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JAMA. 1951;147(14):1361. doi:10.1001/jama.1951.03670310051017.
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Although the exact mechanism by which streptomycin effects its antimicrobial action is not known, there is considerable evidence to indicate that it involves the inhibition of certain metabolic activities of nonproliferating cells of susceptible strains of bacteria.1 Consequently, efforts have been directed toward demonstrating differences in metabolic activities between streptomycinresistant and streptomycin-sensitive bacteria. Thus Seligmann and Wassermann2 reported that acquired resistance is accompanied by certain marked alterations in metabolic activities which they attributed to damage to enzyme systems. Umbreit3 found that susceptible strains of Escherichia coli, but not resistant or dependent variants, possessed an oxidative reaction that is inhibited by streptomycin; he concluded that strains capable of growing in the presence of streptomycin have eliminated the reaction inhibited by the drug. Recently, English and McCoy4 have compared the growth of the sensitive parent and a number of resistant mutants of Micrococcus pyogenes var. aureus in nutrient


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