NAVLE Musculoskeletal

Camelidae and Cervidae Capture Myopathy – NAVLE Study Guide

Capture myopathy (CM), also known as exertional myopathy or exertional rhabdomyolysis, is a non-infectious metabolic disease characterized by severe muscle damage (rhabdomyolysis) resulting from extreme exertion, struggle, or stress during capture,...

Overview and Clinical Importance

Capture myopathy (CM), also known as exertional myopathy or exertional rhabdomyolysis, is a non-infectious metabolic disease characterized by severe muscle damage (rhabdomyolysis) resulting from extreme exertion, struggle, or stress during capture, restraint, handling, or transportation. This condition is of paramount importance in wildlife medicine and is a significant cause of morbidity and mortality in both camelids and cervids.

The condition was first described in 1964 in a Hunter's hartebeest in Kenya and has since been documented in numerous ungulate species worldwide. Camelids (llamas, alpacas, vicunas, guanacos) and cervids (white-tailed deer, elk, moose, caribou, roe deer) are particularly susceptible due to their flighty nature and physiological characteristics. Understanding this condition is essential for veterinarians involved in wildlife capture operations, zoo medicine, farmed cervid management, and camelid practice.

High-YieldCapture myopathy carries a grave prognosis. Prevention through proper capture techniques is far more effective than treatment. Once clinical signs appear (especially dark red-brown urine indicating myoglobinuria), the mortality rate is extremely high despite intensive supportive care.
Syndrome Onset Clinical Signs Pathology
Peracute (Capture Shock) Minutes to 6 hours after capture Sudden death, tachypnea, tachycardia, weak pulse, hyperthermia, lethargy Pulmonary, hepatic, intestinal congestion; multifocal necrosis in multiple organs; few gross muscle lesions
Acute (Ataxic Myoglobinuric) Hours to days after capture Ataxia, torticollis (wryneck), dark red-brown urine (myoglobinuria), stiffness, recumbency Pale, dry muscle lesions in limbs and back; swollen dark kidneys; myoglobin casts in tubules
Subacute (Ruptured Muscle) 1-2 days to weeks after capture Dropped hindquarters, hyperflexed hocks (gastrocnemius rupture), tetraplegia, torticollis Severe muscle necrosis with hemorrhage; rupture of gastrocnemius, cervical, and lumbar muscles
Chronic (Delayed Peracute) Weeks to months; occurs with repeat capture Sudden death during mild stress; animal stops, pupils dilate, collapses Cardiac fibrosis from previous episode; minimal acute muscle changes; death from ventricular fibrillation

Etiology and Pathophysiology

Capture myopathy develops when animals are subjected to extreme physical exertion, psychological stress, or both during capture events. The pathophysiology is complex and involves multiple interrelated mechanisms that ultimately result in severe skeletal and cardiac muscle damage.

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