Alexander Ogston, micrococci, and Joseph Lister.

This paper recalls the notable achievement, in 1880, of Alexander Ogston, a surgeon who, seeking the cause of suppuration, showed that acute abscesses result from micrococci. There were two kinds. One, arranged in chains, had been called streptococci already; the other, in clumps, he named staphylococci. He injected micrococci into animals. If blood poisoning occurred in them, it followed localized tissue infection. This information, applied to surgical events, suggested that the "hospital diseases" were a sequel to wound suppuration and explained why antiseptic surgery controlled both conditions. Ogston's observations are now common knowledge, but Lister rejected them. It is suggested he did so because he relied on intuition rather than experiment. The scene is set for Lister and Ogston's discoveries by a review of the historical background. Patients subjected to surgery faced a terrible ordeal and a very real chance of death from the mysterious hospital diseases. Surgeons viewed the mortality with bland detachment, blaming fate. But Simpson and Semmelweis were deeply concerned. However, puerperal fever was regarded as entirely distinct from the hospital diseases, and neither condition connected in any way with suppuration in wounds. Simpson, Semmelweis, Lister, and Ogston all found their ideas scorned by members of the profession, which may have feared being held responsible for deaths. Ogston's achievement lives on, but he has been forgotten. We should remember him.

Perianal orf.

The parapox viral infection orf is usually diagnosed without difficulty when the lesions have the characteristic morphology and there is an appropriate history of contact with sheep. Two cases of orf in a perineal location in young children are presented to illustrate modification of the physical signs by flexural occluded sites. Electron microscopy of scrapings from the lesions established the diagnosis.

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.

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.

Review of significant progress in clinical dermatology since 1977.

The disease rules all; the patient, except for HLA typing, is in eclipse. Immunology holds the key to new knowledge. Management lingers at present behind scientific advance (systemic lupus erythematosus), or is fired by a new, and possibly overenthusiastic, aggressive spirit (mycosis fungoides). Classification of clinical disease is bound to change (dermatitis herpetiformis). Our concept of Staphylococcus aureus has been widened further (toxic shock syndrome). Psoriasis, a more unpleasant disease than we have cared to admit, may be connected with a generalized enzyme defect. Psoriasis, acne, and other disorders of keratinization respond to newer oral retinoids. Some vignettes of new therapy, new toxicity, new ideas, and old ideas seen anew have been presented.