The mechanism by which drug resistance emerges was studied by Luria and Delbrück in 1943 and by Lederburg and Lederburg in 1952. Further work established that streptomycin resistance emerges as the result of point mutations, at a rate of about one per billion cells, while isoniazid resistance has a mutation rate of one per million. Mainstream textbooks treat this as established science,<ref>''Zinsser Microbiology,'' 1968, pp. 163-167, Appleton-Century-Crofts, Library of Congress 68-8386</ref> and supporters of the Darwinian theory of evolution often cite it as an example of rapid evolution.<ref name=fda/> Creationists dispute this interpretation. Some acknowledge the general correctness of the traditional explanation but argue that it is not analogous to speciation in higher organisms and has no relevance to the evolution of macroorganisms. Others have hypothesized alternative explanations for the arise and spread of drug-resistance in bacteria. | The mechanism by which drug resistance emerges was studied by Luria and Delbrück in 1943 and by Lederburg and Lederburg in 1952. Further work established that streptomycin resistance emerges as the result of point mutations, at a rate of about one per billion cells, while isoniazid resistance has a mutation rate of one per million. Mainstream textbooks treat this as established science,<ref>''Zinsser Microbiology,'' 1968, pp. 163-167, Appleton-Century-Crofts, Library of Congress 68-8386</ref> and supporters of the Darwinian theory of evolution often cite it as an example of rapid evolution.<ref name=fda/> Creationists dispute this interpretation. Some acknowledge the general correctness of the traditional explanation but argue that it is not analogous to speciation in higher organisms and has no relevance to the evolution of macroorganisms. Others have hypothesized alternative explanations for the arise and spread of drug-resistance in bacteria. |