Pesticide resistance

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Pesticide application can artificially select for resistant pests. In this diagram, the first generation happens to have an insect with a heightened resistance to a pesticide (red). After pesticide application, its descendants represent a larger proportion of the population because sensitive pests (white) have been selectively killed. After repeated applications, resistant pests may comprise the majority of the population.

Pesticide resistance describes the decreased susceptibility of a pest population to a pesticide that was previously effective at controlling the pest. Pest species evolve pesticide resistance via natural selection: the most resistant organisms are the ones to survive and pass on their genetic traits to their offspring.[1]

Manufacturers of pesticides tend to prefer a definition that is dependent on failure of a product in a real situation, sometimes called field resistance. For example, the Insecticide Resistance Action Committee (IRAC) definition of insecticide resistance is 'a heritable change in the sensitivity of a pest population that is reflected in the repeated failure of a product to achieve the expected level of control when used according to the label recommendation for that pest species'.[2]

Pesticide resistance is increasing in occurrence. Farmers in the USA lost 7% of their crops to pests in the 1940s; over the 1980s and 1990s, the loss was 13%, even though more pesticides were being used.[1] Over 500 species of pests have evolved a resistance to a pesticide.[3] Other sources estimate the number to be around 1000 species since 1945.[4]

Rachel Carson predicted the phenomenon in her 1962 book Silent Spring.[1]


Propensity of pest populations to evolve resistance is probably caused by a number of factors. First, pest species are usually capable of producing large number of offspring. This increases the probability of random mutations and ensures the rapid build-up in numbers of resistant mutants once such mutations have occurred. Secondly, pest species have been exposed to natural toxins for a long time before the onset of human civilization. For example, many plants produce phytotoxins to protect them from herbivores. As a result, coevolution of herbivores and their host plants required development of the physiological capability to detoxify or tolerate poisons.[5][6] Thirdly, humans often rely almost exclusively on insecticides for pest control. This increases selection pressure towards resistance. Pesticides that fail to break down quickly and remain in the area contribute to selection for resistant organisms even after they are no longer being applied.[7]

In response to pesticide resistance, pest managers may resort to increased use of pesticides, exacerbating the problem.[8] In addition, when pesticides are toxic toward species that feed on or compete with pests, the pest population will likely expand further, requiring more pesticides.[8] This is sometimes referred to as pesticide trap,[8] or a pesticide treadmill, since farmers are continually paying more for less benefit.[4]

Insect preys and parasites which live on other insects generally have smaller populations and are therefore much less likely to evolve resistance than are the primary targets of the pesticides, such as mosquitoes and those that feed on plants. This can compound the pest problem because these species normally keep pest populations in check.[7] But resistant predators of pest species can be bred in laboratories, which can help keep pest populations down.[7]

The fewer sources of food a pest has the more likely it is to evolve resistance, because it is exposed to higher concentrations of pesticides and has less opportunity to breed with populations that have not been exposed.[7] Other factors in the speed with which a species evolves resistance are generation time and fecundity (shorter generations and more offspring lead to resistance more quickly).[7]


Resistance has evolved in a variety of different pest species: Resistance to insecticides was first documented by A. L. Melander in 1914 when scale insects demonstrated resistance to an inorganic insecticide. Between 1914 and 1946, 11 additional cases of resistance to inorganic insecticides were recorded. The development of organic insecticides, such as DDT, gave hope that insecticide resistance was an issue of the past. Unfortunately, by 1947 housefly resistance to DDT was documented. With the introduction of every new insecticide class – cyclodienes, carbamates, formamidines, organophosphates, pyrethroids, even Bacillus thuringiensis – cases of resistance surfaced within two to 20 years.

  • In the US, studies have shown that fruit flies that infest orange groves were becoming resistant to malathion, a pesticide used to kill them.[9]
  • In England, rats in certain areas have evolved such a strong resistance to rat poison that they can consume up to five times as much of it as normal rats without dying.[1]
  • DDT is no longer effective in preventing malaria in some places, a fact which contributed to a resurgence of the disease.[4]
  • Colorado potato beetle has evolved resistance to 52 different compounds belonging to all major insecticide classes. Resistance levels vary greatly among different populations and between beetle life stages, but in some cases can be very high (up to 2,000-fold).[11]

Although the evolution of pesticide resistance is usually discussed as a result of pesticide use, it is important to keep in mind that pest populations can also adapt to non-chemical methods of control. For example, the northern corn rootworm (Diabrotica barberi) became adapted to a corn-soybean crop rotation by spending the year when field is planted to soybeans in a diapause.[12]

Multiple and cross-resistance[edit]

Multiple resistance is the phenomenon in which a pest is resistant to more than one class of pesticides.[7] This can happen if one pesticide is used until pests display a resistance and then another is used until they are resistant to that one, and so on.[7] Cross resistance, a related phenomenon, occurs when the genetic mutation that made the pest resistant to one pesticide also makes it resistant to other pesticides, especially ones with similar mechanisms of action.[7]

Physiology and behavior[edit]

Frequently a pest becomes resistant to a pesticide because it evolves physiological changes that protect it from the chemical.[7] In some cases, a pest may gain an increased number of copies of a gene, allowing it to produce more of a protective enzyme that breaks down the pesticide into less toxic chemicals.[7] Such enzymes include esterases, glutathione transferases, and mixed microsomal oxidases.[7] Alternatively, the number of biochemical receptors for the chemicals may be reduced in the pest, or the receptor may be altered, reducing the pest's sensitivity to the compound.[7] Behavioral resistance has also been described for some chemicals; for example, some Anopheles mosquitoes evolved a preference for resting outside that prevented them from coming in contact with pesticide sprayed on interior walls.[13] Still other mechanisms include increased rates of excretion of toxic molecules, their sequestration and storage inside of the insect body away from vulnerable tissues and organs, and decreased toxin penetration through the insect body wall.[14]

Often, mutation in only a single gene leads to the evolution of a resistant organism. In other cases, multiple genes are involved. Resistant genes are usually autosomal. This means that they are located on autosomes (as opposed to sex chromosomes). As a result, resistance is inherited similarly in males and females. Also, resistance is usually inherited as an incompletely dominant trait. When a resistant and a susceptible individual mate with each other, their progeny has an intermediate level of resistance (more resistant than the susceptible parent, but not as resistant as the resistant parent).

Adaptation to pesticides usually decreases relative fitness of organisms in the absence of pesticides. Resistant individuals often have reduced reproductive output, life expectancy, mobility, etc. Therefore, relatively few of them persist in a population that is not exposed to a particular insecticide to which they have evolved resistance.[15]

Blowfly maggots produce an enzyme that confers resistance to organochloride insecticides. Scientists have researched ways to use this enzyme to break down pesticides in the environment, which would detoxify them and prevent harmful environmental effects.[16] Later they discovered a similar enzyme produced by soil bacteria that also breaks down organochloride insecticides but which works faster and remains stable in a variety of conditions.[16] The product, called Landguard is used in Australia to decontaminate spray equipment, soil and water after pesticide spraying and spills.[16]


Pest resistance to a pesticide can be managed by reducing selection pressure by this pesticide on the pest population. In other words, the situation when all the pests except the most resistant ones are killed by a given chemical should be avoided. This can be achieved by avoiding unnecessary pesticide applications, using non-chemical control techniques, and leaving untreated refuges where susceptible pests can survive.[17][18] Adopting the integrated pest management (IPM) approach usually helps with resistance management.

When pesticides are the sole or predominant method of pest control, resistance is commonly managed through pesticide rotation. This involves alternating among pesticide classes with different modes of action to delay the onset of or mitigate existing pest resistance.[19] Different pesticide classes may have different effects on a pest.[19] The U.S. Environmental Protection Agency (EPA or USEPA) designates different classes of fungicides, herbicides and insecticides. Pesticide manufacturers may, on product labeling, require that no more than a specified number of consecutive applications of a pesticide class be made before alternating to a different pesticide class. This manufacturer requirement is intended to extend the useful life of a product.[20]

Tankmixing pesticides is the combination of two or more pesticides with different modes of action in order to improve individual pesticide application results and delay the onset of or mitigate existing pest resistance.[17]

See also[edit]


  1. ^ a b c d PBS (2001), Pesticide resistance. Retrieved on September 15, 2007.
  2. ^ Insecticide Resistance Action Committee (2007), Resistance Definition. Retrieved on September 15, 2007.
  3. ^ How pesticide resistance develops. Excerpt from: Larry Gut, Annemiek Schilder, Rufus Isaacs and Patricia McManus. Fruit Crop Ecology and Management, Chapter 2: "Managing the Community of Pests and Beneficials." Retrieved on September 15, 2007.
  4. ^ a b c Miller GT (2004), Sustaining the Earth, 6th edition. Thompson Learning, Inc. Pacific Grove, California. Chapter 9, Pages 211-216.
  5. ^ Ferro DN. 1993. Potential for resistance to Bacillus thuringiensis: Colorado potato beetle (Coleoptera: Chrysomelidae) – a model system. American Entomologist 39:38-44.
  6. ^ Bishop BA and EJ Grafius. 1996. Insecticide resistance in the Colorado potato beetle. In: P Jolivet and TH Hsiao. Chrysomelidae Biology, Volume 1. SBP Academic Publishing, Amsterdam.
  7. ^ a b c d e f g h i j k l m Daly H, Doyen JT, and Purcell AH III (1998), Introduction to insect biology and diversity, 2nd edition. Oxford University Press. New York, New York. Chapter 14, Pages 279-300.
  8. ^ a b c Marten, Gerry “Non-pesticide management” for escaping the pesticide trap in Andrah Padesh, India. Retrieved on September 17, 2007.
  9. ^ Doris Stanley (January 1996), Natural product outdoes malathion - alternative pest control strategy. Retrieved on September 15, 2007.
  10. ^ Andrew Leonard, "Monsanto's bane: The evil pigweed",, Aug. 27, 2008.
  11. ^ Alyokhin, A., M. Baker, D. Mota-Sanchez, G. Dively, and E. Grafius. 2008. Colorado potato beetle resistance to insecticides. American Journal of Potato Research 85: 395–413.
  12. ^ Levine E, Oloumi-Sadeghi H, Fisher JR (1992) Discovery of multiyear diapause in Illinois and South Dakota Northern corn rootworm (Coleoptera: Cerambycidae) eggs and incidence of the prolonged diapause trait in Illinois. Journal of Economic Entomology 85: 262-267.
  13. ^ Berenbaum M (1994) Bugs in the System. Perseus Books, New York.
  14. ^ Yu, S.J. 2008. The Toxicology and Biochemistry of Insecticides. CRC Press, Boca Raton.
  15. ^ Stenersen, J. 2004. Chemical Pesticides: Mode of Action and Toxicology. CRC Press, Boca Raton.
  16. ^ a b c Marino M. (August 2007), Blowies inspire pesticide attack: Blowfly maggots and dog-wash play starring roles in the story of a remarkable environmental clean-up technology. Solve, Issue 12. CSIRO Enquiries. Retrieved on 2007-10-03.
  17. ^ a b Chris Boerboom (March 2001), Glyphosate resistant weeds. Weed Science - University of Wisconsin. Retrieved on September 15, 2007
  18. ^ Onstad, D.W. 2008. Insect Resistance Management. Elsevier: Amsterdam.
  19. ^ a b Graeme Murphy (December 1, 2005), Resistance Management - Pesticide Rotation. Ontario Ministry of Agriculture, Food and Rural Affairs. Retrieved on September 15, 2007
  20. ^

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