TY - JOUR
T1 - Characterization of a degenerative cardiomyopathy associated with domoic acid toxicity in california sea lions (Zalophus californianus)
AU - Zabka, T. S.
AU - Goldstein, Tracey
AU - Cross, C.
AU - Mueller, R. W.
AU - Johnson, Christine K
AU - Gill, S.
AU - Gulland, F. M D
PY - 2009/1
Y1 - 2009/1
N2 - Domoic acid, produced by marine algae, can cause acute and chronic neurologic sequela in California sea lions (Zalophus califomianus) from acute toxicity or sublethal exposure. Eight sea lions, representing acute and chronic cases, both sexes, and all age classes, were selected to demonstrate a concurrent degenerative cardiomyopathy. Critical aspects of characterizing the cardiomyopathy by lesion distribution and morphology were the development of a heart dissection and tissue-trimming protocol and the delineation of the cardiac conducting system by histomorphology and immunohis- tochemistry for neuron-specific protein gene product 9.5. Histopathologic features and progression of the cardiomyopathy are described, varying from acute to chronic active and mild to severe. The cardiomyopathy is distinguished from other heart lesions in pinnipeds. Based on histopathologic features, immunopositive staining for cleaved caspase-3, and comparison with known, similar-appearing cardiomyopathies, the proposed pathogenesis for the degenerative cardiomyopathy is the primary or at least initial direct interaction of domoic acid with receptors that are suspected to exist in the heart, l- Carnitine, measured in the heart and skeletal muscle, and troponin-I, measured in serum collected at the time of death from additional animals (n = 58), were not predictive of the domoic acid-associated cardiomyopathy. This degenerative cardiomyopathy in California sea lions represents another syndrome beyond central neurologic disease associated with exposure to domoic acid and may contribute to morbidity and mortality.
AB - Domoic acid, produced by marine algae, can cause acute and chronic neurologic sequela in California sea lions (Zalophus califomianus) from acute toxicity or sublethal exposure. Eight sea lions, representing acute and chronic cases, both sexes, and all age classes, were selected to demonstrate a concurrent degenerative cardiomyopathy. Critical aspects of characterizing the cardiomyopathy by lesion distribution and morphology were the development of a heart dissection and tissue-trimming protocol and the delineation of the cardiac conducting system by histomorphology and immunohis- tochemistry for neuron-specific protein gene product 9.5. Histopathologic features and progression of the cardiomyopathy are described, varying from acute to chronic active and mild to severe. The cardiomyopathy is distinguished from other heart lesions in pinnipeds. Based on histopathologic features, immunopositive staining for cleaved caspase-3, and comparison with known, similar-appearing cardiomyopathies, the proposed pathogenesis for the degenerative cardiomyopathy is the primary or at least initial direct interaction of domoic acid with receptors that are suspected to exist in the heart, l- Carnitine, measured in the heart and skeletal muscle, and troponin-I, measured in serum collected at the time of death from additional animals (n = 58), were not predictive of the domoic acid-associated cardiomyopathy. This degenerative cardiomyopathy in California sea lions represents another syndrome beyond central neurologic disease associated with exposure to domoic acid and may contribute to morbidity and mortality.
KW - Algal blooms
KW - California sea lions
KW - Carnitine, caspase
KW - Conducting system
KW - Heart
KW - Immunohistochemistry
KW - Troponin-I
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U2 - 10.1354/vp.46-1-105
DO - 10.1354/vp.46-1-105
M3 - Article
C2 - 19112124
AN - SCOPUS:63249134755
VL - 46
SP - 105
EP - 119
JO - Veterinary Pathology
JF - Veterinary Pathology
SN - 0300-9858
IS - 1
ER -