Pesticide resistance
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 specimens survive and pass on their acquired heritable changes traits to their offspring. If a pest has "resistance" then the pesticide lacks "efficacy" efficacy and resistance are inversely related. Cases of resistance have been reported in all classes of pests ("i.e." crop diseases, weeds, rodents, "etc."), with 'crises' in insect control occurring early-on after the introduction of pesticide use in the 20th century. 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". Pesticide resistance is increasing. Farmers in the US 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. Over 500 species of pests have evolved a resistance to a pesticide. Other sources estimate the number to be  around 1,000 species since 1945. 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 the field is planted with soybeans in a diapause. , few new weed killers are near commercialization, and none with a novel, resistance-free mode of action. Similarly, discovery of new insecticides is more expensive and difficult than ever. Causes. Pesticide  resistance probably stems from multiple factors: 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. 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. Adaptation. Pests becomes resistant by evolving physiological changes that protect them from the chemical. One protection mechanism is to increase the number of copies of a gene, allowing the organism to produce more of a protective enzyme that breaks the pesticide into less toxic chemicals. Such enzymes include esterases, glutathione transferases, and mixed microsomal oxidases. Alternatively, the number and/or sensitivity  of biochemical receptors that bind to the pesticide may be reduced. Behavioral resistance has been described for some chemicals. For example, some "Anopheles" mosquitoes evolved a preference for resting outside that kept them away from pesticide sprayed on interior walls. 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 Nation's 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. Integrated pest management. The Integrated pest management (IPM) approach provides a balanced approach to minimizing resistance. Resistance can be managed by reducing use of a pesticide. This allows non-resistant organisms to out-compete resistant strains. They can later be killed by returning to use of the pesticide. A complementary approach is to site untreated refuges near treated croplands where susceptible pests can survive. 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. Before glyphosate, most herbicides  would kill a limited number of weed species, forcing farmers to continually rotate their crops and herbicides to prevent resistance. Glyphosate disrupts the ability of most plants to construct new proteins. Glyphosate-tolerant transgenic crops are not affected. A weed family that includes waterhemp ("Amaranthus rudis") has developed glyphosate-resistant strains. A 2008 to 2009 survey of 144 populations of waterhemp in 41 Missouri counties revealed glyphosate resistance in 69%. Weed surveys from some 500 sites throughout Iowa in 2011 and 2012 revealed glyphosate resistance in approximately 64% of waterhemp samples. In response to the rise in glyphosate resistance, farmers  turned to other herbicides—applying several in a single season. In the United States, most midwestern and southern farmers continue to use glyphosate because it still controls most weed species, applying other herbicides, known as residuals, to deal with resistance. The use of multiple herbicides appears to have slowed the spread of glyphosate resistance. From 2005 through 2010 researchers discovered 13 different weed species that had developed resistance to glyphosate. From 2010-2014 only two more were discovered. A 2013 Missouri survey showed that multiply-resistant weeds had spread. 43% of the sampled weed populations were resistant to two different  herbicides, 6% to three and 0.5% to four. In Iowa a survey revealed dual resistance in 89% of waterhemp populations, 25% resistant to three and 10% resistant to five. Resistance increases pesticide costs. For southern cotton, herbicide costs climbed from between a few years ago to about in 2014. In the South, resistance contributed to the shift that reduced cotton planting by 70% in Arkansas and 60% in Tennessee. For soybeans in Illinois, costs rose from about . Section::::"Bacillus thuringiensis". During 2009 and 2010, some Iowa fields showed severe injury to corn producing Bt toxin Cry3Bb1 by western corn rootworm. During  2011, mCry3A corn also displayed insect damage, including cross-resistance between these toxins. Resistance persisted and spread in Iowa. Bt corn that targets western corn rootworm does not produce a high dose of Bt toxin, and displays less resistance than that seen in a high-dose Bt crop. 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.