Introduction

• Cause: systemic Type I hypersensitivity response.
• Signs: facial urticaria and pruritus, vomiting, shock.
• Diagnosis: history and clinical signs.
• Treatment: intravenous fluids, corticosteroids, antihistamine.
• Prognosis: good if responds to immediate emergency treatment.

Pathogenesis

Etiology

• Often iatrogenic:
  • Blood transfusion Anemia: transfusion indications.
  • Cytotoxic drugs Chemotherapy; general principles.
  • Potentially allergenic therapies, eg Vitamin K1 (for anticoagulant poisoning Anticoagulant rodenticide poisoning), tetanus antitoxin Tetanus.
  • Vaccine reactions.
  • Food reactions.
• Insect bites.

Specific

• Previous exposure to allergen.

Pathophysiology

• Mast cell degranulation   →   release of chemical mediators   →   clinical signs.

• Animal must first be sensitized to antigen to produce anaphylactic reaction.
• Production of IgE occurs initially which binds to tissue mast cells and circulating blood basophils which renders these cells 'sensitized'.
• On second exposure antigen binds to IgE on mast cells and basophils   →   degranulation and vasoactive amine release and pro-inflammatory mediator release.
• Multiple effects on many body systems   →   signs of shock ( mainly as a consequence of hypovolemia from increased vascular permeability and pooling of blood from vasodilation).

Timecourse

• Acute (within minutes of exposure in sensitized animal).

Diagnosis

Treatment

Prevention

Outcomes