Severe Vesiculobullous Dermatopathy in a Pacific White-Sided Dolphin (Lagenorhynchus obliquidens) Associated with a Sudden Increase in Caloric Intake
IAAAM Archive
Martin Haulena1; David Huff1; Stephen Raverty2; Sherry Myers3; Marcy Murphy4; Mark Papich4
1Vancouver Aquarium, Vancouver, BC, Canada; 2Animal Health Center, Abbotsford, BC, Canada; 3Prairie Diagnostic Services, SK, Canada; 4College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA


An approximately 18-year-old, 77.8 kg, adult female Pacific white-sided dolphin (Lagenorhynchus obliquidens) maintained in a semi-closed, 1.1 million litre captive display pool was presented for chronic regurgitation, weight loss, ulcerative lesions on the extremities, and small (<5mm diameter) vesicles on the peduncle. Biopsy, culture and polymerase chain reaction (PCR) of the lesions revealed no obvious viral involvement and a mixed population of bacteria associated with the cutaneous ulcers. Gastroscopy revealed no obvious cause for the regurgitation. The skin lesions were thought to represent poor wound healing secondary to weight loss from chronic regurgitation of behavioral origin. Regurgitation was treated by allowing the animal access to unlimited food.

Over the next 9 days, daily food intake increased from 8.5 kg (14,745 kcal/kg) to 19 kg (40,000 kcal) of mixed herring and capelin. Regurgitation stopped within 24 hours of behavioural treatment. After 7 days of access to unlimited food, skin lesions resolved, the dolphin's attitude had improved, and rapid weight gain was noted (99.5 kg; a gain of 22.3 kg).

On the 8th day of access to unlimited food, however, large (7-10 cm diameter) bilaterally symmetrical vesicular lesions developed initially on the nonpigmented regions of the thoracic flank and became generalized throughout the torso (trainers described the dolphin as "swollen"). Skin lesions progressed over the next 10 days to become a severe generalized bullous dermatopathy (affecting 65-75% of the dolphin's surface area) with individual bullae measuring up to 25 cm in diameter. Ruptured bullae drained sero-sanguinous fluid and left free flaps of skin up to 6 mm thick, exposing deep epithelium and dermis. Abnormalities on bloodwork included a mild leukocytosis of 7.6 x 109/L (RI 2.2-6.7 x 109/L), mildly increased fibrinogen of 3.9 g/L (RI 1.5-3.5 g/L), mild anemia (PCV=52%; RI 56-64%) with marked regeneration (18% reticulocytes; RI 0-4%), decreased serum iron of 11 μmol/L (RI 28-37 μmol/L), and increased GGT of 145 U/L (RI 10-55 U/L), AST of 1284 U/L (RI 30-190 U/L), and ALT of 834 U/L (RI 40-256 U/L). Serum vitamin A and E levels were within expected levels. Cytological examination of vesicular fluid revealed low numbers of neutrophils with scattered melanin granules, rare individual to small rafts of acantholytic keratinocytes, faintly eosinophilic strands of material (presumably fibrin) and rare gram-positive cocci and diplococci that were interpreted as incidental. Vesicular fluid aspirates were inoculated for aerobic and anaerobic bacterial culture including special media for Vibrio sp. and fungal culture. No significant growth was recovered. PCR on vesicular fluid and epidermal homogenates for calicivirus, universal herpesvirus, poxvirus, papillomavirus, and morbillivirus, as well as for universal Mycobacterium sp., Nocardia sp., Erysipelothrix sp., Streptococcus sp., and universal fungi were negative. Negative staining electron microscopy of cytospin preparations of the vesicular fluid and epidermis were negative for viral inclusions and no cytopathic effect was noted on Vero or Mabin Dawby cell lines after 3 weeks incubation. Histopathology showed superficial epidermal vacuolation and swelling degeneration, superficial laminar coagulative necrosis of the epidermis, transverse to vertical intraepidermal clefts extending outward from the dermoepidermal junction. The subjacent dermis showed mild to moderate edema with scattered nuclear dust and mild perivascular accumulations of predominantly neutrophils with fewer macrophages and lymphocytes. Based on these results, metabolic disorder (hepatic or pancreatic disease, internal neoplasia), superficial necrolytic dermatitis, immune-mediated skin disease, vasculitis, gas bubble disease and drug eruption were prime differentials.

Despite negative bacterial culture results aggressive antibiotic therapy was initiated due to a suspected viral etiology with secondary bacterial infection. The animal was treated with enrofloxacin, amoxicillin/clavulanic acid, cephalexin, azithromycin, and amoxicillin (not all simultaneously). Antibiotic therapy was changed based on poor response to therapy, cytology results, and to rule out drug reaction to a particular antibiotic. Prophylactic itraconazole therapy was started after multiple antibiotic therapies to prevent secondary mycoses. Very little response to antibiotic therapy was observed in the skin lesions, although blood inflammatory parameters and serum liver enzyme levels improved slightly. Food intake was limited to 12 kg/day. Prednisone at 1 mg/kg was started after 7 days of antibiotic therapy for 7 days due to increasing suspicion of immune-mediated disease. Although the number of new lesions developing may have decreased while the dolphin was treated with prednisone, there was no obvious healing noted. New lesions began developing after approximately 7 days of therapy with prednisone and cyclosporine was substituted at 5 mg/kg PO BID. Because of lack of initial response to therapy, continued increased liver enzyme levels (presumably exacerbated by itraconazole), and the possibility of drug reaction as an underlying cause, all remaining medications (amoxicillin, itraconazole, and cyclosporine) were suspended 17 days after the onset of bullous lesions.

Throughout the entire course of disease, the dolphin interacted normally with trainers and conspecifics, ate well and remained bright, alert, and active without evidence of discomfort, pain, or pruritus. Skin lesions began resolving within 2 days, blood abnormalities normalized within 8 days, and most skin lesions had healed with a return of pigment and scarring (so-called 'tattoo lesions') within 30 days of suspending all medication. Behavioural regurgitation resumed shortly after caloric intake was limited; however, the dolphin remains in good body condition (current weight 96.3 kg). Although a definitive diagnosis was never found, metabolic disease (possibly hepatic lipidosis) related to a sudden increase in caloric intake exacerbated by the use of hepatoxic drugs such as itraconazole is suspected.


The authors would like to thank veterinary technicians Danielle McLaughlin and Chelsea Decolle as well as Bill Van Bonn, Eric Jensen, Lisa Mazzaro, Mike Garner, Greg Bossart, Todd Roebeck, Chris Dold, Hendrik Nollens, Robert Braun, Jim McBain, Brad Blankenship, Tom Reidarsen, John Robinson, Katherine Zaremba, Jeff Matheson, and a whole host of other experts.

Speaker Information
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Martin Haulena, DVM, MS
The Marine Mammal Center, Marin Headlands
Golden Gate National Recreation Area
Sausalito, CA, USA

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