Abstract
The response of marine mammals to stress is of great relevance, since these animals are subjected to stressors from the marine and terrestrial environments that can potentially affect their health. In this context, understanding physiological responses of individual animals to manipulation and sampling also has implications for the well-being of marine mammals. In the Austral summer of 2012, South American fur seal (Arctocephalus australis) pups (n = 150) were captured at several rookeries located at Guafo Island (43° 36'S y 74° 43'W), Southern Chile, as part of a long-term study on infectious disease ecology in fur seal populations. During these procedures, 5 pups from the same rookery died during or within 20 minutes of handling. Necropsies were performed in the field, and most tissues were examined by histopathology. Serum obtained pre-mortem was available from 3 pups for measurements of CK, AST, LDH and Troponin I. Values of these enzymes from three pups, of the same age, subjected to the same handling protocol, but from different rookeries, were used as controls. Tissues of fur seal pups from past studies, dead by acute trauma, were used as controls for assessment of striated muscles and adrenal glands. On gross examination, 4 pups had pale areas in the subendocardial zone of the left ventricle and interventricular septum. Microscopically, there were mild multifocal contraction bands with necrosis of cardiomyocytes. Similar changes were observed in the smooth intestinal muscle in all pups and in the skeletal muscle in one pup. In the adrenal gland, there was diffuse hyperplasia of the zona glomerulosa and nodular hyperplasia of the medulla, and the endothelium of large blood vessels was swollen, collagen fibers were disrupted, and there was occasional margination of neutrophils. Additionally, all pups had moderate to severe chronic inflammatory responses to Orthoalarachne sp. (respiratory mites) and Uncinaria sp. (intestinal hookworm) infections. Plasma levels of AST and CK enzymes were mildly elevated in pups that died from acute stress in comparison with controls. Troponin I concentrations were almost equal in dead and control pups.
Pathologic findings suggest that these pups died from systemic effects of massive catecholamine release. These lesions have been described in cetaceans subjected to by-catch or stranding stress,3 in laboratory animals injected with high doses of catecholamines, and in humans dying from stress cardiomyopathy.1,4 The histologic changes found in the adrenal gland of these pups have been described in cetaceans undergoing chronic stress.2 Mild AST and CK enzyme elevations are correlated with the mild lesions observed in striated muscles and other tissues. Troponin I levels were not correlated with myocardial lesions, as has been reported in stress cardiomyopathy in humans6 and domoic acid cardiomyopathy in California sea lions.5 Chronic parasitism may have played a role in the death of these pups by either decreasing the physiological resistance of a stressful event or by enhancing the release capacity of catecholamines of the adrenal gland, due to hyperplasia of catecholamine producing cells.
Acknowledgements
The authors would like to thank Research and Development Direction, Universidad Austral de Chile for the financial support of the field-work.
* Presenting author
+ Student presenter
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