Suspected capture myopathy in an alpaca (Vicugna pacos) following a dog attack

The relatively recent introduction of alpacas (Vicugna pacos) into Australia and New Zealand has presented a challenge for veterinarians with respect to diagnosis and treatment of disease in this species. It is apparent that alpacas may be susceptible to severe stress-induced disorders, including capture or stress myopathy, which is commonly reported in non-domesticated prey species, and ungulates are considered particularly susceptible (Paterson 2007). This myopathy may also be referred to as exertional rhabdomyolysis because it has a similar clinical presentation to the condition in humans (Bartsch et al. 1977; Paterson 2007). It affects both skeletal and cardiac muscle (Warren et al. 2002) and typical presenting signs in affected animals include ataxia, pain on palpation, recumbency, collapse and sudden death (Bartsch et al. 1977). A marked increase in serum creatine kinase (CK), a biochemical indicator of severe muscle damage, is also typically seen. The primary pathophysiological event underlying the condition appears to be overstimulation of the sympathetic nervous system resulting in vasodilation and hypertension (Roe and Spraker 2012). This leads to excessive aerobic demand and failure of adenosine triphosphate (ATP) production, particularly within skeletal muscle (Williams and Thorne 1996; Criddle 2003). Subsequent reliance on anaerobic metabolism leads to increasing concentrations of lactic acid and accumulation of metabolic wastes in myocytes. Affected cells then undergo necrosis, releasing CK into the circulation (Criddle 2003).Myoglobin released from the damaged myocytes contributes to acute renal failure secondary to tubular obstruction and direct cytotoxicity (Vanholder et al. 2000). Typical clinicopathological changes include marked elevation in the activity of CK in serum and myoglobinuria (Bartsch et al. 1977). Post-mortem findings may vary from minimal in peracute cases to significant multifocal muscular haemorrhage and necrosis, with swelling and darkening of the renal tissue (Bartsch et al. 1977; Roe and Spraker 2012). Histopathological findings may include necrosis and capillary thrombi in affected muscle (Paterson 2007).