Cardiomyopathy in a Stranded Risso's Dolphin (Grampus griseus): A Case Study
IAAAM Archive
Yi-Fan Jen1; Hue-Ying Chiou2; Jiang-Ping Wang3; Pei-Jhong Chen4
1Department of Veterinary Medicine, National Chiayi University, Chai-Yi, Taiwan; 2Division of Animal Medicine, Animal Technology Institute Taiwan, Miaoli, Taiwan; 3Department of Life Sciences, National Cheng Kung University, Tainan, Taiwan; 4DVM, Loving Kindness Animal Hospital, Tainan, Taiwan


Cardiomyopathy could present widely in vertebrate animals. The causes of cardiomyopathy were unknown except the thiamine deficiency can result in myocardial lesions and the release of the massive endogenous catecholamine in the dolphins and whales can cause the contraction band necrosis in the myocardial cells (Turnbull et al., 1998). In 1985, the cardiomyopathies were determined in stranded pygmy and dwarf sperm whales. At necropsy, irregular, pale whitish patches were seen in the myocardium of the adult whales. Microscopic examination revealed interstitial fibrosis, interfibrillar edema and myocellular degeneration in the myocardium of the adult whales (Gregory et al., 1985). In this report, the myocellular degeneration was determined in the myocardium of the dolphin.

September 9th 2006, a juvenile male Risso's dolphin stranded in Shi-Su coast of Tainan County in Taiwan. It was able to keep floating when he was transported into the rehabilitation pool but found imbalanced. Malnutrition, emaciation, and diarrhea with gas were also noticed. Medical treatment and fluid supply were conducted. Blood samples were collected for complete blood count (CBC), serum chemistry analysis and microbiological examination during the period of the rehabilitation. The results of the blood analysis showed that, while the white count was in the normal range, the band cells were found significantly increased, indicating the undergoing severe inflammation in this animal. The outcome of serum chemistry revealed the elevation of ALT, AST and LDH. On October 15th, the dolphin greatly improved and started to swim full-time. On October 16th, oral sedative medicine was provided for the tranquil removal of the dolphin into a larger pool. One hour after this treatment, no signs of life were detected. Full necropsy was performed and histopathologic sampling was collected.

At necropsy, the characteristic of the heart was normal. On histopathology, the pyramidal cells of the 3rd layer of cerebral cortex were shrunken and condensed (neuronal degeneration). The pulmonary alveoli were hyperemic and filled with amorphous, eosinophilic materials (edema fluid). The myocardial cells were multifocally fragmented, swollen and loss of striation. Large numbers of hepatic cells contained variable numbers of clear vacuoles in the cytoplasm. Multiple oval, brown organisms (fluke eggs) were noted in few portal areas associated with marked cholangeal hyperplasia. The epithelial cells of few renal tubules were necrotic and sloughed into the lumen. Few tubules contain proteinacious fluid. The superficial epithelial cells of small intestine were necrotic and the lamina propria was infiltrated by large number of inflammatory cells. According to the clinical signs, histopathological and microbiological findings, our final diagnoses were pneumonia, enteritis, fatty liver with parasite infection, nephropathy, cerebral neuronal degeneration, and acute cardiomyopathy.

Several causes may lead to cardiomyopathy in this case. There was no obvious evidence of heart muscle damage, however, from the results of blood exams on the first few days. (LDH1/LDH2 is 0.38, CK is beneath 300, CK-MB is beneath 0.5) In this case, EKG and image diagnoses (chest radiology and echocardiogram) are critical for the evaluation of the animal's myocardial function while the clinical behavior and the results of the serum chemistry may not provide proper information for the purpose of correct diagnosis. The death of this case may be due to higher sensitivity to diazepam and the respiration might be inhibited by the mechanism of the benzodiazepine family. Another explanation is that the lesion of the myocardium may be caused by the compensatory effects of increased contraction of the heart following the inhibition of the cardiorespiratory function. However no related data was published. In conclusion, the EKG is essential and critical for health evaluation in addition to clinical signs and other examination for stranded cetaceans, and sedative medicine should be used with high caution.


1.  Gregory DB, Odell DK, NH Altman. 1985. Cardiomyopathy in stranded pygmy and dwarf sperm whales. JAVMA 187(11):1137-1140.

2.  Turnbull BS, DF Cowan. 1998 Myocardial contraction band necrosis in stranded cetaceans. J. Comp. Path. 118:317-327.

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Yi-Fan Jen

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