Abstract

Three female white whales were transferred from their normal holding pools inside Mystic Aquarium for an 8-mo stay in outside pools during extensive reconstruction of the Aquarium's main building. One month after their return to the indoor pool system one of the animals, a 16-yr-old (Animal A), developed a marked lymphopenia and a modest increase in immature neutrophils while maintaining a normal appetite and behavior.

In October 1998, approximately 4 mo after her return to the indoor pools, this animal developed intermittent anorexia and showed dermatologic signs of cetacean pox. In January 1999 an endoscopic examination revealed the presence of esophageal ulcers, a condition for which she had previously been treated. A follow-up endoscopic exam after 2 wk of sucralfate administration showed resolution of the ulcers but at this point the animal developed leukocytosis and eruptive skin lesions on its fluke. A biopsy of the erupting lesion revealed mild to moderate, focal, necrotizing dermatitis with intralesional fungal hyphae, the morphology of which was consistent with an Ascomycete, probably Fusarium solani. No fungal growth resulted from a concurrent culture attempt. This was the second presumptive identification of Fusarium from an eruptive lesion on a beluga at Mystic. Six weeks earlier a 15-yr-old female beluga, (Animal B), developed a similar eruptive lesion on her left pectoral appendage from which a Fusarium spp. was isolated. This isolate was subsequently identified as F. solani.

Prior to the diagnosis of fusariomycosis, the animals were treated with intramuscular injections of amikacin (~15 mg/kg) for ~30 days, because systemic Nocardiosis was considered the most probable of the differential diagnoses for the leukocytosis and eruptive skin lesions. Both animals were treated with itraconazole at ~3 mg/kg b.i.d. for 20-30 days. While the skin lesions regressed there were occasional appearances of draining open tracts for a period of ~45 days post diagnosis. Animal B has remained asymptomatic with normal behavior since the lesions regressed nearly 2 yr earlier. Animal A experienced a period of relatively normal behavior for several months post treatment. Both animals were transferred to a new outside beluga habitat approximately 11 mo after the first recognition of clinical signs in Animal A.

Within 1 mo of transfer to the new habitat Animal A began to develop raised pale cutaneous lesions ranging from 3-10 cm in diameter. Concurrent with the development of lesions was an intermittent anorexia, unsociable behavior, lymphopenia, low alkaline phosphatase, and elevated fibrinogen. The lesions developed a dark ring at their edges, became raised, and eventually ruptured. The affected tissue was very friable even prior to rupturing. No etiologic agent was identified initially but later, deeper biopsies demonstrated intralesional acid-fast bacilli as well as filamentous extra-cellular organisms. Deep aspiration of intact lesions yielded copious amounts of thick pus at the blubber-dermal interface. When subsequent lesions developed they were opened up and flushed with dilute betadine twice a day. After a prolonged incubation period on Lowenstein-Jensen medium, we isolated Mycobacterium marinum from several lesions. Prior to the diagnosis of mycobacterial panniculitis the lesions were drained, debrided and flushed with a dilute povidone iodine solution.

After over 1 mo of intense supportive care and a precipitous decline, and 15 mo from the first recognized clinical signs, the animal displayed a brief episode of head thrashing and died. At necropsy, there were multiple, scattered, deep, ulcerated and necrotic skin lesions on the extremities, snout, and ventral abdomen. These skin lesions extended to the blubber, and some of them contained hemorrhagic or purulent cores. There was severe, chronic, proliferative fibrinosuppurative pleuritis with atelectasis of the left lung lobes and severe hemopericardium, hemomediastinum contiguous with severe hemorrhage in the muscles of the ventral neck. A 5-cm full-thickness tear in the descending aorta was identified in a dissecting aneurysmal dilatation 10 cm distal to the aortic arch. The pleural fluid was determined to be a modified transudate with many intact macrophages containing intracytoplasmic acid-fast bacilli and fewer lymphocytes. Impression smears of several skin lesions taken at necropsy revealed suppurative and histiocytic dermatitis with intralesional acid-fast bacilli. Histopathologic examination of skin lesions revealed the presence of multiple granulomata in the deep dermis and panniculus, with intralesional acid-fast bacilli. Lymphohistiocytic interstitial pneumonia was identified in multiple sections of lung, and severe, chronic, proliferative, lymphohistiocytic pleuritis was confirmed. No etiologic agent was identified in the sections of lung parenchyma or pleura. Based on the finding of acid-fast bacilli in the macrophages from pleural fluid and in several skin lesions, the differential diagnoses included bacteria in the family Mycobacteriaceae, including the genera Mycobacterium and Nocardia.

Bacterial cultures taken at the time of necropsy yielded sparse growth of a Mycobacterium spp. with morphologic and growth characteristics most consistent with M. marinum. DNA was extracted from samples of the subcutaneous exudate and several skin lesions that were frozen at necropsy.

Polymerase chain reaction using primers specific for the genus Mycobacterium generated an amplicon of 439 base pairs from DNA samples extracted from skin lesions and from a centrifuged sample of the pleural effusion. Restriction endonuclease digestion of the amplicon from the whale yielded a pattern of cleavage products identical to that generated by a known (i.e., positive control) Mycobacterium marinum isolate of ATCC origin, thus confirming that the mycobacterial DNA from the lesions was derived from a M. marinum isolate. Taken together, the gross and histopathologic findings, and ancillary diagnostic tests support the diagnosis of fatal aortic rupture in a dissecting aneurysm, and chronic, multisystemic mycobacteriosis. No evidence of fusariomycosis was present.