Trisomy 17 in a bonobo (Pan paniscus) and deletion of 3q in a lowland gorilla (Gorilla gorilla gorilla): comparison with human trisomy 18 and human deletion 4q syndrome.

A female bonobo (Pan paniscus) born at the San Diego Zoo exhibited inability to nurse and progressive weakness plus multiple congenital abnormalities including aural canal atresia and stenosis, malformed auricles, clenched hands, lordosis, agenesis of the caudal vertebra and cardiac abnormalities. Chromosome analysis identified the bonobo as being trisomic for chromosome 17, the homolog of human chromosome 18. Genotyping with human microsatellites suggested the extra chromosome was maternal in origin. In addition, a male lowland gorilla (Gorilla gorilla gorilla), also born at the zoo, exhibited postnatal growth retardation, facial dysmorphisms and small hands with short fingers. Karyotype analysis revealed the gorilla carried a deletion of the distal q arm of chromosome 3, the homolog of human chromosome 4. The phenotypic and karyotypic abnormalities found in the bonobo and gorilla were consistent with the characteristics of human trisomy 18 and human deletion 4q syndrome, respectively.

Surgical repair of an atrial septal defect in a juvenile Sumatran orangutan (Pongo pygmaeus sumatraensis).

A systolic heart murmur was auscultated in a 2-yr-old female Sumatran orangutan (Pongo pygmaeus sumatraensis) with a slower than expected growth rate. Cardiac ultrasound revealed an 11-mm atrial septal defect. Cardiac catheterization confirmed the diagnosis. Surgical repair was performed during cardiopulmonary bypass using a pericardial patch. The bypass pump was primed with human albumin and donor orangutan whole blood of a compatible type. Hematuria occurred shortly after the initiation of cardiopulmonary bypass. Successful repair was immediately confirmed with transesophageal ultrasonography. The animal was extubated shortly after returning to spontaneous ventilation but had to be reintubated 4 hr later due to tachypnea and decreased SpO2. Additional extubation attempts failed, necessitating continuous positive pressure ventilation, monitoring, and intensive care environment. Thoracic radiographs suggested adult respiratory distress syndrome. The animal required 14 days of intensive care before extubation of the trachea was successful. After 4 wk of isolation, the orangutan was successfully reintroduced to its family group.

Vaccine-induced canine distemper in European mink, Mustela lutreola.

This report describes vaccine-induced canine distemper virus (CDV) infection in four European mink (Mustela lutreola) induced by the administration of a multivalent, avian-origin vaccine. Clinical signs consisting of seizures, ataxia, facial twitching, oculonasal discharge, hyperkeratosis of footpads, and anorexia developed 16-20 days postvaccination. Conjunctival smears from one animal were positive for CDV antigen by direct fluorescent antibody testing, confirming the clinical diagnosis. The four mink died 16-26 days postvaccination. Gross and microscopic lesions that were diagnostic for CDV infection included interstitial pneumonia, lymphoid depletion, nonsuppurative encephalitis, and dermatitis. Vaccine-strain virus was isolated from tissues of three animals. Cases of vaccine-induced distemper in mustelids using avian-origin vaccine have seldom been reported.

Diurnal urinary corticoid excretion in the human and gorilla.

Urinary corticoids were measured in humans (n = 9) in frequently collected urine samples taken during a 48 hr period, and in captive western lowland gorillas (n = 5) and free-ranging mountain gorillas (n = 3) from samples taken from 0700 to 1800 hr. In each study, the highest concentrations occurred in the morning hours, then declined gradually, reaching the lowest levels in the afternoon to evening. These data show that a similar diurnal pattern of corticoid excretion does occur in these species. We suggest that if single-sample urine collection for determination of hyperadrenal activity is to be used, urine is best collected during hours of low corticoid excretion. © 1994 Wiley-Liss, Inc.

Toxicity of rac-1(3)-myristoyl glycerol to mice.

When a diet containing 30% rac-1(3)-myristoyl glycerol was fed to mice, they developed hypothermia and death occurred within a few days. If 4% safflower oil was added to the diet containing the myristoyl glycerol, hypothermia did not develop and the mortality decreased. There was a pronounced effect of ambient temperature on the toxic effects of rac-1(3)-myristoyl glycerol. Overall, the effects of feeding rac-1(3)-myristoyl glycerol paralleled the previous findings with rac-1(3)-palmitoyl glycerol. Thus there is a general toxicity associated with feeding the monoacylglycerol of any saturated fatty acid that can be reversed by including small amounts of safflower oil in the diet. The only change in plasma lipids that appears to be relevant to the toxicity and its reversal by safflower oil is an increase in cholesteryl linoleate and a corresponding decrease in the cholesteryl ester of the dietary monoacylglycerol. Even though mice ingested large amounts of rac-1(3)-myristoyl glycerol, the percentage of myristic acid in the plasma lipids was not higher than that found when a fat-free diet was fed, and was not affected by the level of myristoyl glycerol in the diet.

The result of feeding palmitoyl glycerol on lymph and plasma lipids.

Palmitoyl glycerol is toxic when fed to mice, but the toxicity is alleviated by supplementing the toxic diet with 2-4% oleate or linoleate at the expense of sucrose. Lipid and fatty acid composition of lymph and plasma were studied in mice fed chow and palmitoyl glycerol diets to help explain the toxicity mechanism. When mice were fed chow, intestinal lymph contained a high proportion of saturated fatty acids; when they were given palmitoyl glycerol, the proportion approached 90% saturated fatty acids. The cholesteryl ester fraction was higher in lymph from mice fed a toxic diet than when the diet was fortified with supplemental safflower oil. However, there were no differences between diets in lipid composition of blood plasma. Similarly, except for plasma cholesterol esters, there were no differences in fatty acid composition between mice fed palmitoyl glycerol as the only fat or supplemented with a protective unsaturated fat. In the plasma, cholesteryl palmitate was elevated and cholesteryl oleate and cholesteryl linoleate were depressed when mice were given a toxic diet. Although a monoacylglycerol was toxic when fed, the percentages of monoacyglycerols in lymph or plasma were not materially elevated. The findings indicate that neither the total proportion of saturated fatty acids nor the amount of circulating monoacylglycerols was directly involved in the toxicity of palmitoyl glycerol.