Abstract

Lysostaphin resistance in the laboratory can arise via single or multistep mutational processes. Inheritance of lysostaphin resistance, moreover, appears to be a stable genotypic trait. Regardless of the level of lysostaphin resistance, mutants are lysed but at much slower rates than are the parent strains. A hypothesis based on differences in the chemical composition of the cell wall structures of lysostaphin-sensitive and lysostaphin-resistant mutants is advanced to explain the acquired resistance to this specific antibiotic. No antibiotic cross-resistance was detected between lysostaphin and seven other clinically useful antibiotics. Thus far, no strains of staphylococci naturally resistant to lysostaphin have been detected in more than 400 clinical isolates of coagulase-positive cultures. In addition, the effects of various environmental factors on lysis of viable S. aureus cells by lysostaphin were investigated.

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