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Vet J. 2013 May;196(2):181-8. doi: 10.1016/j.tvjl.2012.09.021. Epub 2012 Nov 10.

Capture myopathy in live-stranded cetaceans.

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  • 1Department of Comparative Pathology, Instituto Universitario de Sanidad Animal, Facultad de Veterinaria, Universidad de Las Palmas de Gran Canaria, Arucas, Spain.


A group of 51 cetaceans that had been stranded alive on the coasts of the Canary Islands, experienced human capture/rescue interactions and then died, were necropsied over a 12-year period. Of these cetaceans, 25 had haemodynamic lesions indicative of multiorganic vascular shock, degenerative muscle lesions affecting both skeletal and cardiac muscles and myoglobinuric nephrosis typical of capture myopathy (CM). Because macroscopic lesions in muscles and kidneys were not always obvious, a standard protocol was developed where the longissimus dorsi muscle was examined histologically for segmental hypercontraction, contraction band necrosis and segmental muscular degeneration and cardiomyocytes studied for hypereosinophilic wavy fibres, sarcolemmal and perinuclear vacuolation and contraction band necrosis. Light microscopic skeletal and cardiac muscle lesions in all CM animals were confirmed as ante mortem by immunohistochemical assay for myoglobin loss from and fibrinogen entry into affected myofibres. All animals had tubular nephrosis with casts and tubular myoglobin. The oxidative stress-related marker HSP70 was demonstrated immunohistochemically in tubular epithelium. Although the syndrome related to death of live-stranded cetaceans is multifactorial, this study documents that a clinicopathological syndrome comparable to CM of terrestrial wildlife has a role in stranding outcomes.

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