Camelidae and Cervidae Capture Myopathy – NAVLE Study Guide

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.

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.

Stress Response and Catecholamine Surge

The initiating event is the fight-or-flight response triggered by capture stress. This results in massive sympathetic nervous system activation with release of catecholamines (epinephrine and norepinephrine), glucocorticoids, and other stress hormones. Key effects include increased heart rate and cardiac output, peripheral vasoconstriction to redirect blood flow to skeletal muscles, glycogenolysis and increased glucose availability, and upregulation of skeletal muscle metabolism.

Metabolic Cascade

During prolonged exertion, oxygen demand exceeds supply, forcing a switch from aerobic to anaerobic metabolism. This leads to rapid ATP depletion, accumulation of lactic acid causing severe metabolic acidosis, disruption of cellular ion pumps (Na+/K+-ATPase, Ca2+-ATPase), and massive intracellular calcium accumulation.

Rhabdomyolysis: The Central Pathology

The accumulation of intracellular calcium is the key trigger for rhabdomyolysis. Calcium activates destructive proteases and phospholipases, causes persistent myofiber contraction and mechanical damage, leads to mitochondrial dysfunction and cell death, and results in sarcolemmal rupture and release of intracellular contents.

When muscle fibers are damaged, their contents are released into the bloodstream including myoglobin, creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), potassium, and phosphate.

Myoglobinuric Nephropathy

Myoglobin released from damaged muscles causes acute kidney injury (AKI) through three mechanisms: renal vasoconstriction reducing glomerular filtration, intraluminal cast formation causing tubular obstruction, and direct heme-protein cytotoxicity to tubular epithelial cells. The acidic urine environment promotes myoglobin precipitation in renal tubules, forming obstructive casts that appear as the characteristic dark red-brown or port-wine colored urine.

Hyperthermia

Elevated body temperature (greater than 42 degrees Celsius or 107.6 degrees Fahrenheit) is common in capture myopathy. Heat is generated from intense muscle contraction, anaerobic metabolism, and potentially from mitochondrial uncoupling due to oxidative stress. Unlike environmental heatstroke, capture-induced hyperthermia results from excessive endogenous heat production rather than environmental exposure. Importantly, hyperthermia can persist even after exertion has ceased, suggesting ongoing metabolic derangement.

Clinical Syndromes of Capture Myopathy

Capture myopathy has been classified into four distinct clinical syndromes based on time of onset and clinical presentation. Understanding these syndromes is essential for the NAVLE as questions often test differentiation between them.

Species-Specific Considerations

Camelidae (Llamas and Alpacas)

South American camelids including llamas (Lama glama) and alpacas (Vicugna pacos) are susceptible to capture myopathy, though generally considered somewhat less prone than highly flighty species. Key considerations include their relatively calm temperament compared to deer species (though they can still develop CM with improper handling), susceptibility to hyperthermia due to their dense fiber coat, and that repeated chemical immobilization increases risk.

Clinical presentation in camelids: Muscle stiffness and lameness, recumbency and inability to rise, dark red-colored urine, elevated respiratory and heart rates, and hyperthermia (temperature greater than 40 degrees Celsius). Death may occur acutely or be delayed days to weeks.

Cervidae (Deer and Elk)

Cervids are among the most susceptible species to capture myopathy due to their highly flighty nature and intense flight response. Species commonly affected include white-tailed deer (Odocoileus virginianus), mule deer (Odocoileus hemionus), elk (Cervus canadensis), moose (Alces alces), and caribou (Rangifer tarandus).

Risk factors specific to cervids: Extreme flight response when startled or pursued, capture methods involving prolonged chase or physical restraint, hot environmental temperatures, poor body condition or pre-existing disease, pregnancy (particularly late gestation), and inadequate habituation to human presence.

Diagnostic Approach

Clinical History and Signalment

Diagnosis of capture myopathy relies heavily on history of a recent capture, handling, restraint, or transport event. Key historical elements include method of capture (physical vs. chemical immobilization), duration of pursuit or struggle, time since capture event, environmental conditions (temperature, humidity), and any prior capture events (chronic syndrome).

Laboratory Findings

Necropsy Findings

Gross pathology: The hallmark finding is pale, dry, whitish areas in skeletal muscles (hence the alternate name 'white muscle disease'). Commonly affected muscles include the quadriceps femoris, gastrocnemius, cervical muscles, and lumbar epaxial muscles. The kidneys are often swollen and dark red with pale cortex. The bladder may contain dark red-brown urine. Cardiac muscle may show pale streaks, particularly in papillary muscles.

Histopathology: Skeletal muscle shows segmental myofiber degeneration and necrosis with loss of striations, hypereosinophilic sarcoplasm, nuclear pyknosis, contraction band necrosis, and fragmentation of myofibrils. Kidneys demonstrate tubular epithelial necrosis with myoglobin casts (brown granular casts positive for myoglobin on immunohistochemistry). Cardiac muscle may show similar degenerative changes, supporting the term 'capture-induced cardiomyopathy.'

Differential Diagnosis

Several conditions can present similarly to capture myopathy and must be differentiated:

Treatment

There is no specific treatment for capture myopathy, and the prognosis is generally poor to grave once clinical signs develop. Treatment is largely supportive and symptomatic. Prevention is far more effective than treatment.

Prevention Strategies

Prevention is the cornerstone of managing capture myopathy. Proper planning, technique, and species-appropriate handling dramatically reduce incidence.

Pre-Capture Planning

• Assemble experienced capture team with species-specific knowledge
• Avoid capture when ambient temperature exceeds 25 degrees Celsius (77 degrees Fahrenheit)
• Prefer early morning or late evening capture operations
• Have all equipment prepared and functional before initiating capture
• Establish contingency plans for complications

Capture Techniques

• Minimize pursuit duration (less than 5 minutes ideal)
• Use chemical immobilization (remote delivery via dart) rather than physical chase when possible
• For cervids: Xylazine + Ketamine combination may reduce CM risk
• Avoid repeated chemical immobilization events
• Net guns or drop nets should minimize struggle time

Handling and Transport

• Keep handling time to absolute minimum
• Blindfold animals to reduce visual stress
• Minimize noise and sudden movements
• Ensure adequate ventilation in transport vehicles
• Monitor body temperature throughout; cool if exceeds 40 degrees Celsius
• Consider long-acting tranquilizers for transport
• Use species-appropriate trailers/containers

Post-Capture Monitoring

• Observe animals for clinical signs for up to 2 months post-capture
• Allow adequate habituation time before repeat handling
• Document all capture parameters for future reference

Board Tip - Prevention Mnemonic: 'CALM CAPTURE' Cool temperatures preferred Avoid prolonged pursuit Limited handling time Minimize stress and noise Chemical immobilization when possible Adequate planning Prepared equipment Trained personnel Use appropriate tranquilizers Remote delivery of drugs Early morning/evening timing

Prognosis

The prognosis for capture myopathy is generally poor to grave. Once clinical signs appear, particularly myoglobinuria, mortality approaches 80-100% despite intensive treatment. Key prognostic factors include the syndrome type (peracute syndrome is almost uniformly fatal), presence of myoglobinuria (grave prognosis), degree of azotemia (renal failure indicates poor prognosis), severity of hyperkalemia (cardiac arrhythmia risk), and time to treatment initiation. Animals that survive the acute phase may develop chronic cardiac fibrosis and are at risk of sudden death during subsequent stressful events (chronic/delayed peracute syndrome).