A resistance gene that evolves in one bacterial species can potentially be disseminated to many others by means of molecules known as plasmids, which are transmitted among suitable hosts by cell contact. The molecular evolution of antibiotic resistance is similar to the process that bacteria have used for millenia to evolve resistance to naturally occurring antibiotics and to soil contaminated with lethal concentrations of heavy metals. In many cases, the resistance genes are contained in mobile genetic elements that can be transmitted from one organism to the next, and their spread has resulted in the wide dissemination of the resistance genes among pathogenic and nonpathogenic forms. In this case, the overuse of inexpensive antibiotics, not only in medicine but in animal feed, fish culture, and agriculture, has promoted the evolution of antibiotic resistance in a wide spectrum of microorganisms. The rapid, repeated evolution of insecticide resistance in many parts of the world reflects the operation of this simple mathematical principle.Ī similar situation accounts for the repeated evolution of antibiotic resistance in bacteria: Rare bacterial types containing genes for resistance are favored in the presence of the antibiotic and eventually displace the normal sensitive types. The phenomenon occurs because the time required to evolve significant resistance depends on the logarithm of the total increase in frequency of the resistance gene as a result of the pesticide application, which over a wide range of realistic values is effectively limited to 5 to 50 generations. Exposure to the insecticide gives an advantage to these mutants, and over several generations, they gradually increase in frequency at the expense of the normal types until very few of the normal sensitive types remain.Ī remarkable principle in population genetics states that insecticide resistance can be expected to evolve in approximately 5 to 50 pest generations, irrespective of the insect species, geographical region, nature of the pesticide, frequency and method of application, and other seemingly important variables.
The evolution of resistance to insecticides is so common because the insect populations often contain rare mutant variants that are already resistant. Resistance in the mosquito Aedes aegypyti is also associated with a DDTase enzyme, but not the one found in the housefly. Mutant forms of the enzyme convert DDT into the relatively harmless compound DDE. In the common housefly, resistance results from the presence of an enzyme called DDTase, the natural function of Which is unknown. In many cases, the insecticide resistance results from the action of a single gene, although multiple other genetic changes that can modify the response to insecticides also occur. In fact, more than 200 species of insects had become resistant to DDT by 1976 some species have evolved multiple resistance to four or more groups of chemical insecticides.
The introduction and widespread use of each of these was quickly followed by the evolution of resistance in large numbers of insect species. After the initial success of DDT, many other exotic chemical compounds were introduced as insecticides.
As a consequence, DDT was quickly employed worldwide to control houseflies, mosquitoes, and a variety of other insect pests. DDT appeared to have many advantages because, in proper dose, it was toxic to insects but not to humans. The first synthetic organic insecticide to be adopted for practical use was DDT, which was introduced in 1941. The Processes and Results of Evolution Are Exemplified in the Evolution of Insecticide Resistance in Insects and Antibiotic Resistance in Bacteria
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