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STAPHYLOCOCCUS AUREUS is one of the most versatile human pathogens. In the late 1930s, sulfonamides offered the first challenge to S. aureus, but they failed because of their poor clinical performance in the presence of pus and the acquisition of resistance by the bacteria.1 In the early 1940s the introduction of benzylpenicillin (penicillin G) temporarily solved the problem of staphylococcal infections, but the continued use of this agent caused the selection of resistant strains, which produced penicillinase (β-lactamase). By 1948 the prevalence of resistant strains had seriously reduced the value of benzylpenicillin.2 By the end of the 1950s, S. . . .
Brumfitt et al. (Thu,) studied this question.