Clinical and pathological findings in a Dwarf Red Brocket Mazama rufina (Mammalia: Cetartiodactyla: Cervidae) attacked by dogs

Capture myopathy is a common fatal syndrome in wild ungulates resulting from anthropogenic stressful events such as the capture or transport of specimens. There are, however, few published data on this issue due to predator attacks. The present report describes for the first time the capture myopathy syndrome in a Dwarf Red Brocket Mazama rufina following dog Canis familiaris attack. Clinical signs included pale mucous with increase capillary refill time, tachycardia, tachypnea, hypertension, hypothermia, hypoglycemia, and red brown urine. Muscle tremors, ataxia, prostration, paralysis, and opisthotonus were progressively observed. Laboratory tests showed increased levels of cortisol, creatinine, creatine kinase, lactate dehydrogenase, and potassium; decreased blood urea nitrogen-creatinine ratio; and myoglobinuria. The animal died 72 hours after hospital admission. At necropsy, findings included injuries on both hindlimbs with edema, emphysema, and soft-friable texture in affected muscles, dark kidneys and brown urine in bladder. Histopathological exams were indicative of skeletal-cardiac muscle degenerative lesions and myoglobinuric nephrosis. Immuno-histochemistry revealed myoglobin depletion in degenerate muscles and myoglobin accumulation in renal tissues. We strongly recommend that treatment for capture myopathy be initiated when a wild ungulate is admitted with history of predator attack, since the syndrome may have already established. This report adds to the instances of negative impacts caused by domestic dogs on threatened wildlife species.

Capture Myopathy and Stress Cardiomyopathy in a Live-Stranded Risso’s Dolphin (Grampus griseus) in Rehabilitation

Capture myopathy (CM) is described in wild animals as a metabolic syndrome resulting from the extreme stress suffered during and after capture, handling, restraint, and transport. Although CM has been characterized in many species of cetaceans, descriptions of cardiac injury—an important component of this syndrome, and, according to previous authors, comparable to the existing human pathology so-called stress cardiomyopathy (SCMP)—are still rare. Therefore, the main aim of this report is to illustrate, for the first time, the biochemical analysis, and gross, histopathological, histochemical and immunohistochemical features of CM, and more specifically of the SCMP involved in this syndrome, caused by the live-stranding and consequent rehabilitation attempt, for a certain period of time, in a juvenile male Risso’s dolphin (Grampus griseus). The animal presented elevated values of creatine kinase, cardiac troponin I and blood urea nitrogen, with some variations during the rehabilitation period. Histologically, we detected vascular changes and acute degenerative lesions analogous to the ones observed in humans with SCMP. We consider this study to be an important contribution to the study of cetaceans since it could help in decision-making and treatment procedures during live-strandings and improve conservation efforts by reducing the mortality of these animals.

Conserving wildlife in a changing world: Understanding capture myopathy—a malignant outcome of stress during capture and translocation

The number of species that merit conservation interventions is increasing daily with ongoing habitat destruction, increased fragmentation and loss of population connectivity. Desertification and climate change reduce suitable conservation areas. Physiological stress is an inevitable part of the capture and translocation process of wild animals. Globally, capture myopathy—a malignant outcome of stress during capture operations—accounts for the highest number of deaths associated with wildlife translocation. These deaths may not only have considerable impacts on conservation efforts but also have direct and indirect financial implications. Such deaths usually are indicative of how well animal welfare was considered and addressed during a translocation exercise. Importantly, devastating consequences on the continued existence of threatened and endangered species succumbing to this known risk during capture and movement may result. Since first recorded in 1964 in Kenya, many cases of capture myopathy have been described, but the exact causes, pathophysiological mechanisms and treatment for this condition remain to be adequately studied and fully elucidated. Capture myopathy is a condition with marked morbidity and mortality that occur predominantly in wild animals around the globe. It arises from inflicted stress and physical exertion that would typically occur with prolonged or short intense pursuit, capture, restraint or transportation of wild animals. The condition carries a grave prognosis, and despite intensive extended and largely non-specific supportive treatment, the success rate is poor. Although not as common as in wildlife, domestic animals and humans are also affected by conditions with similar pathophysiology. This review aims to highlight the current state of knowledge related to the clinical and pathophysiological presentation, potential treatments, preventative measures and, importantly, the hypothetical causes and proposed pathomechanisms by comparing conditions found in domestic animals and humans. Future comparative strategies and research directions are proposed to help better understand the pathophysiology of capture myopathy.

Use of Diazepam-Ketamine in Prevention of Capture Myopathy in the Ostrich (Struthio camelus): A Case Report

Capture or exertional myopathy is an attendant complication of manual restraint in ratites, asides physical injuries that handlers may suffer. This work was carried out to restrain and immobilize two ostriches (Struthio camelus) in a bid to facilitate their clinical examination and transportation from one location to another, without subjecting the birds to capture myopathy that arises from the stress and exertion associated with physical restraint and capture. Two ostriches, male and female, weighing 120kg and 105kg respectively, were requested to be immobilized for relocation from Onireke to Jericho area in Oyo State, Nigeria. The birds were fasted overnight, administered with diazepam (3mg/kg) orally and ketamine (10mg/kg) intramuscularly. Mild sedation was achieved with diazepam after one hour. The birds were successfully transported. Complete recovery was achieved at about 8hours post-administration of ketamine. Anaesthetic agents did not alter the haematologic parameters. We conclude that the diazepam-ketamine combination is generally safe for ratites and that oral administration of diazepam accompanied by intramuscular administration of ketamine provides restraint in ratites while also avoiding the risk of capture myopathy. It is suggested that the current dose of diazepam might need to be increased if the oral route is to be employed so as to shorten the onset of sedation and increase the depth of sedation.

Delayed peracute capture myopathy in a Himalayan Ibex Capra sibirica (Mammalia: Cetartiodactyla: Bovidae)

The present study focused on the capture myopathy as a fatal consequence of capture and rescue operation in an endangered Himalayan Ibex kid. The Ibex died 48 hours after being captured without showing specific clinical signs. Post-mortem examination revealed renal cortical necrosis, degeneration of tubular cells and congestion as the main histopathological findings in kidneys. Myocardial lesions consisted of multifocal degenerative changes of myofibres, hyalinization and nuclear degeneration with pyknosis. Skeletal muscles that appeared grossly normal showed mild to moderate degeneration and fragmentation with intermittent loss of striation. The pathological findings were indicative of delayed peracute capture myopathy. This is believed to be the first report of capture myopathy in an endangered Himalayan ibex from India underlining the importance of understanding the causes of mortality in such endangered wild species as a prerequisite to successful conservation programme.