The use of butorphanol as an analgesic in a psittacine species was evaluated by determining its isoflurane-sparing effects. The Effective Dose 50 (ED50) of isoflurane was determined using a bracketing technique based on the purposeful movement elicited by pressure applied to a digit with a hemostat. The ED50 of isoflurane for 11 cockatoos (four greater sulfur crested, three lesser sulfur crested, and four citron crested) was determined to be 1.44 +/- 0.07%. After the administration of 1 mg/kg of butorphanol tartrate intramuscularly (IM), the ED50 was significantly (P < .05) decreased to 1.08 +/- 0.05%. Physiological variables that changed significantly included decreases in heart rate, tidal volume (Vt), inspiratory (Ti) and expiratory times (Te), and an increase in respiratory rate. No complications resulted because of these changes. Based on the results, butorphanol produces an isoflurane-sparing effect in cockatoos and has the potential to be a useful analgesic in psittacines.

Two alpha2-adrenoceptor agents, xylazine and medetomidine, in combination with midazolam and ketamine safely and effectively immobilized Siberian tigers (Panthera tigris altaica). The medetomidine protocol used smaller drug volumes, and induction and recovery times were shorter. Although cardiopulmonary abnormalities were noted, none were likely to be life threatening.

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Mycobacterium intracellulare (MIT) was diagnosed postmortem by culture and supporting histopathology in seven birds from a flock of little blue penguins (Eudyptula minor) at the Henry Doorly Zoo (HDZ). These birds represented 20% of the deaths in the population over a 4 yr period. Clinical signs in affected birds included severe respiratory distress characterized by open-mouth breathing with chronic debilitation. On exam, plaques were noted in the larynx, trachea, and soft tissue of the caudal oropharynx. Index cases were identified on necropsy in two birds on loan to another institution in 2003. Following a case confirmed antemortem at the HDZ, a three-drug protocol of rifampin (15 mg/kg p.o. s.i.d.), ethambutol (15 mg/kg p.o. s.i.d.), and clarithromycin (10 mg/kg p.o. s.i.d.) was started on this bird in 2004 and extended to the entire flock in 2005. Gastric wash, fecal samples, and throat plaques were obtained antemortem on five birds within the flock, selected because of the presence of oral plaques, and tested by culture followed by a polymerase chain reaction assay. MIT was detected in gastric washes from four birds and in throat plaques from all five. Three more birds died during treatment. After the seventh bird died, antimicrobial susceptibility testing performed in July 2007 indicated that the MIT was now resistant to most antibiotics tested, including rifampin and ethambutol. The treatment regimen was changed to minocycline (10 mg/kg p.o. b.i.d.) and clarithromycin (10 mg/kg p.o. s.i.d.). Oral plaques were not seen on monthly rechecks of the flock through November 2008. The proposed mechanism of transmission is exposure to wild birds but the source has not been determined. These cases of avian mycobacteriosis caused by MIT are the first known cases reported in little blue penguins.

This study evaluated the pharmacokinetics of florfenicol in the white-spotted bamboo shark (Chiloscyllium plagiosum). In addition to the pharmacokinetics, the potential application for treatment of bacterial meningitis was explored. A pilot study was used to compare doses of 30, 40, and 50 mg/kg i.m. Following that study, 10 adult sharks were administered a single i.m. dose of florfenicol at 40 mg/kg. Plasma and cerebrospinal fluid were collected and analyzed for florfenicol by a sensitive and specific high-pressure liquid chromatographic method. Pharmacokinetic analysis was performed using both non-compartmental and compartmental techniques. The absorption produced an average peak at 54 (+/-19) hr from the i.m. site of administration, and the half-life was prolonged, averaging 269.79 hr (+/-135.87). Florfenicol plasma concentrations peaked at an average of 11.85 microg/ml (+/-1.45) and were maintained above our target minimum inhibitory concentration of 4-8 microg/ml for at least 120 hr. Cerebrospinal fluid concentrations peaked at an estimated 9 microg/ml around 48 hr, surpassing the target minimum inhibitory concentration for at least 72 hr.