Pesticide resistance

Pesticide resistance probably stems from multiple factors: • Many pest species produce large numbers of offspring, for example insect pests produce large broods. This increases the probability of mutations and ensures the rapid expansion of resistant populations. • Pest species had been exposed to natural toxins long before agriculture began. 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. Secondary metabolites or allelochemicals produced by plants inhibit insect feeding, but insects have evolved enzymes to metabolize or detoxify them by converting them into non-toxic metabolites. The same enzymes may also detoxify insecticides by converting lipophic compounds into ones that are excreted or otherwise removed from the insect. Greater exposure to insect-inhibiting secondary metabolites or allelochemicals is more likely to increase pesticide resistance. One group of chemicals produced by insects to detoxify toxins are esterases which can detoxify organophosphates and pyrethroid. Conditions that affect how resistant some insects are to insecticides include exposure to different amounts of secondary metabolites or allelochemicals, which are variable among plant species in response to different degrees of herbivory pressure. The way an insect feeds on a plant impacts their exposure; insects that feed on the vascular tissue (sap sucking insects like aphids) are generally exposed to less insect-inhibiting compounds than insects that consume the leaves. Plants produce a wide range of defensive chemical compounds and generalist insects that feed on different types of plants can increase their exposure to them increasing their likelihood of developing pesticide resistance. • Humans often rely almost exclusively on pesticides for pest control. This increases selection pressure towards resistance. Pesticides that fail to break down quickly contribute to selection for resistant strains even after they are no longer being applied. • In response to resistance, managers may increase pesticide quantities/frequency, which exacerbates the problem. In addition, some pesticides are toxic toward species that feed on or compete with pests. This can paradoxically allow the pest population to expand, requiring more pesticides. This is sometimes referred to as the pesticide trap, or a '''', since farmers progressively pay more for less benefit. • Unfamiliarity with variation in regulatory enforcement can hamper policy makers' ability to produce real change in the course of resistance evolution. ==Examples==

Resistance has evolved in multiple 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 were recorded. The development of organic insecticides, such as DDT, gave hope that insecticide resistance was a dead issue. However, by 1947 housefly resistance to DDT had evolved. 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. • Studies in America have shown that fruit flies that infest orange groves were becoming resistant to malathion. • In Hawaii, Japan and Tennessee, the diamondback moth evolved a resistance to Bacillus thuringiensis about three years after it began to be used heavily. • In the southern United States, Amaranthus palmeri, which interferes with cotton production, has evolved resistance to the herbicide glyphosate and overall has resistance to five sites of action in the southern US . • The Colorado potato beetle has evolved resistance to 52 different compounds belonging to all major insecticide classes. Resistance levels vary across populations and between beetle life stages, but in some cases can be very high (up to 2,000-fold). • The cabbage looper is an agricultural pest that is becoming increasingly problematic due to its increasing resistance to Bacillus thuringiensis, as demonstrated in Canadian greenhouses. Further research found a genetic component to Bt resistance. • The widespread introduction of Rattus norvegicus (the brown rat) combined with the widespread use of anticoagulent rodenticides such as warfarin has produced almost equally widespread resistance to vitamin K antagonist rodenticides around the world. • In aquatic environments, non-target organisms have also demonstrated pesticide resistance. A study on Gammarus roeselii and Hyalella azteca found that after only two generations of exposure to the neonicotinoid thiacloprid, tolerance levels nearly doubled. The research suggests that developmental plasticity, rather than genetic mutations alone, may contribute to rapid resistance in some species. ==Consequences==

Insecticides are widely used across the world to increase agricultural productivity and quality in vegetables and grains (and to a lesser degree the use for vector control for livestock). The resulting resistance has reduced function for those very purposes, and in vector control for humans. ==Multiple and cross-resistance==

• Multiple-resistance pests are resistant to more than one class of pesticide. This can happen when pesticides are used in sequence, with a new class replacing one to which pests display resistance with another. • Cross-resistance, a related phenomenon, occurs when the genetic mutation that made the pest resistant to one pesticide also makes it resistant to others, often those with a similar mechanism of action. ==Adaptation==

Pests becomes resistant by evolving physiological changes that protect them from the chemical. Resistance may involve rapid excretion of toxins, secretion of them within the body away from vulnerable tissues and decreased penetration through the body wall. Mutation in only a single gene can lead 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 allosomes, also known as 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 individual mates with a susceptible individual, their progeny generally has a level of resistance intermediate between the parents. Adaptation to pesticides comes with an evolutionary cost, usually decreasing relative fitness of organisms in the absence of pesticides. Resistant individuals often have reduced reproductive output, life expectancy, mobility, etc. Non-resistant individuals sometimes grow in frequency in the absence of pesticides - but not always - so this is one way that is being tried to combat resistance. 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. A similar enzyme produced by soil bacteria that also breaks down organochlorides works faster and remains stable in a variety of conditions. Resistance to gene drive forms of population control is expected to occur and methods of slowing its development are being studied. The molecular mechanisms of insecticide resistance only became comprehensible in 1997. Guerrero et al. 1997 used the newest methods of the time to find mutations producing pyrethroid resistance in dipterans. Even so, these adaptations to pesticides were unusually rapid and may not necessarily represent the norm in wild populations, under wild conditions. Natural adaptation processes take much longer and almost always happen in response to gentler pressures. ==Management==

In order to remediate the problem it first must be ascertained what is really wrong. Assaying of suspected pesticide resistance - and not merely field observation and experience - is necessary because it may be mistaken for failure to apply the pesticide as directed, or microbial degradation of the pesticide. The United Nations' World Health Organization established the Worldwide Insecticide resistance Network in March 2016, due to increasing need and increasing recognition, including the radical decline in function against pests of vegetables. When pesticides are the sole or predominant method of pest control, resistance is commonly managed through pesticide rotation. This involves switching among pesticide classes with different modes of action to delay or mitigate pest resistance. The Resistance Action Committees monitor resistance across the world, and in order to do that, each maintains a list of modes of action and pesticides that fall into those categories: the Fungicide Resistance Action Committee, the Weed Science Society of America (the Herbicide Resistance Action Committee no longer has its own scheme, and is contributing to WSSA's from now on), and the Insecticide Resistance Action Committee. The U.S. Environmental Protection Agency (EPA) also uses those classification schemes. Manufacturers may recommend no more than a specified number of consecutive applications of a pesticide class be made before moving to a different pesticide class. Two or more pesticides with different modes of action can be tankmixed on the farm to improve results and delay or mitigate existing pest resistance. == Status ==

Glyphosate Glyphosate-resistant weeds are now present in the vast majority of soybean, cotton, and corn farms in some U.S. states. Weeds resistant to multiple herbicide modes of action are also on the rise. Products such as Capture LFR (containing the pyrethroid bifenthrin) and SmartChoice (containing a pyrethroid and an organophosphate) have been increasingly used to complement Bt crops that farmers find alone to be unable to prevent insect-driven injury. Multiple studies have found the practice to be either ineffective or to accelerate the development of resistant strains. ==See also==