Leighton E. Cluff

CELLULAR REACTIONS IN THE PATHOGENESIS OF STAPHYLOCOCCAL INFECTION

Inflammation associated with microbial multiplication is the essence of infection. How microorganisms initiate an inflammatory reaction, however, is poorly understood.’ Bacteria may be chemotactic;’ they may elaborate “toxic” substances influencing vascularity or causing direct injury to cells; they may elaborate enzymes which facilitate or impede the spread of infection.‘ On the other hand, activation of host factors may initiate inflammation and determine its course irrespective of any specific attribute or characteristic of the microorganism.:’ Whatever its cause, alteration of the inflammatory reaction may have a profound influence upon the pathogenesis of infection. Staphylococci rarely, if ever, invade and infect normal tissues, but become pathogenic only after invasion of previously injured or inflamed mucocutaneous surfaces. With these bacteria, therefore, we are not solely concerned with the inflammation induced by infection, but also with the influence of previously inflamed or injured tissue upon the infectivity of the microorganism. Staphylococci are indigenous to man and can be recovered from mucocutaneous surfaces of all human beings repeatedly or intermittently. Colonization, therefore, is the rule, and infection rarely, if ever, develops without alteration of local or systemic resistance. Nevertheless, everyone probably acquires staphylococcal infection, but some more frequently and severely than others4 The uniform colonization and infection of human beings, even though variable in severity and frequency, is further illustrated by the demonstration of immunological reactivity to staphylococcal antigens in most persons.’ Therefore, infection by these bacteria is usual in individuals possessing hypersensitivity or immunological reactivity to the microorganism. The possible implication of hypersensitivity in the cellular reaction occurring with staphylococcal infection cannot be overlooked. Acquired immunity has not been previously considered particularly important in the control of staphylococcal infection. There are observations, however, showing that the cellular reaction to staphylococcal disease may be influenced by immunization with specific bacterial

Adrenal Hemorrhagic Effect of Thorotrast.

Summary Thorotrast administered intravenously has been shown to produce bilateral adrenal hemorrhage in rabbits. This effect is directly related to the dosage of Thorotrast employed, and is more frequently observed in larger rabbits than in small rabbits. Adrenal hemorrhage was dependent upon the particulate material in Thorotrast (thorium dioxide) and was not produced by the dextrin medium alone. The possible role of at least 3 demonstrated activities of Thorotrast—adrenal stimulation, production of multiple coagulation defects, and vascular wall injury is discussed.

Identification of toxinogenic C. diphtheriae with fluorescent antitoxin: demonstration of its nonspecificity.

Summary 1. Immunofluorescent staining of various Corynebacteria and other microorganisms with fluorescein labelled diphtheria antitoxin resulted in staining of toxinogenic and atoxinogenic strains of C. diphtheriae, as well as of certain other Corynebacteria and unrelated microorganisms. 2. Specificity of this staining for identification of toxinogenic C. diphtheriae could not be improved by alterations in conditions of staining, or by chemical manipulation of antitoxin solutions. 3. This lack of specificity is felt to be due to multiple non-antitoxic (accessory) antibodies present in the antitoxin preparations which cross-react with a variety of bacterial antigens. 4. It is suggested that stainable diphtheria toxin may not be present at or on the surface of viable, intact diphtheria organisms, and specific identification of toxinogenic C. diphtheriae by fluorescent antitoxin may not be possible. 5. On the basis of data presented here, this technic as currently described would seem to offer little more than a gram stain to the diagnostic bacteriology of diphtheria.