In early times, scientists considered antibiotic resistance in terms of adaptation to the toxic agents. For instance, Ehrlich worked on development of p-rosaniline resistance to Trypanosoma brucei as early as 1904. The resistance was observed during the treatment of trypanosome infections as the organisms emerged that were resistant to p-rosaniline. The drug inactivation was also discovered early as well. In 1919, Neuschlosz reported Paramecium caudatum resistance to quinine and a dye that acquired the ability to destroy the toxic agent. The emerging resistance in clinical isolates to penicillin was reported as early as 1941, resistance to sulfonamide in 1939. Miller and Bohnhoff observed resistance to streptomycin in 1947. The streptomycin was initially represented as the first breakthrough in the chemotherapy of tuberculosis. However, relapses were soon observed with streptomycin-resistant Mycobacterium tuberculosis. The resistance continued to develop for other antimicrobials as well. It was soon realized that resistance could emerge even in the absence of an antibiotic by transfer of antibiotic genes.
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