Immediate

Immediate (type I) hypersensitivity reaction is the most common serious adverse event following vaccination in dogs. This reaction is mediated by immunoglobulin E (IgE), the principal cellular component is the mast cell or basophil, and the reaction is amplified or modified by eosinophils, neutrophils, and platelets. The precise mechanism by which some patients are more prone to type I hypersensitivity is not clear. It has been shown in people that some individuals preferentially produce more type 2 helper T cells that secrete interleukin-4 (IL-4), IL-5, and IL-13, which favor IgE activation. IgE produced preferentially in response to certain antigens or allergens links with the allergen at receptors on mass cells and basophils to trigger mass cell degranulation. Mediators of immediate hypersensitivity include preformed agents such as histamine, tryptase, and kininogenase, and newly generated mediators such as leukotrienes and prostaglandins. These mediators increase vascular dilation and permeability and cause smooth muscle contraction.

Antigens within vaccines that can cause type I hypersensitivity reactions include foreign proteins such as residual culture media proteins, additives, preservatives, and possibly adjuvants. Protein of bovine origin from fetal calf serum has been incriminated as an IgE allergen causing hypersensitivity reactions in some dogs (Ohmori et al, 2005). Different vaccines, even with the same label antigen (e.g., Leptospira), may contain differing quantities of foreign proteins after the vaccine manufacturing process. Thus practitioners may observe different reaction rates when using the same antigen vaccines from different manufacturers. Continued vaccine quality improvements, however, have reduced hypersensitivity reaction rates for many vaccines in the last decade.

A dose-response relationship has been observed between the number of vaccines administered at one time and the likelihood of an immediate hypersensitivity reaction (Moore et al, 2005). This relationship derives from the increased risk associated with individual vaccines in smaller dogs (i.e., <10 kg) as well as the increase in risk as additional vaccines are given at one time to any dog. It is therefore prudent to limit the number of parenterally administered vaccines administered at one time, particularly to smaller dogs or dogs at high risk. Increased risk has been demonstrated for some small breeds such as dachshunds, pugs, miniature pinschers, Boston terriers, and Chihuahuas, and selected large breed dogs such as boxers and weimaraners. This increased risk most likely represents genetic predisposition to rapid mast cell degranulation in the face of low quantities of antigen. The optimal separation time between administration of different vaccines is not known, but a 2-week interval is considered reasonable.

Clinical signs of type I hypersensitivity commonly are noted in the skin and vascular systems and include facial or periorbital edema, wheals, urticaria, pruritus, hypotensive shock, or collapse. Vomiting with or without diarrhea and respiratory distress are noted less commonly. Treatment of immediate hypersensitivity reactions should be tailored to the severity of the clinical signs. Treatment may include the H₁ antihistamine diphenhydramine to block histamine receptors, rapidly soluble glucocorticoids to block arachidonic pathways, and intravenous crystalloid fluids to counteract hypotensive shock. Epinephrine and oxygen therapy are not often necessary but are indicated for cyanosis and respiratory distress. In patients with documented immediate hypersensitivity reactions to previous vaccinations, prevaccination administration of diphenhydramine (2 to 3 mg/kg IM) may prevent recurrence of type I reactions; untreated dogs may or may not demonstrate adverse effects after subsequent vaccinations.