Toxic shock syndrome (TSS) in humans is a systemic disease caused by the release of bacterial toxins with superantigen activity. Most cases in humans are related to production of toxic shock syndrome toxin‐1 (TSST‐1) by strains of Staphylococcus aureus. Clinically, they manifest with high fever, hypotension, diarrhoea, myalgia, skin rash and oedema, often progressing to desquamation of the skin. External or internal infections may be the origin. In dogs, the most common bacterial organism isolated from cases of bacterial pyoderma is Staphylococcus intermedius. This bacterium has also been shown to produce exotoxins, including TSST‐1. Retrospectively, 11 dogs with clinical presentations and histopathological lesions closely resembling TSS in humans were evaluated. The animals ranged in age from 1.5 to 13 years, with a mean of 4.65 years. No sex predisposition was found. The breeds represented in the study were varied, including small breeds (pug, Boston terrier) and large breeds (golden retriever, Labrador retriever). The most common clinical presentation was multicentric to generalized cutaneous erythema (n = 10) and oedema (n = 7), in some cases with vesicles (n = 4) and pustules (n = 3) evolving to ulcers (n = 3). The extremities, ears and ventrum were frequently involved. Systemic signs were invariably present. Mild anaemia (n = 8), hypoalbuminaemia (n = 8), depression (n = 8) and neutrophilia (n = 7) were the most consistent abnormalities. Fever (n = 5) and thombocytopenia (n = 5) were also observed. Complete clinical history was not obtained in two cases that were compatible with this condition on histopathological exam. In general, there was a good response to systemic treatment with cephalexin (n = 4); in cases for which early antibiotic therapy was not instituted, the outcome was usually fatal(n = 5). In the only case cultured, pustular lesions yielded a mixed population of coagulase‐positive Staphylococcus spp. and Pseudomonas spp. Histologically, the most characteristic pattern was superficial dermatitis with epidermal neutrophilic exocytosis and necrotic (apoptotic) keratinocytes, often with neutrophilic satellitosis. The lesions evolved to panepidermal necrosis with ulceration in some dogs, a phenomenon unrelated to the final outcome. The pathogenesis of the skin lesions in human cases of TSS seems to be related to the nonspecific stimulation of lymphocytes by the bacterial superantigen and the release of high levels of cytokines, specifically TNFα. Until further characterization of the process is obtained, biopsies with features of neutrophilic exocytosis and apoptosis should warrant consideration of TSS, and immediate antibiotic treatment (cephalexin) should be instituted to prevent potential fatal progression of the disease. Funding: Self‐funded.
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