Capture myopathy in active stranded cetaceans

Abstract

Capture myopathy (CM) is a poorly characterized disease in cetaceans. CM is a metabolic muscle disease described in wild mammals and birds associated with stress of capture, restraint, and transportation. The pathologic findings include mild to moderate rhabdomyolysis affecting the cardiac and skeletal muscle and myoglobinuric nefrosis. Spraker (1993) described four clinical syndromes in animals: capture shock, ataxic myoglobinuric, ruptured muscle and delayed peracute syndrome. In this communication we report a series of 51 active stranded cetaceans in Canary Islands since 1996 to 2008, in order to describe the skeletal, cardiac and renal lesions, which characterized this pathology in cetaceans. Selected tissue samples were fixed in 10% neutral buffered formalin, embedded in paraffin wax, and sections (4 μm) were stained with haematoxylin and eosin, PTAH, Masson’s Trichome and PAS techniques. In addition, immunohistochemical examination to detect myoglobin and fibrinogen was performed. Type, severity and distribution of both muscular and renal lesions were related to the time to death and human interaction. Skeletal muscular lesions varied from marked hypercontraction and segmental necrosis of type 1 myofibres, to diffuse rhabdomyolysis with evidences of inflammatory reaction. Animals that were under close human contact, and died 24-48 hrs after to active stranding showed the most severe muscular lesions with affectation of both type 1 and type 2 muscular fibres. Degenerate myofibres showed depletion of myoglobin and an intracytoplasmic immunoreaction for fibrinogen, which is indicative of in vivo, acute ischemic muscular damage. Similar myocardial lesions were observed. Renal lesions also were related to muscular damage and time to death and varied from minimal changes to extensive myoglobinuric nephrosis. Granules and casts in Bowman’s space, tubular lumens, and cytoplasm of degenerate tubular cells were strongly labelled by the antimyoglobin antibody.