Fish display robust neuroendocrine and physiologic stress responses to noxious stimuli. Many anesthetic, sedative, or analgesic drugs used in other vertebrates reduce stress in fish, decrease handling trauma, minimize movement and physiologic changes in response to nociceptive stimuli, and can be used for euthanasia. But extrapolating from limited published anesthetic and sedative data to all fish species is potentially harmful because of marked anatomic, physiologic, and behavioral variations; instead, a stepwise approach to anesthetizing or sedating unfamiliar species or using unproven drugs for familiar species is advisable. Additionally, knowledge of how water quality influences anesthesia or sedation helps limit complications. The most common method of drug administration is through immersion, a technique analogous to gaseous inhalant anesthesia in terrestrial animals, but the use of injectable anesthetic and sedative agents (primarily intramuscularly, but also intravenously) is increasing. Regardless of the route of administration, routine preprocedural preparation is appropriate, to stage both the animals and the supplies for induction, maintenance, and recovery. Anesthetic and sedation monitoring and resuscitation are similar to those for other vertebrates. Euthanasia is most commonly performed using an overdose of an immersion drug but injectable agents are also effective. Analgesia is an area in need of significant research as only a few studies exist and they provide some contrasting results. However, fish have mu and kappa opiate receptors throughout the brain, making it reasonable to expect some effect of at least opioid treatments in fish experiencing noxious stimuli.

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The human MHC class I gene, HLA-B27, is a strong risk factor for susceptibility to a group of disorders termed spondyloarthropathies (SpAs). HLA-B27-transgenic rodents develop SpAs, implicating HLA-B27 in the etiology of these disorders. Several nonhuman primates, including gorillas, develop signs of SpAs indistinguishable from clinical signs of humans with SpAs. To determine whether SpAs in gorillas have a similar HLA-B27-related etiology, we analyzed the MHC class I molecules expressed in four affected gorillas. Gogo-B01, isolated from three of the animals, has only limited similarity to HLA-B27 at the end of the α1 domain. It differs by several residues in the B pocket, including differences at positions 45 and 67. However, the molecular model of Gogo-B*0101 is consistent with a requirement for positively charged residues at the second amino acid of peptides bound by the MHC class I molecule. Indeed, the peptide binding motif and sequence of individual ligands eluted from Gogo-B*0101 demonstrate that, like HLA-B27, this gorilla MHC class I molecule binds peptides with arginine at the second amino acid position of peptides bound by the MHC class I molecule. Furthermore, live cell binding assays show that Gogo-B*0101 can bind HLA-B27 ligands. Therefore, although most gorillas that develop SpAs express an MHC class I molecule with striking differences to HLA-B27, this molecule binds peptides similar to those bound by HLA-B27.

Six adult female tigers (Panthera tigris) were anesthetized repeatedly for elective medical procedures using 3 mg medetomidine and 200 mg ketamine i.m. Inductions were rapid and smooth, although supplemental ketamine was needed for safe transport after induction in 6 of 17 procedures. Reversal of the medetomidine-induced sedation with 15 mg atipamezole i.m. 59-232 min after induction resulted in smooth, rapid recoveries.

No abstract

An emaciated 2.36-kg juvenile green sea turtle, Chelonia mydas, was found floating off of Melbourne Beach, Florida, USA (28 degrees 2'4"N, 80 degrees 32'32"W). The turtle exhibited signs of cachexia, positive buoyancy, lethargy, and obstipation; was covered with barnacles; and was anorexic at the time of presentation. Dorsal-ventral radiographs with positive contrast confirmed obstruction of the gastrointestinal tract. Serum chemistry abnormalities reflected metabolic/nutritional deficiencies. Gastrointestinal prokinetics and oral/enema mineral oil applications were effective in relieving gastrointestinal obstruction with the turtle defecating a total of 74 foreign objects over a period of a month. After the removal of the foreign material, the turtle quickly regained normal behavior and health. The lack of blood parameters demonstrating infection or inflammation; the failure to respond to antibiotic and antifungal treatment as well as the parallel improvement in behavior and health after incremental evacuation of the plastic is highly suggestive of a cause and effect association.

Cotton-top tamarins (Saguinus oedipus) are a critically endangered species that have been bred successfully in captivity for many years. For two decades, the Cotton-top Tamarin SSP(©) has been challenged with a high rate of reproduction combined with a history of contraceptive failures and nonrecommended births using the current Depo Provera(®) (medroxyprogesterone acetate) injection followed by MGA (melengestrol acetate) implant contraception combination. To address these issues we have developed and tested the use of levonorgestrel (LNG) as an effective contraception option for cotton-top tamarins. LNG was delivered in an injectable, gel matrix consisting of polylactic-co-glycolic acid, triethyl citrate and N-methylpyrrolidone. This gel matrix forms a biodegradable depot at the subcutaneous injection site providing slow release of the active ingredient. Gel matrix composition and LNG concentration were adjusted in four gel formulations to maximize the duration of contraceptive efficacy while minimizing immediate post-injection increases in fecal LNG concentration. LNG treatment (68.44 ± 8.61 mg/kg) successfully eliminated ovarian cycles (fecal pregnanediol-3-glucuronide (PdG) and estrone conjugates (E(1) C)) for 198.8 ± 70.3 days (formulation four; range 19-50 weeks). It was demonstrated that subcutaneous LNG depot injection was an effective, reversible contraceptive option for the management of cotton-top tamarins in captivity.

Toxicosis associated with benzimidazole anthelmintics has been reported with increasing frequency in zoologic collections. Clinical signs, clinicopathologic abnormalities, and gross and histologic lesions are primarily the result of damage to the gastrointestinal and hematopoietic systems. Profound leukopenia, especially granulocytopenia, is the most common and severe clinicopathologic change associated with benzimidazole administration. Death usually occurs from overwhelming systemic bacterial and/or fungal infections secondary to severe immunosuppression. In this 125-day study, six male Hermann's tortoises (Testudo hermanni) were treated orally with two 5-day courses of fenbendazole 2 wk apart at a dosage of 50 mg/kg. Serial blood samples were used to assess hematologic and plasma biochemical changes before, during, and following the treatment period. Although the tortoises remained healthy, blood sampling indicated an extended heteropenia with transient hypoglycemia, hyperuricemia, hyperphosphatemia, and equivocal hyperproteinemia/hyperglobulinemia, which were considered to be in response to fenbendazole administration. Changes in several other clinicopathologic parameters appeared to correlate with fenbendazole administration. The hematologic and biochemical changes seen in the healthy animals in this study should be considered when treating compromised tortoises with fenbendazole. Hematologic and plasma biochemical status of tortoises/reptiles should be determined before treatment and monitored during the treatment period. The risk of mortality of an individual from nematode infection should be assessed relative to the potential for metabolic alteration and secondary septicemia following damage to hematopoietic and gastrointestinal systems by fenbendazole.