Efficacy of a low-dosage combination of butorphanol, azaperone, and medetomidine (BAM) to immobilize Rocky Mountain elk.

We compared dosages of a combination of sedatives, which included butorphanol tartrate, azaperone tartrate, and medetomidine HCl (BAM) in captive adult Rocky Mountain elk (Cervus elaphus nelsoni). All three BAM dosages (low, medium, and high) effectively immobilized elk and produced an adequate level of sedation in all subjects. Induction times were similar among the three groups (mean ± SD: low=6.9 ± 1.1 min; medium=6.3 ± 0.9 min; high=4.7 ± 1.3 min). Most elk became hypoxemic regardless of BAM dosage, but hypoxemia tended to be most severe in the high-BAM group; regardless of BAM dosage, oxygen supplementation improved the percentage of oxygen saturation and stabilized the vital rates. Recovery after administration of antagonists (3 mg atipamezole/mg medetomidine and 2 mg/kg tolazoline) was comparable among groups (range of means=9 ± 1.5-11.7 ± 1 min). Based on the findings from clinical trials and field data from free-ranging elk immobilizations, we recommend low-dose BAM (2 mL dose; equivalent to 46 mg butorphanol, 30 mg azaperone, and 18 mg medetomidine) and supplemental oxygen for adult elk; immobilization should be antagonized using 3-5 mg atipamezole/mg medetomidine and 2 mg/kg tolazoline, with tolazoline injected about 5-10 min before atipamezole to smooth out recovery.

Immunization with a synthetic peptide vaccine fails to protect mule deer (Odocoileus hemionus) from chronic wasting disease.

Chronic wasting disease (CWD) adversely affects both wild and captive cervid populations. A vaccine to prevent CWD would be a highly desirable tool to aid in disease management. To this end, we tested in mule deer a combination of CWD vaccines consisting of cervid prion peptide sequences 168-VDQYNNQNTFVHDC-182 and 145-NDYEDRYYRENMYRYPNQ-164 that had previously been shown to delay onset of clinical disease and increase survival in a mouse-adapted scrapie model. Thirteen captive mule deer (Odocoileus hemionus) were divided into vaccine (n=7) and control groups (n=6), and given prime and boost vaccinations intramuscularly 5 wk apart. Eight weeks postprime (3 wk postboost), all animals were challenged via natural exposure to an environment contaminated with infective CWD prions. Deer were monitored intermittently for prion infection by rectal and tonsil biopsies beginning 275 days postchallenge. All vaccinates responded to both peptide conjugates present in the combination vaccine as measured by enzyme-linked immunosorbent assay. However, all deer eventually became infected regardless of vaccine status.

Failure of fallow deer (Dama dama) to develop chronic wasting disease when exposed to a contaminated environment and infected mule deer (Odocoileus hemionus).

We monitored a herd of fallow deer (Dama dama) for evidence of prion infection for 7 yr by periodic postmortem examination of animals from the herd. The fallow deer were exposed to the chronic wasting disease (CWD) agent from mule deer by living in a paddock considered contaminated with infectivity from its history of housing CWD infected deer and, after the first year of the study, by comingling with infected mule deer (Odocoileus hemionus). At least 8 of 12 mule deer serving as sentinels for prion transmission and 25 additional mule deer serving as sources of infectivity developed clinical CWD or were otherwise confirmed to be infected with CWD via lymphoid tissue immunohistochemistry (IHC). In contrast, none of the 41 exposed fallow deer showed clinical signs suggestive of CWD, IHC staining of disease-associated prion in lymphoid or brain tissues, or evidence of spongiform degeneration in sections of brain stem at the level of the obex when sampled 18 mo to 7 yr after entering the mule deer paddock. The absence of clinical disease and negative IHC results in fallow deer housed in the same contaminated paddock for up to 7 yr and almost continuously exposed to CWD-infected mule deer for up to 6 yr suggests a species barrier or other form of resistance preventing fallow deer infection by the CWD agent or delaying progression of the disease in this species.

Evaluation of intramuscular butorphanol, azaperone, and medetomidine and nasal oxygen insufflation for the chemical immobilization of white-tailed deer, Odocoileus virginianus.

Chemical immobilization of wildlife often includes opioids or cyclohexamines. These substances are problematic as a result of their required storage, handling, and record-keeping protocols. A potentially useful alternative sedation protocol includes a combination of butorphanol, azaperone, and medetomidine (BAM: 0.43 mg/kg butorphanol, 0.36 mg/kg azaperone, 0.14 mg/kg medetomidine). One risk of wildlife immobilization with any drug combination is hypoxemia. This may be of particular importance when using an alpha 2 agonist such as medetomidine because of its powerful vasoconstrictive effect. In this prospective study, the BAM combination was evaluated for chemical immobilization of white-tailed deer. Additionally, selected physiologic parameters associated with BAM immobilization, including oxygen saturation via pulse oximetry and arterial blood gas measurement, with and without nasal insufflation of oxygen at a relatively low flow of 3 L/min, were evaluated. The BAM combination resulted in a predictable onset of sedation, with a mean induction time to lateral recumbency of 9.8 +/- 3.6 min. All deer recovered smoothly within a range of 5-20 min after reversal with intramuscular administration of naltrexone, atipamazole, and tolazoline (NAT). Clinically relevant decreases in arterial partial pressure of oxygen (PaO2) and oxygen saturation (SpO2) were observed in animals not receiving supplemental oxygen, while both parameters significantly improved for oxygen-supplemented deer. Pulse oximetry with this protocol was an unreliable indicator of oxygen saturation. In this study, altitude, recumbency, hypoventilation, butorphanol- and medetomidine-specific effects, as well as the potential for alpha 2 agonist-induced pulmonary changes all may have contributed to the development of hypoxemia. Overall, capture of white-tailed deer with the BAM/NAT protocol resulted in excellent chemical immobilization and reversal. Because the BAM combination caused significant hypoxemia that is unreliably detected by pulse oximetry but that may be resolved with nasal oxygen insufflation, routine use of oxygen supplementation is recommended.