Robert J. Wright, Extension Entomology Specialist
Insecticides differ in their modes of action, or how they act against a target pest. This NebGuide discusses insect resistance management and provides modes of action for insecticides used for Nebraska field crops.
Insecticide resistance is becoming an increasing problem worldwide; over 500 insects are documented to be resistant to one or more insecticides. Although we often think of insecticide resistance as a problem in tropical areas, or in greenhouses where insects can produce many generations in a year, Nebraska also has had problems with insecticide resistance.
Western corn rootworms have developed resistance to insecticides twice: in the 1950s to persistent soil insecticides such as aldrin, dieldrin, and heptachlor and more recently, in the 1990s to foliar insecticides such as methyl parathion and carbaryl that were used to control adult corn rootworms in central Nebraska. Also, some greenbug populations are resistant to chlorpyrifos. We now have a greater diversity of types of insecticides labeled for use on Nebraska field crops than in the past. Understanding available modes of action of these insecticides and not repeatedly using products with the same mode of action can play an important role in reducing future problems with insecticide resistance.
Pesticide resistance may be defined as a decreased response of a population of animals or plants to a pesticide or control agent as a result of previous exposure to the pesticide. Resistance is different from “tolerance,” which is the innate ability to survive a given toxicant dose without prior exposure and evolutionary change.
Insecticide resistance can be thought of as “accelerated evolution” or a population responding to an intense selective pressure and survival of those individuals that possess genes conferring resistance. Insecticide resistance occurs as a response to insect management practices over multiple years.
Resistance develops as a result of random mutations, producing a small number of individuals which possess traits that allow survival of normally lethal doses of insecticides. The insecticide itself does not produce a genetic change.
IRAC is an international industry consortium providing a coordinated response to prevent or delay the development of resistance in insect and mite pests. Its website (www.irac-online.org) has a great deal of additional information. The following text from the IRAC website has been modified with permission.
In most cases, not only does resistance render the selecting compound ineffective, it often also confers cross-resistance to other chemically related compounds. This is because compounds within a specific chemical group usually share a common target site within the pest, and thus share a common mode of action. For example, both carbamates such as Furadan® and Sevin® and organophosphates such as Lorsban® and Counter®, are acetylcholine inhibitors. Carbamates and organophosphates are subgroups with a similar mode of action.
It is common for resistance to develop based on a genetic modification of this target site. When this happens, the selecting compound’s interaction with its target site is impaired and the pesticide loses its pesticidal efficacy. Because all compounds within the chemical subgroup share a common mode of action, there is a high risk that the resistance that has developed will automatically confer cross-resistance to all the compounds in the same subgroup. It is this concept of cross-resistance within chemically related insecticides or acaricides that is the basis of the IRAC mode of action classification.
The objective of successful Insecticide Resistance Management (IRM) is to prevent or delay the evolution of resistance to insecticides, or to help regain susceptibility in insect pest populations in which resistance has already arisen. Effective IRM is an important element in maintaining the efficacy of valuable insecticides. It is important to recognize that it is usually easier to proactively prevent resistance from occurring than it is to reactively regain susceptibility.
Experience has shown that all effective insecticide or acaricide resistance management strategies seek to minimize the selection for resistance from any one type of insecticide or acaricide. In practice, alternations, sequences, or rotations of compounds from different mode of action groups provide a sustainable and effective approach to IRM. This ensures that selection from compounds in any one mode of action group is minimized. The IRAC mode of action classification is provided as an aid to insecticide selection for these types of IRM strategies.
This classification was developed and endorsed by IRAC and is based on the best available evidence of the mode of action of available insecticides. IRAC companies have agreed to the classification details and internationally recognized industrial and academic insect toxicologists and biochemists have approved the classification.
Table I. Mode of action of insecticides
Main Group and Primary Site of Action | Chemical Subgroup or Exemplifying Active Ingredient | Active Ingredient (Representative Trade Names®) |
---|---|---|
1. Acetylcholine esterase inhibitors |
1A Carbamates |
Aldicarb (Temik®) |
Carbaryl (Sevin®, others) |
||
Carbofuran (Furadan®) |
||
Methomyl (Lannate®) |
||
Oxamyl (Vydate®) |
||
Thiodicarb (Larvin®) |
||
1B Organophosphates |
Acephate (Orthene®) |
|
Chlorethoxyfos (Fortress®) |
||
Chlorpyrifos (Lorsban®, others) |
||
Dimethoate (Dimethoate, others) |
||
Ethoprop (Mocap®) |
||
Malathion (Fyfanon®, others) |
||
Methamidophos (Monitor®) |
||
Methidathion (Supracide®) |
||
Methyl parathion (Penncap-M®) |
||
Phorate (Thimet®) |
||
Phosmet (Imidan®) |
||
Tebupirimphos (Aztec®) |
||
Terbufos (Counter®) |
||
2. GABA-gated chloride channel antagonists |
2A Cyclodiene organochlorines |
Endosulfan (Thionex®, others) |
2B Phenylpyrazoles (fiproles) |
Fipronil (Regent®) |
|
3. Sodium channel modulators |
3A Pyrethroids Pyrethrins |
Permethrin (Ambush®, Pounce®) |
Bifenthrin (Capture®, others) |
||
Beta-cyfluthrin (Baythroid®) |
||
Deltamethrin (Decis®) |
||
Esfenvalerate (Asana®) |
||
Zeta-cypermethrin (Mustang® MAX) |
||
Gamma-cyhalothrin (Proaxis™) |
||
Lambda-cyhalothrin (Warrior) |
||
Tefluthrin (Force®) |
||
3B DDT Methoxychlor |
||
4. Nicotinic acetylcholine receptor agonists |
4A Neonicotinoids |
Thiamethoxam (Cruiser®) |
Imidacloprid (Gaucho®) |
||
Clothianidin (Poncho™) |
||
4B Nicotine |
||
4C Sulfoximes |
Sulfoxaflor (Transform®) |
|
4D Butenolides |
Flupyradifurone (Sivanto®) |
|
5. Nicotinic acetylcholine receptor allosteric activators |
Spinosyns |
Spinosad (Entrust™, Success®, Tracer®) |
Spinetoram (Radiant®) |
||
6. Chloride channel activators |
Avermectins Milbemycins |
|
7. Juvenile hormone mimics |
7A Juvenile hormone analogues |
|
7B Fenoxycarb |
||
7C Pyriproxyfen |
||
8. Miscellaneous nonspecific (multi-site) inhibitors |
||
9. Selective homopteran feeding blockers |
9B Pymetrozine |
Pymetrozine (Fulfill®) |
9C Flonicamid |
||
10. Mite growth inhibitors |
10A Clofentezine Hexythiazox (Onager®) |
Hexythiazox (Onager) |
10B Etoxazole |
Etoxazole (Zeal®) |
|
11. Microbial disruptors of insect midgut membranes |
Bacillus thuringiensis or Bacillus sphaericus and the insecticidal proteins they produce |
Cry proteins used in Bt corn hybrids, Dipel®, and others |
12. Inhibitors of mitochondrial ATP synthase |
12A Diafenthiuron |
|
12B Organotin miticides |
||
12C Propargite |
Propargite (Comite® II) |
|
12D Tetradifon |
||
13. Uncouplers of oxidative phosphorylation via disruption of the proton gradient |
Chlorfenapyr DNOC |
|
14. Nicotinic acetylcholine receptor channel blockers |
Nereistoxin analogues |
|
15. Inhibitors of chitin biosynthesis, type 0, Lepidopteran |
Benzoylureas |
Diflubenzuron (Dimilin®) |
16. Inhibitors of chitin biosynthesis, type 1, Homopteran |
Buprofezin |
|
17. Moulting disruptor, Dipteran |
Cyromazine |
|
18. Ecdysone receptor agonists |
Diacylhydrazines |
Methoxyfenozide (Intrepid®) |
19. Octopamine receptor agonists |
Amitraz |
|
20. Mitochondrial complex III electron transport inhibitors (Coupling site II) |
20A Hydramethylnon |
|
20B Acequinocyl |
||
20C Fluacrypyrim |
||
21. Mitochondrial complex I electron transport inhibitors |
21A METI acaricides |
Fenpyroximate (Portal®) |
21B Rotenone |
||
22. Voltage-dependent sodium channel blockers |
22A Indoxacarb |
Indoxacarb (Steward®) |
22B Metaflumizone |
||
23. Inhibitors of acetyl CoA carboxylase |
Tetronic and Tetramic acid derivatives |
Spiromesifen (Oberon®) |
24. Mitochondrial complex IV electron transport inhibitors |
24A Phosphine |
|
24B Cyanide |
||
25. |
||
26. |
||
27. |
||
28. Ryanodine receptor modulators |
Diamides |
Flubendiamide (Belt™) Rynaxypyr (Coragen®) |
Un Compounds of unknown or uncertain mode of action |
Azadirachtin |
Azadirachtin (Azatin® XL Plus) |
Benzoximate |
||
Bifenazate |
||
Chinomethionat |
||
Cryolite |
||
Dicofol |
||
Pyridalyl |
Based on information obtained from www.irac-online.org, IRAC (Insecticide Resistance Action Committee) Mode of Action Classification Version 8.1, issued April 2016.
Extension is a Division of the Institute of Agriculture and Natural Resources at the University of Nebraska–Lincoln cooperating with the Counties and the United States Department of Agriculture.
© 2011–2016, The Board of Regents of the University of Nebraska on behalf of the University of Nebraska–Lincoln. All rights reserved.
University of Nebraska–Lincoln Extension educational programs abide with the nondiscrimination policies of the University of Nebraska–Lincoln and the United States Department of Agriculture.