ABSTRACT
The Jekyll and Hyde nature of the body’s immune response mechanism was recognized early by Clemens von Pirquet (Figures 1 and 2), who introduced the term ‘allergy’ to denote a state of altered reactivity1. It was found that some types of allergy or hypersensitivity could be passively transferred to previously non-reactive individuals with serum, whereas others required lymphoid cells. Coca and Cooke introduced the term ‘atopy’, which means ‘out of place’ or ‘strange disease’,
to characterize certain hypersensitivity states which were considered to be heritable and to be limited in occurrence to the human being2 (Figures 3-5). The atopic diseases include allergy to foods, hay fever and pollen, and constitute the so-called clinical allergies. Antibodies in the blood sera of atopic patients were described as being different
from the precipitins and agglutinins involved in common serological reactions. The reagins, as these antibodies were called, are now known to
belong to the IgE class of immunoglobulin. Two physicians, Prausnitz (Figure 6) and Küstner, transmitted sensitivity to fish from one of them to the other by the injection of serum3. They were the first to demonstrate the passive transfer of specific reactivity with serum from atopic individuals to local skin sites in normal recipients, who subsequently demonstrate a wheal and flare response following injection of specific antigen into the same site. In studies on the relationship of hypersensitivity to immunity, Arthus, in 1903, observed that repeated injections of protein antigen into the same skin site of rabbits led to a hemorrhagic and necrotic reaction4 (Figure 7). This local hypersensitivity reaction was subsequently demonstrated to be caused by immune complexes, classified by Coombs and Gell as type III hypersensitivity (Figures 8 and 9). This phenomenon, known since that time as the Arthus reaction, is proven by its specificity and dependence upon immune complexes to be immunologic in nature. By contrast, the Shwartzman phenomenon, which is remarkably similar to the Arthus reaction in many respects, is not immunologic. In 1928, Gregory Shwartzman found that a hemorrhagic and necrotic reaction could be produced at a local site 4 h following a provocative intravenous injection of a small amount of Salmonella typhi culture filtrate
in rabbits treated 24 h previously by an intradermal injection of an agar culture washing of the microorganisms (Figures 10-13). This led to the localized Shwartzman reaction. If both injections were administered intravenously, the generalized Shwartzman reaction took place with features closely resembling disseminated intravascular coagulation (DIG)5.
