In the late 1980s, Sea World of Ohio had four cases of pinnipeds (three California sea lions, one ringed seal) with skin ulcers involving the pelvic and axillary skin folds. Mild cases resolved with antibiotic therapy. The most severe case was in an adult male. Lesions involved the epidermis, dermis and the hypodermic and were histologically characterized as ulcerative and necrotizing dermatitis of unknown etiology. Bacteria and inflammation seen in the sections were thought to be a secondary response to the ulcers. These lesions appeared to wax and wane with little apparent response to antibiotic therapy and medicated flushes. Prednisolone therapy provided only temporary reduction of lesion size. Three of the four cases failed to resolve.

Hematologic, biochemical and culture findings were unremarkable in all cases. Multiple skin biopsies and cultures revealed no definitive etiology over a two-year period. The most severely affected animal was euthanized.

Since early 1994, a ten-year old male, castrated, captive-born California sea lion has had continuous axillary skin ulceration, similar to those described in the Sea World animals. This animal has been housed at a central California zoo since birth. The lesions appeared following the onset of ventral abdominal and pectoral flipper alopecia. The lesions are primarily confined to the axillary regions bilaterally and affected the entire epidermal, dermal, and hypodermal layers, exposing underlying connective tissue and muscle. The affected areas measure approximately 25 cm X 30 cm at there most advanced stage. No complete reepithelialization has occurred since the onset of this condition.

This animal experiences a waxing and waning of the lesions. At each recrudescence the lesions appear worse than previous episodes with a decreased degree of healing. During each episode regional alopecia occurs over the ventral abdomen, thorax, and neck. The alopecia often extends up the lateral trunk and affected areas around the head and shoulders. The sea lion received a complete physical examination and diagnostic work-up ten months after the onset of the lesions.

Diagnostic tests included negative anaerobic and fungal cultures, small numbers of coagulase-positive Staphylococcus, beta-hemolytic Streptococcus and yeast by aerobic culture. Hematologic and serum chemistry parameters were within expected limits for this species. Biopsies of the lesions and adjacent non-ulcerated skin revealed ulcerative, pyogranulomatous dermatitis and superficial, lymphocytic, plasmacytic and neutrophilic dermatitis. No microorganisms were identified. Viral elements were not detected by electron microscopy. T4 levels were deemed low normal based on comparison with four other sea lions from another facility. Mammals may have decreased T4 levels during illness. Retrospective samples would help in interpretation of T4 levels.

Treatment with antimicrobial and antifungal agents did not resolve the lesions. The most significant healing occurred during initial cephalosporin and Itraconazole therapy when the animal was confined out of the pool immediately after the anesthetic episode. After one month of confinement, the animal escaped from the enclosure and returned to the pool. Healing has not occurred since this time.

Thyroid supplementation has been attempted with inapparent response after 6 months of treatment. Modifications and corrections in diet' supplementations, and food thawing and handling procedures have not had an effect on this animal's illness. Changes in water disinfection are being pursued by this facility. At the present time, chlorine is added at the filtration system. Levels are monitored with a poolside chlorine test Skin conditions causing full thickness ulcerations have been reported in elephant seals. In the case of elephant seal skin disease, the distribution of lesions is generalized and excoriative, affecting primarily wild juveniles in the spring. The distribution of these sea lion/seal lesions has been much more focal. To the authors' knowledge, this condition has only been documented in captive, adult pinnipeds. The occurrence of similar lesions in wild pinnipeds is unknown.

Differentials for the sea lion lesions include pox virus, San Miguel Sea Lion virus, endocrinopathy, immunodeficiency disease, and poor water quality. Pox virus has been ruled out in these cases due to the distribution of the lesions and lack of demonstrable viral inclusions on histopathology. Lesion distribution and lack of response to antimicrobials and supportive care make San Miguel Sea Lion virus unlikely. Other etiologies are more difficult to rule out due to the paucity of information on normal endocrine values in this species in captivity. The involvement of water quality in this condition has not been completely evaluated. Holding this animal out of the water for an extended period of time and monitoring healing is being considered again. This is the only animal of five in this pool that has alopecia and skin ulcers. It is the authors' opinion that these lesions are far more persistent and widespread than could be accounted for by trauma.

In the past several months this animal's condition has declined as the lesions have progressed. Areas of ulceration now include the skin over the pelvic limbs. The axillary lesions have increased in size and severity. Further diagnostic results are pending. This animal's prognosis for long-term survival is poor at this time. He continues to be the only animal affected in this group of five sea lions.

Any information on similarly affected sea lions at other facilities would be greatly appreciated. Suggestions on other possibilities and treatments that have been successfully used in similar cases are welcome.

Dierauf, L. 1990. Handbook of Marine Mammal Medicine. CRC Press, Boca Raton, Florida, USA.