Abstract

A young male (estimated 8-9 years), 214 cm long rough-toothed dolphin (Steno bredanensis) stranded in Hong Kong on 14 May 2004. Attempts to return him to sea by the local authorities were unsuccessful and the dolphin was transported to Ocean Park quarantine facilities for treatment and rehabilitation. He presented emaciated with a mass of 75 kg, had extensive scarring and was unable to float unaided. Supportive care, initially with fluids then fish mash and antibiotics were given. He improved and swam unaided in a couple of days and ate dead fish voluntarily within 3 days. He was tactile, interacted with trainers and responded to enrichment items. Diagnostics within the first week included: hematology and biochemistry, serology, fecal, gastric and blowhole samples, ultrasonography and gastroscopy. Findings were generally unremarkable except those relating to the gastrointestinal system. Thickened intestinal walls were detected on ultrasound and he had small frequent defecations or constipation with flatulence and sticky, firm feces. Contrast radiographs did not reveal any abnormality. However, after an encouraging start, his appetite dropped from about 4 kg for a few days to an average of 0.9 kg fish/day for 34 days, then nil thereafter. He subsequently received complete nutritional support by tube feeding 4-5 times a day and later by being force fed whole fish until his death on 6 March 2005. His body condition appeared normal and his mass increased with the enforced feeding, but he exhibited irregular behavior and a lack of interest in feeding. Erratic behavior included bursts of activity between periods of lethargy with a hunched posture, which was attributed to possible lack of social interaction and stimuli and action was taken to try to alleviate this. However in November he developed apparent ventral abdominal edema, followed by elevated fibrinogen and globulins in December, and finally clinical and behavioral deterioration in February until his death in March 2005.

On necropsy excessive cerebral spinal fluid was found within the cranium and the cerebral vessels were congested. Other findings included evidence of a hepatopathy, gastric and esophageal ulceration and generalised edematous lymph nodes. The significant findings on histopathology were a spongiform leukoencephalopathy in the cerebral hemispheres associated with glioisis, indicating chronicity. There was no evidence of inflammation or inclusion bodies. The histopathological changes are consistent with lesions caused by prions or viruses. This is the first reported case of a spongiform encephalopathy in a cetacean and illustrates the importance of thorough necropsies on stranded cetaceans including examinations of the brain and spinal cord, and the greater implications for public health if a prion is involved.

Acknowledgments

The authors are grateful to Katrina Gregory, Nimal Fernando, Gary Wong, Harriet Chiu and the rest of the Marine Mammal Department, the staff of Ocean Park's clinical laboratory and staff of the Hong Kong Agriculture Fisheries and Conservation Department for their involvement in the treatment and attempted rehabilitation of this dolphin. Also thanks to Drs. Fiona Brook, Jim McBain, Charles Manire, Geraldine Lacave and Con Metreweli for their advice and professional contributions to this case.

The costs of the support and treatment of this case were covered by the Hong Kong Ocean Park Conservation Foundation.