Antibiotic Resistant Genes in Natural Environment

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 [1]. In 1919, Neuschlosz reported Paramecium caudatum resistance to quinine and a dye that acquired the ability to destroy the toxic agent [1]. The emerging resistance in clinical isolates to penicillin was reported as early as 1941, resistance to sulfonamide in 1939 [2-4]. Miller and Bohnhoff observed resistance to streptomycin in 1947 [5,6]. The streptomycin was initially represented as the first breakthrough in the chemotherapy of tuberculosis [7]. However, relapses were soon observed with streptomycin-resistant Mycobacterium tuberculosis [8]. 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 [1]. For instance, Hotchkiss demonstrated that penicillin resistance could be transferred to susceptible pneumococcus [1,9]. However, the most important step was to understand the prevalence of R-plasmids that help to better understand the resistance acquisition and dissemination [1]. The excessive usage of antibiotics in agriculture, aquaculture and livestock has resulted in selection for resistant bacteria [10]. The spread of antibiotic resistance genes by horizontal gene transfer via plasmids and mobile elements such as transposons has increased the acquisition of antibiotic resistance genes among species from antibiotic producers to commensal and pathogen bacteria [11,12]. Today, the focus is to understand the function of these resistance genes in their natural environmental hosts and understand the mechanisms involved in the emergence, and spread of antibiotic resistance.