Antivenin‐associated serum sickness in a dog

Abstract

Objective:To describe a case of documented serum sickness in a dog following administration of a single dose of a novel antivenin crotalidae polyvalent. Case Summary:A 4-year-old female neutered mixed breed dog developed recurrent signs of hypersensitivity (swelling, edema, urticaria/hives, gastrointestinal signs, vasculitis) at 1 and 2 weeks following administration of a single unit of a novel antivenin crotalidae polyvalent plasma product. Both episodes were treated with antihistamines and glucocorticoids and signs improved rapidly, with a prolonged course of glucocorticoids and antihistamines administered following the second occurrence. Diagnosis of serum sickness was based on clinical appearance of delayed hypersensitivity following exposure to novel biologic product, absence of other inciting cause of hypersensitivity, complement testing, and skin biopsies confirming vasculitis. New or Unique Information Provided:This case documents the first report of delayed hypersensitivity with a novel antivenin plasma product. This is the only case report of serum sickness to a single unit of antivenin. Additionally, the dog developed recurrence of hypersensitivity following the initial episode at 1 week; appropriate identification and prolonged treatment could have prevented recurrence and additional hospitalization. Cost and benefit analysis should be considered with antivenin administration. K E Y W O R D Sanatomy, anesthesiology, cardiovascular, coagulation, fluid balance

In vitro evaluation of canine whole blood with the addition of Crotalus atrox (Western Diamondback Rattlesnake) venom and antivenom using thromboelastography

“…There is a possibility that if venom from a different snake species had been used, then different outcomes might have occurred. Antivenom is composed of antibodies to various aspects of snake venom and can include whole immunoglobulin G or antigen‐binding fragments formed after pepsin digestion (F(ab’)2) 2,5–7,9,12,17,23,26,27 . The North American antivenom product contains both the fragment crystallizable region of antibody (Fc) and F(ab’)2 portions of the antibody structure 2,5–7,9,12,17,22,26,27 .…”

“…Antivenom is composed of antibodies to various aspects of snake venom and can include whole immunoglobulin G or antigen‐binding fragments formed after pepsin digestion (F(ab’)2) 2,5–7,9,12,17,23,26,27 . The North American antivenom product contains both the fragment crystallizable region of antibody (Fc) and F(ab’)2 portions of the antibody structure 2,5–7,9,12,17,22,26,27 . b Since the Fc portion of the antibody binds complement, it is considered to be the most immunogenic, which has been shown in other Fc‐containing antivenom products 5,9,27 .…”

Retrospective comparison of three antivenoms for the treatment of dogs with crotalid envenomation

“…14,24 However, when an animal is given a whole immunoglobulin product from a different species, antibodies can be found in that animal's bloodstream in 14 to 21 days. 9,21 This raises a question not explored in our study as to which product would be safest to use if a dog is given a fractionated or whole immunoglobulin antivenom product during its initial crotalid envenomation and then has another envenomation episode. We were unaware of any literature indicating a significantly higher reaction rate in dogs or people who have received antivenom on > 1 occasion.…”

“…However, the Fc portion also increases the risk of acute type I and delayed type III hypersensitivity reactions. [7][8][9] Two IgG products 10,11 are currently approved by the USDA for use in animals with crotalid envenomation (referred to subsequently as antivenoms C and D).…”

Intramyocardial haematoma causing right ventricular outflow obstruction after brown snake (Pseudonaja species) envenomation in a dog

“…38 The prevalence of serum sickness in dogs after administration of antivenom is unknown, but three case reports have been published reporting its occurrence after different antivenoms for viper envenomation in the United States. [41][42][43] In human medicine, there is no consensus regarding the diagnostic criteria for serum sickness; however, it is usually a clinical diagnosis. Australian authors have suggested that clinical signs, risk factors and laboratory data may contribute to a diagnosis.…”