Successful Management and Resolution of a Severe Necrotizing Dermatopathy in a Golden-Headed Lion Tamarin (Leontopithecus chrysomelas)
An 8-year-old female golden-headed lion tamarin (Leontopithecus chrysomelas) with a prior history of metabolic bone disease and cholelithiasis presented with a full thickness, 3 cm × 2 cm ulceration on the right lateral thorax and abdomen, with multiple furuncles at the wound edges and on the lateral aspect of the right arm. Unknown trauma with secondary infection was the most likely etiology. Histopathology indicated an ulcerative dermatitis with colonies of coccoid bacteria; severe, necrotizing cellulitis; and pyogranulomatous furunculosis. An aerobic culture grew Staphylococcus aureus that was sensitive to most common antibiotics. Initial treatments consisted of amoxicillin/clavulanic acid (Pfizer, New York, NY, USA), ciprofloxacin (Lupin Limited, Baltimore, MD, USA), and meloxicam (Boehringer Ingelheim, St. Joseph, MO, USA), and evaluations were performed every 3–5 days for topical treatments with dilute chlorhexidine (Agrilabs, St. Joseph, MO, USA) and/or betadine (Purdue Products, Stamford, CT, USA), and topical silver sulfadiazine (SSD 1%, Ascend Laboratories, LLC, Parsippany, NJ, USA). Within 2 weeks, the initial wounds had contracted, but thick, raised, brown plaques had developed. At 4 weeks, the plaques had spread over the right side of the body (7.6 cm × 3.5 cm). Repeat skin biopsies showed severe necrosis and neutrophilic infiltration with mixed bacterial infection of the epidermis and dermis, and macrophage-engulfed granules that were suspected to be related to ointments. Possible etiologies for the extensive response included a staphylococcal toxin reaction, a reaction to systemic or topical medications (SSD, or betadine), or an underlying immune pathology leading to a pyoderma vegetans-type lesion.1-3 Topical chlorhexidine and oral amoxicillin/clavulanic acid and ciprofloxacin were continued, clindamycin (Greenstone Brand, Peapack, NJ, USA) was added due to its anti-toxin effects, and an anti-inflammatory course of prednisone (Boehringer Ingelheim, St. Joseph, MO, USA) was administered and tapered.4 At week 7, the plaques had spread to cover approximately 40% of the dorsum and the right side of the thorax and abdomen. Repeat biopsies showed severe ulceration bordered by severe hyperplastic epidermis covered with a crust of exudate, degenerate neutrophils and bacteria. Chemical debridement with hydrogen peroxide (H2O2) was initiated, consisting of covering the area in H2O2-soaked gauze for 5–10 min, and then using H2O2-soaked cotton tipped applicators to mechanically debride the plaques. This procedure was repeated every 3–5 days for the first 2 weeks, and immediate improvement and epithelialization of the borders of the affected tissue were seen. Repeat debridements were performed every 2–4 weeks for 4 months. During this time, oral clindamycin was the only oral treatment administered. Complete resolution of the lesion was seen 4 months after H2O2 debridement was initiated, with limited scarring, and normal hair coverage. This case highlights the importance of chemical debridement in management of necrotizing dermatopathies.
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