule is simple: rotate between group numbers, not between labels. Two different trade names, two different manufacturers, and two different formulations can carry the same IRAC group, and using them in sequence applies the same selection pressure twice.
How resistance develops
Resistance is not an individual pest becoming tolerant. It is a population changing composition:
- Within any large population, a few individuals carry a gene conferring survival against a given mode of action.
- Treatment kills the susceptible majority; the resistant few survive and reproduce.
- Because the survivors' competitors are gone, the resistant genotype now dominates the next generation.
- Repeat, and the mode of action stops working at label rate.
Factors that accelerate it:
- Short generation time and high reproductive rate - aphids, mites, whiteflies, many fungi.
- Repeated use of a single mode of action - the strongest single driver.
- Persistent residues that hold a sublethal dose over many days.
- Sublethal rates, whether from a deliberate rate cut or from an under-calibrated sprayer.
- Closed systems with little immigration of susceptible individuals - greenhouses, stored product facilities.
A related phenomenon is cross-resistance, where selection for resistance to one material confers resistance to others sharing its mode of action, and multiple resistance, where a population accumulates resistance to several distinct modes of action.
Managing resistance
+------------------------------------------------------------------+
| RESISTANCE MANAGEMENT |
+------------------------------------------------------------------+
| ROTATE modes of action - by IRAC/FRAC/HRAC group NUMBER, |
| ideally by pest generation rather than by spray |
| TREAT only when a scouting THRESHOLD is reached |
| APPLY the FULL LABEL RATE - never a reduced rate |
| MIX modes of action where the labels permit and both are |
| effective at the rate used |
| PRESERVE REFUGES of untreated, susceptible population |
| USE NON-CHEMICAL TACTICS: resistant varieties, sanitation, |
| rotation, biological control, exclusion |
| SCOUT after treatment and record what worked |
+------------------------------------------------------------------+
The rate point deserves emphasis because it runs against intuition. Cutting rates to "save money and reduce exposure" is one of the most reliable ways to select for resistance, because it lets partially resistant individuals survive. The correct range is the label range, chosen for the pest pressure and the size of the target stage - and exceeding the label maximum is never lawful under FIFRA or Pes 502.01.
Secondary consequences of over-reliance on chemicals extend beyond resistance. Secondary pest outbreaks occur when a broad-spectrum material removes the natural enemies that had been holding a minor pest in check, and pest resurgence occurs when the target pest rebounds faster than its predators after a spray. Both are arguments for selective chemistry and threshold-based treatment.
Worked example
A greenhouse has sprayed for two-spotted spider mite four times in six weeks with three different product names and is losing control.
- Check the group numbers. If two or three of those products share an IRAC group, the grower has applied one mode of action three times, not three modes once.
- Check the stage. Miticides differ sharply in activity against eggs, motiles, and adults; a product with no ovicidal activity applied on a 7-day interval can miss each successive hatch.
- Check coverage. Spider mites live on leaf undersides; without sufficient carrier volume and underside deposition, no product works.
- Check the environment. Hot, dry greenhouse conditions accelerate mite development and shorten the generation interval, compressing the selection cycle.
- Rebuild the program: rotate by IRAC group per generation, apply the full label rate, add predatory mites where the chemistry allows them to survive, raise humidity, and remove heavily infested plants.
- Greenhouses are a closed system with little immigration of susceptible individuals, which is exactly why mite resistance appears there first.
An applicator wants to rotate insecticides to slow resistance. What is the correct basis for rotation?
Why does applying a pesticide at less than the label rate increase the risk of resistance?
What distinguishes a second-generation anticoagulant rodenticide from a first-generation product?