Determination of the pathophysiological consequences of capture and capture-induced hyperthermia in blesbok (Damaliscus pygargus phillipsi)

Abstract

An unacceptable number of wild animals die or experience morbidity as a result of capture-related complications. Capture-induced hyperthermia is believed to play a role in the morbidity and mortality of captured animals. The aims of this research were to gain a better understanding of the pathophysiological consequences of capture and capture-induced hyperthermia and to better understand the association between capture-induced hyperthermia and capture myopathy. We aimed to determine whether cooling could reduce the pathophysiological consequences of capture and protect against capture related complications like capture myopathy. Forty wild blesbok were captured from the wild and then housed in bomas at Groenkloof Nature Reserve for the duration of the study. These animals were divided into three groups which included a group of animals that were chased and cooled during immobilization (C+C), a group that was chased but not cooled during immobilization (CNC) and a control group that was not chased before or cooled during immobilization (Ct). The control group received powder diazepam in their feed two hours before they were darted to minimize their stress response to capture. The treatment groups were chased for 15 minutes before they were darted. All the animals were darted and immobilized with etorphine and azaperone. The chased and cooled group were doused with 10L of 4°C water over a 10 minute period during the immobilization. The immobilization period lasted for forty minutes in all the animals. A number of clinical and physiological parameters were measured in all the animals directly after induction into immobilization, 40 minutes later, and then on day 2, 16 and 30 post the initial capture. On these subsequent days the animals were not chased but they were simply all immobilized in their holding bomas, for data and sample collection, after they received in feed diazepam. The parameters measured and analysed included muscle and rectal temperature, PaO2, PaCo2, pH, lactate, GGT, GLDH, creatinine, BUN, CK, AST, cardiac troponin I and cortisol. The animals in the control group had normal values for all the variables measured except they were hypoxic during the immobilization. The animals that were chased developed hyperthermia, hypoxia and mild acidaemia, and they had mildly elevated concentrations of GLDH, AST, CK and creatinine indicating mild hepatic, renal and skeletal muscle damage. These animals also had severe increases in lactate and cardiac Troponin I concentrations indicating cardiac damage possibly as a result of the hypoxia that occurred during the chase and the immobilization. Despite cooling correcting the hyperthermia, it did not prevent or protect against any of these pathophysiological effects. Therefore, this capture-induced hyperthermia appeared to play a limited role in causing these effects. Therefore, capture that involves chasing animals before immobilization appears to primarily cause cardiac muscle damage. This capture-induce cardiomyopathy may have profound secondary consequences, which could result in mortality or other capture related complications.