Fenbendazole treatment without environmental decontamination eradicates Syphacia muris from all rats in a large, complex research institution.

Syphacia muris parasitism was eliminated from rats and voles by feeding fenbendazole-medicated chow (150 ppm) for five 7-day periods; treatment periods were separated by 7-day periods of feeding non-medicated chow, yielding atotal treatment course of 9 weeks. No other manipulations to facilitate eradication, including the use of filter tops, autoclaved cages, environmental decontamination, colony depopulation, breeding cessation, and research restriction, were done. The examination of 3143 cellophane-tape impressions of the anus and 160 cecal examinations from euthanized rats and voles during the treatment period and for 7 months afterwards confirmed the efficacy of treatment. Treatment was rapidly effective in voles. In rats, pinworm eggs persisted at high levels for 2 weeks after the start of treatment, but no eggs were found after 22 days.

The effectiveness of a microisolator cage system and sentinel mice for controlling and detecting MHV and Sendai virus infections.

Experiments were conducted to determine (a) whether BALB/c mice housed on soiled bedding can be used as sentinels for the detection of Sendai virus and MHV from infected mice housed in microisolators, and (b) whether the microisolator caging system protects mice against Sendai virus and MHV infections. Sentinel mice were housed in microisolator cages, exposed continuously to soiled bedding and bled at 21 and 42 days for serology. All sentinel mice were seropositive for MHV by 42 days; however, sentinel mice exposed to soiled bedding were seronegative for Sendai virus at 21 and 42 days. These results suggest that sentinels housed on soiled bedding may not detect all infectious murine viruses. This study also showed that the microisolator caging system provided an effective barrier against MHV infection at the cage level and suggests that the microisolators should protect mice against other infectious agents.

Fatal fatty liver-kidney syndrome in obese monkeys.

A fatal syndrome associated with brief periods of anorexia or acute weight loss was noted in monkeys. Affected monkeys died unexpectedly or after a very short illness. Consistent gross findings at necropsy were enlarged, pale yellow livers, pale tan to yellow kidneys, abundant deposits of body fat and empty gastrointestinal tracts. Fatty change of the liver and kidney was the predominant and characteristic lesion found microscopically. Most of the monkeys were female Macaca fascicularis greater than 8 years of age. However, monkeys of other species and ages, and one male also died of this syndrome. Affected monkeys generally had losses of 8-33% of body weight (last measured weight--weight at death). In some animals, this syndrome was associated with a location change forcing new social interactions. A common clinical pathologic finding was azotemia. These findings suggest that obese monkeys may be prone to a fatal syndrome characterized by fatty change of the liver and kidney, and weight loss.

Simian varicella infection in the African green monkey (Cercopithecus aethiops).

A severe and highly fatal disease occurred in African green monkeys (Cercopithecus aethiops). The disease was marked by an extensive maculo-vesicular rash. In fatal cases, multifocal necrosis and hemorrhage were found characteristically in many organs and tissues. New cases of the disease occurred over a 39-day period. Nine of 49 exposed African green monkeys were affected and five of the nine died. Four cynomolgus (Macaca fascicularis) and 31 stumptailed monkeys (Macaca arctoides) which were exposed were not affected. Delta Herposvirus was isolated from affected African green monkeys. Stumptailed monkeys housed in association with the African green monkeys, as well as those housed elsewhere, had significant serum concentrations of neutralizing antibodies to this agent.

Electrocardiographic effects of right atrial pacing and nitroglycerin in atherosclerotic rhesus monkeys.

Right atrial pacing at rapid heart rates induced ischemic S-T segment changes in 19 atherosclerotic, male rhesus monkeys. Prior administration of nitroglycerin (100 mug/kg, i.v.) prevented the S-T segment alteration at a given pacing rate in 5 animals, attenuated it in 12 others, and had no effect in the remaining 2. The results of these studies are similar to earlier ones in atherosclerotic rabbits.

Evaluation of chromic oxide, glycerol triether, and beta-sitosterol as fecal flow markers in two species of nonhuman primates.

Recovery of beta-sitosterol, glycerol triether (1-hexadecyl-2,3-didodecyl glycerol triether), and chromic oxide was studied in African green monkeys and stumptail macaques consuming diets containing 0.75 mg/Cal cholesterol and 38% of calories as safflower oil or butter. Following oral administration of these compounds, feces were collected daily for 9 days. For all animals, excretion of beta-sitosterol and glycerol triether paralleled one another almost exactly. Except for two animals, this was also true for chromic acid. Essentially 100% of the administered beta-sitosterol and 90-95% of the glycerol triether were recovered; excretion of these markers virtually was complete by day 3. Ninety-two percent of the beta-sitosterol was isolated in the nonsaponifiable lipid extract of the feces with less than 6% in the remaining aqueous phase. A maximum of 3.1% of the beta-sitosterol and 1.8% of the glycerol triether were found in the blood. For stumptail macaques, the major excretory form of beta-sitosterol was the 5 beta-derivative. African green monkeys were more variable; one animal excreted the bulk of the beta-sitosterol unchanged while others excreted greater than 80% as the ring-saturated 5 beta-derivative. Animals consuming the safflower oil containing diet consistently excreted a greater percentage of the beta-sitosterol unchanged, compared with those animals eating the butter containing diet. There was no evidence for steroid ring degradation in any of the animals used in this study.