The staphylococcal scalded skin syndrome in historical perspective: emergence of dermopathic strains of Staphylococcus aureus and discovery of the epidermolytic toxin. A review of events up to 1970

Abstract

The gradual recognition of dermopathic strains of Staphyloccus aureus, which cause staphylococcal impetigo, pemphigus neonatorum, Ritter's disease, and what was originally called staphylococcal toxic epidermal necrolysis, is described. Obstacles delaying their recognition included an entrenched belief that staphylococci should produce pus, the striking dissimilarity of their main clinical effects (impetigo and scalding), the strongly held opinions of von Rittershain, and controversy over the cause of impetigo. Phage typing and histopathology confirmed the common etiology of these diseases and established the existence of dermopathic strains securely. The important contributions made by Melish and Glasgow were to provide an experimental model for these strains and to discover the epidermolytic toxin, whose action of splitting the epidermis underlies the pathogenesis of all these diseases (which have become known collectively as the staphylococcal scalded skin syndrome). Clinically, however, the impetigo effects and the scalding effects differ markedly, so it is proposed that staphylococcal impetigo should be retained as a separate clinical entity, and that staphylococcal impetigo and the modified staphylococcal scalded skin syndrome should be known collectively as the staphylococcal epidermolytic toxin syndrome.