Systemic blastomycosis in a horse.

Progressive multisystemic disease caused by Blastomyces dermatitidis was diagnosed in a 17-year-old Quarter horse broodmare. The mare had been treated unsuccessfully with antibiotics for mastitis 3 months postpartum. The disease progressed to exudative cutaneous lesions affecting the ventrum, pectoral region, and limbs accompanied by weight loss across several months. Yeast bodies were observed in swabs of the cutaneous exudate, suggesting a clinical diagnosis of blastomycosis. Following referral, pleural effusion, cavitated lung lesions, and hyperproteinemia were identified, and the mare was euthanized because of poor prognosis. Necropsy revealed extensive pyogranulomas in the mammary gland, skin, subcutaneous tissues, and lungs, accompanied by thrombi in major blood vessels of the lungs and hind limbs. Histologically, pyogranulomatous inflammation was evident in many tissues, and fungal organisms were seen in sections of mammary gland, skin, subcutis, pericardium, and lung. Blastomyces dermatitidis was cultured from mammary tissue, lungs, lymph node, and an inguinal abscess. Although blastomycosis is endemic in the area of origin of the mare in northwestern Wisconsin, the disease is extremely rare in horses and hence easily misdiagnosed. Unique features of this case included the extent of mammary gland involvement and the presence of thrombi in multiple sites.

Infarctive purpura hemorrhagica in five horses.

Five horses were examined because of signs of muscle stiffness, colic, or both. All 5 had been exposed to Streptococcus equi within 3 weeks prior to examination or had high serum titers of antibodies against the M protein of S equi. Horses had signs of unrelenting colic-like pain and focal areas of muscle swelling. Four horses were euthanatized. The fifth responded to treatment with penicillin and dexamethasone; after 3 weeks of treatment with dexamethasone, prednisolone was administered for an additional 10 weeks. Common hematologic and serum biochemical abnormalities included neutrophilia with a left shift and toxic changes, hyperproteinemia, hypoalbuminemia, and high serum creatine kinase and aspartate transferase activities. Necropsy revealed extensive infarction of the skeletal musculature, skin, gastrointestinal tract, pancreas, and lungs. Histologic lesions included leukocytoclastic vasculitis in numerous tissues and acute coagulative necrosis resembling infarction. These horses appeared to have a severe form of purpura hemorrhagica resembling Henoch-Schönlein purpura in humans and characterized by infarction of skeletal muscles. Early recognition of focal muscle swelling, abdominal discomfort, neutrophilia, hypoalbuminemia, and high serum creatine kinase activity combined with antimicrobial and corticosteroid treatment may enhance the likelihood of a successful outcome.