Sulfonamide-resistant strains of Staphylococcus aureus produce greater amounts of p-aminobenzoic acid than do their parent strains. This synthesis occurs both in the absence and in the presence of sulfonamides. The quantity of p-aminobenzoic acid synthesized by resistant strains appears sufficient to account for their resistance to sulfonamide drugs. On the basis of this evidence, it is suggested that the development of ability to synthesize p-aminobenzoic acid in excess of the normal metabolic requirements, as a result of continued exposure to sulfonamides, explains the phenomenon of sulfonamide fastness in Staphylococcus aureus.
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