The discovery of anaphylaxis

In 1902, Richet and Portier were attempting to immunize dogs with venom extracted from sea anemones (Actinia). To their surprise, instead of being protected, some dogs had apparently become more sensitive to the effect of the venom: they became acutely ill and died within minutes of the second injection. They had expected protection (prophylaxis) but had, they thought, achieved the opposite, which they termed anaphylaxis. It soon became clear that this was not enhanced toxicity of the venom, but rather a dangerously severe acute allergic reaction that could equally be triggered by non-toxic proteins. Prausnitz demonstrated in 1921 that this hypersensitivity could be transferred by a heat-labile component of the serum, but it was not until 1966 that the Ishizakas identified this component as immunoglobulin E (IgE).

Hypersensitivity reactions take many forms and these were classified in 1968 by Gell and Coombes; IgEmediated hypersensitivity was labelled type I. More recently, the nomenclature committee of the European Academy of Allergy and Clinical Immunology (EAACI) has recommended it should simply be called “IgE-mediated hypersensitivity.”

Definitions of anaphylaxis

The term “anaphylaxis” has been used for all types of acute life-threatening illness triggered by abnormal sensitivity to a trigger agent, and for apparently spontaneous attacks with similar features (idiopathic anaphylaxis). This has made it difficult to define. The EAACI Nomenclature Committee proposed the following broad definition: