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A chronic ulcerative and eosinophilic dermatitis occurred in 20 captive cheetahs (Acinonyx jubatus) with persistent feline herpes virus 1 (FHV1) infection. Affected animals had erythematous, ulcerated plaques primarily on the face and forelegs in sites of contact with lachrymal and salivary secretions. The dermatitis was characterized by dense infiltrates of eosinophils and plasma cells and pseudoepitheliomatous hyperplasia. Rare keratinocytes within the lesions had nuclei with marginated chromatin and small eosinophilic inclusions composed of herpes virus nucleocapsids. Virus isolated from lesions was confirmed to be FHV1. Lesions persisted and progressed unless removed by cryoexcision. The occurrence of this unusual reaction to FHV1 in approximately 5% of captive North American cheetahs suggests a species propensity for a Th2-dominant response to herpes virus infection. This atypical immune reaction may indicate a heritable trait or modulation of the immune response by other factors such as chronic stress.

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To evaluate the association between corneal lipid infiltration (corneal arcus) and dietary cholesterol in Cuban tree frogs (Osteopilus septentrionalis), 47 wild-caught frogs were fed diets of either regular or high-cholesterol crickets containing 0.7% and 1.7% cholesterol dry matter, respectively. Serum total cholesterol and triglycerides were measured when the frogs were euthanized after 17 mo. In a subsample of frogs, serum lipoproteins were characterized using high-performance liquid chromatography. The first case of corneal lipid deposition occurred in a female frog after 13 mo on the high-cholesterol diet. In the subsequent 4 mo, 5/11 males and 11/35 females developed the disease. Four of these affected frogs were females on the regular diet. Frogs with corneal lipid deposition had elevated serum total cholesterol (27.3 +/- 19.8 mmol/L) and low-density lipoproteins (LDL, 17.8 +/- 18.9 mmol/L) compared with unaffected captive frogs (16.5 +/- 20.4 and 9.0 +/- 7.6 mmol/L, respectively). Corneal lipid deposition was more prevalent in frogs on the high-cholesterol diet, and this group had higher serum total cholesterol (34.1 +/- 15.2 mmol/L in females, 22.8 +/- 14.8 mmol/L in males) than did frogs on the diet of regular crickets (12.3 +/- 8.7 mmol/L in females, 10.4 +/- 3.1 mmol/L in males). Captive frogs on both diets had higher serum total cholesterol than did wild frogs (3.1 +/- 2.1 mmo/L in females, 5.3 +/- 2.6 mmo/L in males). This additional serum cholesterol was primarily carried on very low-density lipoproteins (VLDL) and LDL rather than high-density lipoproteins (HDL), as indicated by the significantly higher ratio of VLDL cholesterol and LDL cholesterol over HDL cholesterol in captive frogs compared with wild frogs. Elevation in this ratio was significantly higher in captive females than in captive males. There was no evidence that increased serum cholesterol in captive females was directly related to the process of vitellogenesis.

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Sera from nine species of clinically healthy nonhuman primates were assayed for T4 and thyroid-stimulating hormone (TSH) using human immunoassays (a fluorescence polarization immunoassay for T4, a microparticle enzyme immunoassay for TSH). The T4 levels ranged from 20 to 132 nmol/L (x +/- SD = 62.8 +/- 24.7 nmol/L). Levels of TSH were detected only in western lowland gorillas (Gorilla gorilla gorilla) and Sumatran orangutans (Pongo pygmaeus abelii) (range, 0.4-10.8 mIU/L; detectable limit = 0.01 mIU/L). The results suggest that the antibodies used in the commercial TSH immunoassay assessed in this study cross-react with gorilla and orang-utan TSH but not with TSH of primates of the genera Macaca, Papio, Erythrocebus, Ateles, Leontopithecus, and Lemur.

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Eight 8-wk-old raccoon pups (Procyon lotor) with maternal canine distemper virus (CDV) neutralizing antibodies (NAb) and 24 8-wk-old seronegative pups were administered a commercial modified-live CDV vaccine (Galaxy, D, Solvay Animal Health, Inc., Kitchener, Ontario, Canada). All 24 seronegative raccoons had detectable serum CDV NAb titers 14 days after the initial dose. Titers rose to maximum levels 4 wk post-vaccination. Mean titers for groups of vaccinated seronegative pups were maintained between 1:256 and 1:2,048 for the remainder of the 3 mo observation period. Geometric means of the serum CDV NAb titer of eight seronegative pups given a single vaccine dose at 8 wk of age did not differ significantly from those of eight pups that were given serial doses at 8, 12, and 16 wk of age, or from those of eight pups vaccinated once at 16 wk of age. Seven unvaccinated 8-wk-old raccoon pups used as controls remained seronegative throughout the trial. Seven out of eight 8-wk-old pups with maternal antibodies, vaccinated at 8, 12, and 16 wk of age, failed to develop a rise in their CDV NAb titers until at least 18 wk of age, 2 wk after the third vaccination. Titers in eight unvaccinated raccoons with maternal antibodies declined steadily to undetectable levels at 20 wk of age. A half-life of 10.55 days was calculated for maternally-derived CDV NAb in raccoon pups. Sixteen vaccinated raccoons were protected from clinical disease following experimental oronasal challenge with a virulent raccoon strain of CDV, 13 to 23 wk after vaccination. Serum CDV NAb titers at the time of challenge ranged from 1:12 to 1:384 and increased during the period of observation. Three of four unvaccinated seronegative raccoons used as controls failed to mount any detectable CDV NAb and were euthanatized after developing clinical signs of canine distemper 26, 29, and 30 days post-challenge (PC). Necropsies confirmed the diagnosis. The fourth control raccoon exhibited transient equivocal clinical signs, mounted a sluggish humoral response, but was clinically normal when euthanatized 42 days PC. In this raccoon, there was focal non-suppurative encephalitis with intranuclear inclusion bodies typical of CDV infection.

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Primary hypothyroidism was diagnosed in a 26-yr-old female western lowland gorilla (Gorilla gorilla gorilla) on the basis of serum levels of thyroxine (T4), free T4, and thyroid-stimulating hormone (TSH) measured by human immunoassays. Compared with clinically normal gorillas, the TSH level (107 mlIU/L) was markedly elevated, and T4 (<14.0 nmol/L) and free T4 (5.0 pmol/L) levels were decreased. Thyroid hypofunction could explain the weight gain, unsettled appetite, anxious behavior, lethargy, and poor intraspecies interactions shown by this gorilla. The antibodies in the commercial immunoassay used in this study apparently cross-reacted with gorilla TSH. Supplementation with levothyroxine sodium was initiated and was followed by a marked decrease in circulating TSH and a noticeable improvement in the animal's physiologic status and activity level.

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Amphibians present unique challenges for the clinician in the diagnosis and treatment of life-threatening conditions. Their adaptability to both aquatic and terrestrial lifestyles leaves them vulnerable to dehydration and fluid overload, either of which may accompany serious disease. This article presents the most common emergency conditions in amphibians, the physiologic basis of disease, and a guide to the diagnosis and treatment of amphibian emergencies.

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The anatomy of the renal portal system of the red-eared slider (Trachemys scripta elegans) is described, based on dissection of six double latex-injected specimens (three males, three females). The anatomy of these vessels, which had not previously been described in this species, was found not to differ significantly from the fundamental chelonian pattern. Fluoroscopic radioangiography revealed that venous blood returning from the hindlimbs flowed predominantly to the liver and bypassed the kidneys. Blood from the tail either flowed to the kidneys or bypassed them and flowed directly to the liver. A putative valve is described that governs venous blood flow from the caudal body to or around the kidneys.

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The premise that drugs not be injected into the caudal body of reptiles because they will be carried by the renal portal system to the kidneys, where they may be nephrotoxic or rapidly excreted, was tested by comparing the pharmacokinetics of gentamicin (excreted via glomerular filtration in mammals) and carbenicillin (excreted partly via renal tubular secretion in mammals) following injection into the forelimb or hindlimb of red-eared sliders (Trachemys scripta elegans). Ten sliders received intramuscular gentamicin (10 mg/kg) in a forelimb (n = 5) or a hindlimb (n = 5), and plasma levels of the drug were assayed over time. Following drug clearance, the experiment was repeated with the site of injection reversed so that each animal acted as its own control. Another 10 sliders were similarly treated, using intramuscular carbenicillin (200 mg/kg). Injection site of gentamicin had no effect on any pharmacokinetic parameter (time to maximum plasma concentration, maximum plasma concentration, half-life, area under the curve, clearance, and volume of distribution). However, the area under the curve of plasma carbenicillin concentration vs. time was significantly lower following hindlimb injection, in comparison with forelimb injection, at 1, 4, and 8 hr, which may reflect reduced bioavailability of the drug, as would be expected with renal portal perfusion and tubular excretion on first pass through the kidney. This effect on carbenicillin likely is not clinically important because plasma levels remained above recommended minimum inhibitory concentrations. Because blood draining the caudal body of reptiles passes through the kidneys or the liver before reaching the central circulation, the effect on the pharmacokinetics of a drug injected in that region will vary with its renal or hepatic extraction rate. Generally, this effect is unlikely to be significant.

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Proliferative periosteal disease was identified in 6 black lemurs (Eulemur macaco macaco) of 2 family groups. Bilaterally symmetric formation of periosteal new bone at the metaphyseal regions of major long bones was first detected at the stifle and tarsal areas and was detected later at the carpal areas. Bony changes were accompanied by progressive renal disease. The syndrome progressed for 6 to 16 months before the lemurs were euthanatized because of debility. Necropsy revealed changes confined to the skeleton and kidneys. Formation of new bone was detected at all affected joints, and chronic renal disease was evident in each lemur. A specific cause was not identified. Although indistinguishable histologically from hypertrophic osteoarthropathy, several important differences were apparent. Distribution of the periosteal new bone was in the metaphyseal rather than diaphyseal areas. Thoracic or gastrointestinal lesions, typically seen with hypertrophic osteoarthropathy, were not detected, and substantial renal disease was evident. A genetic component may be involved in the development of this condition.

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Over a 3-year period, 32 Dall's sheep (Ovis dalli dalli) embryos were transferred into 24 domestic sheep (O. aries) recipients and 4 were transferred into 2 Dall's sheep recipients. In the first year, none of the 10 O. aries recipients was diagnosed pregnant. In the following 2 years, 9 (37%) of the domestic sheep recipients were pregnant on Day 18, 8 (33%) on Day 40, 6 (25%) on Day 90 and 4 (16%) on Day 120; 1 aborted at Day 125 and another at Day 145. Pregnancies were established only in ewes that had previously been recipients of Dall's sheep embryos. The 2 remaining pregnant sheep were treated with progesterone from Day 125 until the fetuses were determined to be dead at Day 145. Both of the Dall's sheep recipients (Year 2) established pregnancies; 1 live Dall's sheep lamb was born 174 days after mating. No differences in serum progesterone, oestrone, prostaglandin F-2 alpha metabolites or cortisol concentrations could be detected during pregnancy between recipients carrying Dall's sheep embryos, recipients receiving progesterone treatment or domestic ewes carrying domestic sheep pregnancies. Six fetuses were necropsied (1 at Day 125 and 5 at Day 145-146): all fetuses were premature and had various degrees of hydranencephaly. No significant differences were found when cotyledon numbers were compared among domestic ewes carrying Dall's sheep lambs. Dall's sheep ewes lambing naturally and domestic ewes lambing naturally. These results demonstrate that the transfer of Dall's sheep embryos to domestic ewes results in the establishment but subsequent loss of pregnancy and that these losses occur throughout gestation.

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In late spring of 1986, 10 of 23 Dall's sheep (Ovis dalli dalli) at the Metropolitan Toronto Zoo were moved to a new exhibit, where all developed severe respiratory signs refractory to anthelmintic and antibiotic therapy. In July, two animals died with chronic active bronch-pneumonia, and a third was euthanized because of pneumonia several months later. Bacteria were not isolated from the lungs of the first, steptococci and Pasteurella hemolytica were isolated from the other two, respectively; Mycoplasma ovipneumoniae was isolated from both. Pulmonary lesions in all three sheep were consistent with Mycoplasma sp. infection. Nasal swabs of the remaining animals yielded no consistent bacterial isolates; however, four of eight sheep were positive for M. ovipneumoniae. Viral cultures yielded an as yet unidentified herpesvirus. Sheep in the original and new herds had no serologic titers to parainfluenza-3, equine viral rhinopneumonitis, or infectious bovine rhinotracheitis, and had variable titers against bovine respiratory syncytial virus. No titers against M. ovipneumoniae were present in 13 sheep still in the original exhibit, but titers varied from 1:32 to 1:256 in eight pneumonic sheep. Sera taken from three sheep before or early in the outbreak were all negative for antibody to M. ovipneumoniae. Two of the affected Dall's sheep had been in contact with domestic sheep in the winter of 1985-1986, and M. ovipneumoniae was subsequently cultured from the domestic flock. Exposure to a new pathogen, and environmental and social stress in a new exhibit may have resulted in this severe disease in Dall's sheep.

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Geopetitia aspiculata was found in 12 species of Passeriformes, one species of Coraciiformes, and one species of Charadriiformes which died in a free-flight area in the Tropical House at the Assiniboine Park Zoo, Winnipeg, Canada. The nematodes occurred in chronic inflammatory cysts attached to the serosa of the posterior end of the esophagus, proventriculus, and the anterior part of the gizzard. Posterior ends of worms were observed to extend from the cyst into the lumen of the proventriculus. Birds hatched and raised in the Tropical House acquired infections, probably through the agency of feral crickets. Experimental studies showed that G. aspiculata developed to the infective third stage in the fat body of Acheta domesticus (L.). This is the first transmission cycle of Geopetitia spp. to be elucidated and the egg, first, third, and early fifth stages of the parasite are described. The absence of spicules in males of G. aspiculata is confirmed. Geopetitia aspiculata was probably introduced to the Zoo by infected tropical birds obtained from dealers or other zoos. The wild source of the parasite is not known since G. aspiculata has never been reported in wild birds; the report of G. aspiculata in wild Piciformes in Cuba by Barus (1971) is in error.

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In an episode of tularemia in a Canadian zoologic garden, three black and red tamarins (Sanguinus nigricollis) and one talapoin (Cercopithecus talapoin) died. A second talapoin developed abscesses in the tongue and submandibular area; this animal recovered with treatment. Francisella tularensis was isolated from lung, liver, and spleen from each dead monkey and from pus collected from the tongue abscess of the sick talapoin. The attending veterinarian contracted the disease from a tamarin bite. The source of the disease was identified as wild ground squirrels, and the causative organism was recovered from the liver and spleen of one squirrel and from fleas found on it.

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