Kevin L. Anderson
Evolutionists frequently point to the development of antibiotic resistance by bacteria as a demonstration of evolutionary change. However, molecular analysis of the genetic events that lead to antibiotic resistance do not support this common assumption. Many bacteria become resistant by acquiring genes from plasmids or transposons via horizontal gene transfer. Horizontal transfer, though, does not account for the origin of resistance genes, only their spread among bacteria. Mutations, on the other hand, can potentially account for the origin of antibiotic resistance within the bacterial world, but involve mutational processes that are contrary to the predictions of evolution. Instead, such mutations consistently reduce or eliminate the function of transport proteins or porins, protein binding affinities, enzyme activities, the proton motive force, or regulatory control systems. While such mutations can be regarded as “beneficial,” in that they increase the survival rate of bacteria in the presence of the antibiotic, they involve mutational processes that do not provide a genetic mechanism for common “descent with modification.” Also, some “relative fitness” cost is often associated with such mutations, although reversion mutations may eventually recover most, if not all, of this cost for some bacteria. A true biological cost does occur, however, in the loss of pre-existing cellular systems or functions. Such loss of cellular activity cannot legitimately be offered as a genetic means of demonstrating evolution. Read more…
