Bullous Pemphigoid in a Dog

Suélen Dalegrave, Denner Francisco Tomadon Fiorin, Eduarda Gabriela Mansour, Monica Regina de Matos, Renato Herdina Erdmann, Laís Rezzadori Flecke, Luana Baptista de Azevedo, Eduardo Conceição de Oliveira

Abstract


Background: In dogs, bullous pemphigoid (BP) is a subepithelial autoimmune disease, a rare dermatopathy in the clinical routine. BP is characterized by formation of vesicles and subepidermal blisters that result from dissolution of the dermal-epithelial junction. Clinical signs of BP usually include severe dermatological alterations with a variable prognosis. The aim of this work is to report a case of BP in a dog to contribute information for diagnosis, and to present clinical and pathological aspects that emerge during development of BP.

Case: An adult male mongrel dog exhibited hyperemic, exudative, crusty lesions on the lip commissure and periocular areas. Results from laboratory tests were normal. Results from parasitological and mycological tests on skin scrapings were negative. Imprint cytology of the crusts revealed presence of gram-positive cocci bacteria. In the histopathological analysis of punch biopsy material, the epidermis was detached from the dermis, leading to formation of vesicles. There were inflammatory infiltrates containing neutrophils, eosinophils, and high amounts of fibrin, and areas of multifocal orthokeratotic hyperkeratosis. Multifocal infiltrates containing lymphocytes, histiocytes, and plasma cells were observed on the superficial portions of the dermis, which indicated a diagnosis of BP. After the definitive clinical diagnosis, the animal was treated with enrofloxacin (Baytril Flavour®; 5 mg/kg once a day for 10 days), and prednisolone (Prediderm®; 2 mg/kg once a day until further instructions). On the follow-up visit, 15 days later, the clinical picture had improved, and the lesions had decreased. Continuity of the treatment was prescribed, along with a gradual decrease in the corticoid dose. The dose of prednisolone was initially reduced to 1 mg/kg once a day, and later to 0.5 mg/kg until improvement of the clinical status of the patient. Remission of the lesions was observed 13 weeks later.

Discussion: The diagnosis of BP was established after identification of the clinical cutaneous lesions and observation of microscopic findings on punch biopsy material obtained from the ocular and lip regions. BP does not exhibit breed or sex predisposition, and affects adult dogs. The clinical signs of BP are characteristic of autoimmune diseases that affect the dermoepidermal junction, and consist of erythematous, ulcerated, crusty, and painful lesions on the nose, dorsal area of the muzzle, and periorbital region. However, these lesions must be differentiated, by histological analysis, from several other conditions with a similar clinical presentation. Diseases that must be considered in the differential diagnosis comprise other variants of the pemphigus complex, lupus erythematosus, drug eruption, erythema multiforme, toxic epidermal necrolysis, epitheliotropic lymphoma, inherited bullous epidermolysis, mucous membrane pemphigoid, and lymphoreticular neoplasia. The clinicopathological findings indicated that the lesions were compatible with BP. The occurrence of necrotic and erythematous lesions is due to production of antibodies accompanied by a strong response of neutrophils, which results in loss of cell adhesion and epidermal necrosis. The presence of detachment of the epidermis from the dermis, inflammation in the superficial portion of the dermis, and infiltrates containing lymphocytes, histiocytes and plasma cells observed at the histopathological examination indicated the occurrence of BP. The skin histopathological examination warranted establishment of a diagnosis and therapeutic success. The lack of recurrence of clinical manifestations 43 weeks after the end of the glucocorticoid treatment demonstrated that the therapeutic approach and the cooperation of the owner are essential for success of the treatment.

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DOI: https://doi.org/10.22456/1679-9216.106575

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