Capture Myopathy (CM): An Important Non-infectious Disease of Wild Animals

Capture Myopathy (CM): An Important Non-infectious Disease of Wild Animals

Capture myopathy is a serious condition that can occur in wild and domestic animals wherein muscle damage results from extreme exertion, struggle, or stress. It is also known as exertional myopathy, overstraining disease and exertional rhabdomyolysis.Capture myopathy most often occurs as a result of capture, transport or chemical immobilization, but it can also be the result of other natural causes of stress, such as in prey animals attempting to avoid or struggling with predator animals. It is of particular concern in cases when it is a cause of death in wild animals that are handled by humans.

Capture Myopathy is one of the important pathological changes that occur in case of wild animals due to the stress factors during the restraint operation.This condition may affect different species of wild animals that may endanger the life of the wild fauna and hence, the attending veterinarian needs to understand base line information about the various features pertaining to the capture myopathy.

Every wildlife rancher, wildlife translocator, veterinarian and wildlife auctioneer fear these words: capture myopathy. The so-called condition is the Achilles heel of the wildlife industry. Capture myopathy (CM) is a noninfectious, metabolic disease of wild and domestic animals that can lead to significant morbidity and mortality. The condition is most commonly associated with pursuit, capture, restraint, transport, secondary to other diseases and natural hazards encountered in the environment. It is characterized by metabolic acidosis, muscle necrosis, and myoglobinuria.

Capture myopathy can occur naturally when animals are attempting to avoid predation, but capture myopathy is more often the result of animals being captured and/or immobilized with or without chemical means being involved. When animals overexert themselves (e.g., struggling in a trap or attempting to flee a capture team) to the extent that physiological imbalances develop and result in severe muscle damage, capture myopathy results.¹ Increased ambient temperatures and repeated chemical immobilization can increase the risk of animals suffering from capture myopathy.

Clinical signs of capture myopathy can vary depending on the species and the cause of exertion.² The method of capture and restraint is also a determinant in occurrences of capture myopathy. The clinical signs during early onset include elevated respiratory rate, heart rate, and body temperature.^1,3 Body temperature increases during exertion, with higher temperatures being associated with death due to capture myopathy. The increase in body temperature can be above 42°C.⁴Muscle spasms, stiffness and lameness are also clear signs of CM. Animals often become recumbent and may stumble. If dark red-colored urine is noted, this is an indication that the animal’s muscles are breaking down and that its kidneys have been severely affected.Death of the animal usually follows.

There is no treatment for capture myopathy, prevention being the best method of avoiding this condition. Care should be taken in case of handling of animals that tend to be more susceptible to capture myopathy. An anesthetic protocol consisting of good anesthetic agents can aid significantly in preventing capture myopathy.

Clinical signs include muscle stiffness, severe muscle pain, ataxia, paresis, torticollis, prostration, and paralysis. Animals typically become obtund, anorexic, and unresponsive. Death can occur from within minutes or hours of capture to days or weeks after the inciting event. The first recorded pathological description of capture myopathy was from 1964 in Hunter‘s hartebeest (Beatragus hunteri), currently one of the most critically endangered antelope species.. CM has been termed muscular dystrophy, white muscle disease, overstraining disease, capture disease, cramp, leg paralysis, spastic paresis, stress myopathy, transport myopathy, incipient myopathy, degenerative polymyopathy, muscle necrosis, and idiopathic muscle necrosis throughout the literature. The condition is now most commonly referred to as CM, exertional myopathy, or exertional rhabdomyolysis (Spraker, 1993). Capture myopathy (CM) in wildlife may be a model for stress cardiomyopathy (e.g. Takotsubo Syndrome, Broken-Heart Syndrome) in humans. Peracute CM (a subtype of CM in which symptoms emerge soon after exposure to the stressor) in particular, shares many features with Takotsubo Syndrome/Broken-Heart Syndrome in humans (Blumstein et al., 2015).

Etiology

Exertional rhabdomyolysis, or CM, in animals is distinguishable from other types of rhabdomyolysis by its pathophysiology, as it affects both skeletal and cardiac muscles in response to extreme stress and muscular exertion. CM is an inherent mechanism that facilitates a symbiotic relationship between predator and prey. The stresses of fear and anxiety are the triggering mechanisms for CM that may be modified by genetic or acquired predispositions to the disease (Meyer, 2009). These factors, in turn, may be exacerbated by iatrogenically induced circumstances, such as overexertion, disturbance, excessive handling, transportation, and shock. It is a complex and multifactorial disease (Landau et al., 2012).

Predisposing factors

There are many predisposing or contributing factors for CM which include Species, Environment, Capture related, Other diseases, Nutrition Drugs, and Signalment.

Species

Prey species are considered the most susceptible to CM in the mammalian taxa, particularly ungulates. Highly susceptible species include zebra, deer, giraffe, nyala, tsessebe, duiker, roan antelope, red hartebeest, eland, springbok, kudu, giraffe, white-tailed deer, pronghorn, fallow, and hog deer. The long-legged wading birds are particularly predisposed to CM within the avian taxa. The combination of struggle during capture and restraint in bags or cages where the birds cannot stand increases their susceptibility to CM. Reports of CM in carnivores are rare but the disease can occur under certain conditions (Cattet et al., 2008).

Environment

Environmental factors that can increase the incidence of CM include extremes in ambient temperature, rain, and high humidity. The need for animals to negotiate steep terrain, difficult footing, or water hazards can also hasten the onset of CM.

Capture related

Techniques that involve high chase speeds, prolonged exertion without rest, excessive handling, prolonged restraint, the restraint that promotes struggling from unnatural positioning, crating, transport, subjection to fear stimuli over periods, and renewed stresses, such as repeated moving and transport predispose animals to CM (Ebedes et al., 2002). Injuries induced by capture techniques, or by other animals, can also increase the incidence of CM. Underlying diseases and infections can make an animal more susceptible to CM. Severe worm and tick infections cause anemia and weaken the animal. Heartworm infection may compromise cardiopulmonary circulation.

Nutrition

Animals with a pre-existing vitamin E or selenium deficiency may be predisposed to developing CM. Individuals on a high nutritional plane and carrying excess body fat, such as premigratory birds, may also be at higher risk .

Drugs

Potent opioids, such as fentanyl, etorphine, carfentanil, and thiafentanil, are often used in combination with alpha-2 agonists, butyrophenones, benzodiazepines, and cyclohexamines for wildlife capture (Paterson et al., 2009). Wildlife species immobilized with opioid-based combinations frequently demonstrate side effects, such as excitement, spontaneous movement, muscle rigidity, hypoventilation, catecholamine release, and hyperthermia (Radcliffe et al., 2000). These effects, combined with hypoxemia and elevated fluid loss, may significantly increase the risk of CM. It is important to recognize that nonopioid drug combinations can also cause similar side effects and predispose anesthetized animals to CM (Caulkett et al., 2000).

• Stiffness
• Torticollis
• Tremor
• Lameness
• Emaciation
• Hemoglobinuria
• Myoglobinuria etc.
• Cramping of muscles in strange or unnatural positions may be seen in the affected wild animals.
• Death may occur finally if not attended in a proper manner.

• Depending on the clinical status, corticosteroids may be given to combat the inflammatory responses.
• The animals have to be attended with vitamin E injection and Selenium-vitamin E combinations.
• Sodium bicarbonate may be given by means of intra-venous route at rate of four to six mEq per kg body weight.
• Parenteral B complex vitamins may be provided along with balanced nutrition.
• Corrective measures against the hyperkalemia and the thermo-regulatory derangements.
• Respiratory problems need to be corrected if any.
• The affected wild animal needs to be kept in a place with cool environment.

• Keep the calm status in the environment prior tothe immobilization
• Don’t chase the animal to the possible extentprior to the chemical immobilization.
• Never excite the wild animal to be immobilized with medicaments
• Avoid making unnecessary sounds near the animal enclosure
• Avoid taking strangers nearer to the wild animal to be sedated
• Try to immobilize the wild animal after the confinement in a smaller space. This helps to avoid the unnecessary stress by chasing during the targeting activities.
• Avoid placement of ruminants like blackbuck  in lateral recumbency for prolonged periods, during therapy.

DR RK DESHMUKH,WTI

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