Chronic otitis externa/media with total ear canal ablation and bulla curettage in a North American bison (Bison bison).

An adult female North American bison (Bison bison) with a chronic otitis externa/media of the right ear was examined because of a 4-mo history of intermittent anorexia, apparent painful behavior, and auricular discharge from the right ear. Computerized tomography (CT) demonstrated osteolysis of the tympanic, petrous, and squamous aspects of the temporal bone with soft tissue replacement and sclerosis of the right bulla. A total ear canal ablation with bulla curettage was performed, and cefazolin-impregnated polymethacrylate beads were left within the right bulla and the remnant temporal bone. Six months after the surgery, the bison had no clinical signs of otitis media.

Butorphanol and azaperone as a safe alternative for repeated chemical restraint in captive white rhinoceros (Ceratotherium simum).

Anesthesia in the white rhinoceros (Ceratotherium simum) has routinely involved potent narcotic anesthetic agents such as etorphine or carfentanil with their associated adverse side effects. In captive rhinoceroses conditioned to routine handling, a combination of butorphanol and azaperone at mean (+/- SD) doses of 69.3 +/- 18.0 mg and 103.1 +/- 20.9 mg, respectively, was used to produce levels of neuroleptanalgesia ranging from light "standing" sedation to deeper planes of anesthesia producing sternal and lateral recumbency. This combination was used for repeated (minimum repeat frequency of 3 days between events) anesthetic episodes (n = 26) in two animals, with the remaining episode performed in a white rhinoceros with chronic renal disease. The action of butorphanol was satisfactorily reversed with naltrexone (125 mg i.v. and 125 mg i.m.). Results (mean +/- SD) include sternal recumbency achieved in 14.1 +/- 8.1 min after i.m. dosing, standing and ambulation occurred in 1.7 +/- 0.6 min after reversal, heart rate was 62.0 +/- 10.1 beats/min, respiratory rate was 14.7 +/- 5.6 breaths/min, and percentage of oxygen saturation of hemoglobin (Spo2) was 89.2 +/- 3.0%. Without supplementation, the total elapsed time ranged from 44.9 min to 103.0 min, whereas elapsed times up to 214.3 min were achieved with supplementation (mean time to supplementation was 28.0 +/- 13.9 min after initial dosing). Butorphanol and azaperone produced adequate muscle relaxation and apparently adequate analgesia for minor surgical interferences, including abdominal laparoscopy. Respiratory rates and Spo2 measurements were improved compared with reports of using more potent opioids in this species.

Bilateral aural hyalohyphomycosis in sable antelope (Hippotragus niger).

Three juvenile sable antelope (Hippotragus niger) were diagnosed with bilateral aural hyalohyphomycosis based on histopathology. All three animals were suspected to be immunodeficient based on low IgG levels determined using the zinc sulfate turbidity test. The serum and hepatic copper levels of one animal were below the bovine reference range. Clinical signs in the three animals included bilateral ventral deviation of the pinnae with multifocal subcutaneous aural tumefaction and poor body condition. Numerous septate, nonpigmented fungal hyphae were found within the auricular cartilage, dermis, and subcutaneous granulomas. No significant fungal agents were isolated by culture, and no signs of systemic fungal dissemination were identified except for a concurrent fungal rhinitis in one animal.

Bacterial cholecystitis with cardiac and pulmonary dissemination in a blue-naped mousebird (Urocolius macrourus).

A blue-naped mousebird (Urocolius macrourus) was diagnosed by gross necropsy and histopathology as having a chronic, fibrosing bacterial cholecystitis. Acute, severe, necrotizing pneumonia and myocarditis also were present with intralesional gram-negative bacteria. The bacteria within the lungs and heart were suspected to have spread from the biliary tract because of the pattern of distribution and similar gram-staining characteristics. Enterobacter sp. and Escherichia coli were cultured from the pulmonary lesions. Cloacal cultures in clinically normal blue-naped mousebirds and speckled mousebirds (Colius striatus) yielded both Enterobacter sp. and E. coli. We hypothesize a pathogenesis in this bird consisting of biliary stasis of unknown etiology and eventual infection of the biliary tract by the normal gram-negative gastrointestinal flora. Death was believed to be a result of cardiac and respiratory dysfunction secondary to the bacterial dissemination from the biliary tree and endotoxemia.

Enhanced dopamine release and phosphorylation of synapsin I and neuromodulin in striatal synaptosomes after repeated amphetamine.

Repeated, intermittent treatment of rats with amphetamine followed by a withdrawal period leads to an enhancement in amphetamine-induced dopamine release. We previously reported an increased stoichiometry of site 3-phospho-synapsin I and increased levels of phospho-Ser41-neuromodulin in striatum after repeated amphetamine. In this study, we examined whether the enhanced amphetamine-induced dopamine release and increased levels of these phosphoproteins would be detected in synaptosomes from rats pretreated and withdrawn from repeated amphetamine. Enhanced amphetamine-induced dopamine release was detected in striatal synaptosomes from rats treated with repeated amphetamine compared with controls. The enhanced dopamine release was Ca++ dependent. State-specific antibodies were used to measure the levels of site 3-phospho-synapsin I, phosphorylated by CaM kinase II, and phospho-Ser41-neuromodulin, phosphorylated by protein kinase C, in incubated striatal S1 fractions and synaptosomes. The levels of site 3-phospho-synapsin I and phospho-Ser41-neuromodulin were increased by 40% and 30%, respectively, in amphetamine-pretreated rats compared with controls. Total neuromodulin and synapsin I was not altered. There was a significant 26% increase in CaM kinase II activity in the synaptosomes from amphetamine-pretreated rats but no change in content. No change in protein kinase C activity or content of the alpha-isozyme was detected after repeated amphetamine. Our results demonstrate that the enhanced amphetamine-induced dopamine release and occurring after repeated amphetamine can be detected in synaptosome preparations. Repeated amphetamine leads to alterations in phosphorylation/dephosphorylation activities that can be detected in the incubated synaptosomes. Because the enhanced amphetamine-induced dopamine release after repeated amphetamine appears to be Ca++ sensitive, it is possible that the altered phosphorylation systems, and perhaps site 3-phospho-synapsin I and phospho-Ser41-neuromodulin, play a role in the enhanced dopamine release.

Increased in vivo phosphorylation state of neuromodulin and synapsin I in striatum from rats treated with repeated amphetamine.

Repeated, intermittent treatment of rats with amphetamine results in a sensitization of locomotor and stereotyped behaviors that is accompanied by an enhancement in stimulus-induced dopamine release. The effects of repeated treatment with amphetamine on the phosphorylation state of neuromodulin and synapsin I, proteins involved in neurotransmitter release, were investigated. Rats were injected with 2.5 mg/kg AMPH, twice a week for 5 weeks (intermittent treatment). One week after the last injection, a challenge dose of 2.5 mg/kg AMPH was given 30 min before sacrifice. We previously reported an increase in neuromodulin phosphorylation with this sensitization paradigm. Site 3-phospho-synapsin I, site 1-phospho-synapsin I and phosphoser41-neuromodulin were detected with phosphorylation state-specific antibodies. Acute treatment with amphetamine did not increase the state of synapsin phosphorylation at either site 1 or site 3, but both site 1-phospho-synapsin I and site 3-phospho-synapsin I were increased (38% and 34%, respectively) after repeated, intermittent amphetamine. Immunoreactivity for phosphoser41-neuromodulin was increased by acute amphetamine. Site 3-phospho-synapsin I, site 1-phospho-synapsin I and phosphoser41-neuromodulin were also measured in striatum from rats receiving a different regimen in which amphetamine is given in escalating doses for 4 weeks. With this regimen, behavioral sensitization and enhanced dopamine release are exhibited in rats withdrawn 4 weeks, but not 3 days, after pretreatment. Small but significant increases in site 3-phospho-synapsin I and phosphoser41-neuromodulin were found in rats withdrawn 4 weeks from the escalating dose regimen, but not in those withdrawn 3 days. The increase in the phosphorylation state of synapsin I and neuromodulin reflect changes in the presynaptic signal transduction pathways which could play a role in the behavioral sensitization and contribute to the enhanced dopamine release reported in amphetamine-sensitized rats.

Phosphorylation of neuromodulin in rat striatum after acute and repeated, intermittent amphetamine.

Repeated, intermittent treatment of rats with amphetamine results in a sensitization of locomotor and stereotyped behaviors that is accompanied by an enhancement in stimulus-induced dopamine release. Increased phosphorylation of the neural specific calmodulin-binding protein, neuromodulin (GAP-43, B-50, F1) has been demonstrated in other forms of synaptic plasticity and plays a role in neurotransmitter release. To determine whether neuromodulin phosphorylation was altered during amphetamine sensitization, the in vivo phosphorylated state of neuromodulin was examined in rat striatum in a post hoc phosphorylation assay. Female, Holtzman rats received saline or 2.5 mg/kg amphetamine twice weekly for 5 weeks. One week after the last dose of amphetamine, rats were challenged with either 1 mg/kg or 2.5 mg/kg amphetamine or saline and the rats were sacrificed 30 min later. Purified synaptic plasma membranes were prepared in the presence of EGTA and okadaic acid to inhibit dephosphorylation, and were subsequently phosphorylated in the presence of purified protein kinase C and [gamma-32P]ATP. The protein kinase C-mediated post hoc phosphorylation of neuromodulin was significantly reduced in groups that received either acute or repeated amphetamine suggesting that neuromodulin in those groups contained more endogenous phosphate. The acute, challenge dose of amphetamine increased neuromodulin phosphorylation in the saline-treated controls but not in the repeated amphetamine-pretreated group. Anti-neuromodulin immunoblots showed no change in neuromodulin levels in any group. There was no significant change in protein kinase C activity in any treatment group. To further investigate the effect of acute amphetamine, the ability of amphetamine to alter neuromodulin phosphorylation in 32Pi-preincubated Percoll-purified rat striatal synaptosomes was examined. Amphetamine (10 microM) significantly increased phosphorylation of a 53 kDa band that migrated with authentic neuromodulin in the synaptosomes by 22% while 500 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) increased neuromodulin phosphorylation by 45%. These data suggest that one injection of amphetamine can increase neuromodulin phosphorylation in rat striatum and that this increase is maintained for at least 1 week following a repeated, sensitizing regimen of amphetamine. Since sensitization can be induced with one dose of amphetamine, it is possible that enhanced neuromodulin phosphorylation could contribute to neurochemical events leading to enhanced release of dopamine and/or behavioral sensitization.