Etiology

• Drugs, infectious organisms, foods, pollens, and insects can be responsible for urticaria.
• In humans antibodies against the high affinity high IgE receptors may be found.

Pathophysiology

• Urticaria and angioedema are generally immunological reactions to a wide variety of causative agents including insect and arthropod bites and stings Insect stings, infections, feedstuffs including those with fungal growth, drugs, blood transfusion Blood transfusion and vaccines (often those produced using horse serum), physical trauma and plants such as stinging nettles. Also auto-allergy to casein in milk.
• These are classical type I immediate hypersensitivity reactions.
• The pathogenesis of urticaria and angioedema theoretically requires the animal to be sensitized to the causative allergen by prior exposure. However in the case of incompatible blood transfusions and in some cases of vaccine-induced reactions, urticaria occurs on the administration of the first dose of vaccine. In such cases it is possible that there is sensitization to a cross-reactive environmental allergen that permits the reaction, or that non-IgE-mediated mast cell degranulation occurs, but this has been poorly investigated.
• The pathogenesis of type I hypersensitivity involves the production of allergen-specific IgE (and subtypes of IgG) antibody following sensitization. These antibodies attach to specific receptor molecules on the surface of cutaneous or mucosal mast cells, circulating basophils and epidermal Langerhans dendritic cells. On subsequent exposure to the sensitizing allergen, there is mast cell degranulation with ensuing vasodilation, tissue edema and inflammation, smooth muscle contraction (bronchoconstriction) and pruritus.
• The urticarial reaction that may occur with incompatible blood transfusion is a type I hypersensitivity reaction, and the causative allergen is most likely protein within the donor blood. By contrast, the hemolytic transfusion reactions involve type II hypersensitivity with sensitization to a cell-associated antigen (eg blood group antigen) and the production of IgG and IgM antibodies. This might occur by prior incompatible blood transfusion, or alternatively in the case of some blood group antigens, spontaneously occurring alloantibodies are present (presumptively due to prior exposure to cross-reactive environmental antigens). Exposure to the causative antigen permits binding of the IgG/IgM antibodies, with activation of the classical complement pathway and generation of the anaphylactic mediators C3a and C5a. These may directly cause mast cell degranulation and mediate a similar anaphylactic-type response.
• In some cases Type III hypersensitivity may be responsible for recurrent urticaria.

Timecourse

• These are acute onset reactions following exposure to the inciting allergen.