Resistance to antimicrobial agents has been recognized since the dawn of the antibiotic era. Paul Ehrlich, the father of modern chemotherapy, observed that, during treatment of trypanosome infections, organisms sometimes emerged that were resistant to the agent being used. Resistance was specifi c in the sense that a fuchsin dye-resistant strain was still susceptible to an arsenic compound, while a strain resistant to the arsenic compound retained sensitivity to the dye. He showed that resistance, once acquired, was stably inherited and in 1908 proposed that resistance was due to “reduced avidity of the chemoreceptors so that they are no longer able to take up” the drug (1). Substitute “target” for “chemoreceptor” and one of the major mechanisms for antimicrobial resistance was revealed as was its specifi city for particular compounds. Drug inactivation was discovered early as well. In 1919 Neuschlosz reported that Paramecium caudatum resistant to quinine and to certain dyes acquired the ability to destroy the toxic agents (2).
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Jacoby, G.A. (2009). History of Drug-Resistant Microbes. In: Mayers, D.L. (eds) Antimicrobial Drug Resistance. Infectious Disease. Humana Press. https://doi.org/10.1007/978-1-59745-180-2_1
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