It is widely upheld that evolution is the result of two essential forces: variability (chance) and selection (necessity). This assumption is confi rmed by a number of simple phenomena in antibiotic resistance. Variability is created by random mutation, and some of these variants (for instance those with a mutation in the antibiotic target) become resistant. These variants are selected by antibiotic use and consequently they increase the frequency of resistance. If we increase variability (as in a hyper-mutable strain) or the intensity of selection (antibiotic hyper-consumption), the result is more resistance. This is true, but not the whole truth. Most determinants of antibiotic resistance are not based on simple mutations, but rather on sophisticated systems frequently involving several genes and sequences; moreover, resistance mutations are seldom transmitted by lateral gene transfer. The acquisition of any type of resistance produces a change. In biology, any change is not only an opportunity, but is also a risk for evolution. Bacterial organisms are highly integrated functional structures, exquisitely tuned by evolutionary forces to fi t with their environments. Beyond the threshold of the normal compliance of these functions, changes are expected to disturb the equilibrium. Therefore, the acquisition of resistance is not suffi cient to survive; evolution should also shape and refi ne the way of managing the resistance determinants.
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© 2009 Humana Press, a part of Springer Science+Business Media, LLC
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Baquero, F., Cantón, R. (2009). Evolutionary Biology of Drug Resistance. In: Mayers, D.L. (eds) Antimicrobial Drug Resistance. Infectious Disease. Humana Press. https://doi.org/10.1007/978-1-59745-180-2_2
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DOI: https://doi.org/10.1007/978-1-59745-180-2_2
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