Anaphylaxis
Basic Information 
Epidemiology
Risk Factors
• Previous exposure and sensitization to antigens suspected to cause allergies increases the risk, but this is not always recognized.
• May be triggered by antigens in vaccines, hormones, antibiotics, or antiparasitic agents.
• IV penicillin may trigger acute anaphylaxis in horses.
• Geography and seasonality: Insect-related anaphylaxis may be a summer disease.
Clinical Presentation
Disease Forms/Subtypes
• Anaphylactoid reactions: Under some circumstances, mast cell degranulation may occur in the absence of immunoglobulin E (IgE) antibodies and without prior sensitization. Thus these reactions do not require previous exposure to antigens.
• Anaphylactic reactions: Occur when an antigen (allergen) binds to IgE molecules located on the mast cell surface. These IgE molecules are induced by prior exposure to allergens.
Etiology and Pathophysiology
• Initial exposure to an allergen results in a Th2 response and the production of IgE antibodies. These antibodies bind to Fc receptors on the surface of mast cells and basophils.
• Subsequent exposure of the primed animal to the antigen results in antigen binding to the bound IgE and signaling to the mast cells and basophils, resulting in their rapid degranulation.
• Granules release the primary mediators, notably histamine and heparin.
• Degranulated cells synthesize secondary mediators, namely prostaglandins and leukotrienes, through the arachidonic acid cascade.
• Within a few hours, degranulated cells synthesize multiple cytokines, notably interleukin (IL)-4 and IL-13.
• The initial stages include acute hypotension combined with pulmonary arterial hypertension coinciding with histamine release. In a second phase, beginning about 3 minutes after exposure, venous blood pressure increases, coinciding with serotonin release. About 8 to 12 minutes after exposure, a third phase begins characterized by a reflex increase in blood pressure and alternating apnea and dyspnea. Subsequently, prostaglandin and leukotriene release lead to a phase of prolonged hypotension.
• The changes in vascular tone, increased vascular permeability, and bronchospasm lead to pulmonary congestion, edema, emphysema, and eventual death from hypoxia.
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