Anaphylaxis

Portier and Riehet, in 1902, first described anaphylaxis in dogs as the capacity of a toxic agent, after repeated attempts to induce immunization, to elicit an adverse reaction as opposed to the desired prophylaxis. Anaphylaxis, literally meaning "backward protection," required a latent period for sensitization and subsequent re-exposure to the sensitizing agent. This agent could be a hapten or foreign protein and its tissue accumulation was not necessary.¹. In humans, anaphylaxis occurred in minutes to hours after administration of an inducing agent. Clinical manifestations included urticaria, angioedema, laryngoedema, bronchospasm followed by respiratory distress, hypotension, shock, and, at times, death. Earlier, the most common causative agents of anaphylaxis were horse sera used for tetanus and diphtheria antitoxin, hymenoptera venom used in desensitization, and diagnostic and therapeutic agents. Subsequently, the discovery and widespread use of penicillin allowed for its becoming the major cause of anaphylactic deaths in the United States, causing an estimated 300 fatalities per year.^2,3.