Helicobacter pullorum outbreak in C57BL/6NTac and C3H/HeNTac barrier-maintained mice.

Helicobacter pullorum is a bacterial pathogen in humans. By using microaerobic culture techniques, H. pullorum was isolated from the feces of barrier-maintained mice and identified, on the basis of biochemical, restriction fragment length polymorphism, and 16S rRNA gene sequence analyses. This finding presents an opportunity to study H. pullorum pathogenesis in mice.

Respiratory diseases of rodents and rabbits.

This article is written to provide differential diagnostic help for the practitioner who suspects respiratory disease in rodents or rabbits. The authors are laboratory animal veterinarians who work with rodents and rabbits on a herd health basis but also have considerable experience dealing with individual mice, rats, guinea pigs, hamsters, gerbils, and rabbits. The article presents descriptions of the presentation, pathology, treatment, and control of the primary respiratory pathogens of these species, along with an explanation of conditions that may confuse the diagnostic efforts. The article also mentions reported pathogens of secondary importance and provides extensive references.

Aged murine T-lymphocytes are more resistant to oxidative damage due to the predominance of the cells possessing the memory phenotype.

Glutathione (GSH) is the most important cytosolic antioxidant. Since GSH levels are decreased with age, we hypothesized that T-lymphocytes from old mice would be more sensitive to oxidative stress. T-lymphocytes from young and old mice were exposed to hypoxanthine/xanthine oxidase, and lymphocyte viability, proliferation, GSH content, and calcium signaling were measured. Before exposure, proliferation of T-lymphocytes from young mice was greater than that of old; following exposure, the converse was true. This was in spite of the fact that old mice had lower total GSH levels and greater levels of glutathione disulfide. After oxidative challenge, intracellular calcium responses to anti-CD3 were decreased in naive T-lymphocytes from all mice, while memory lymphocytes were less affected. Higher proportions of memory lymphocytes in old mice resulted in their greater overall preservation of lymphocyte function following oxidative injury, contrary to expectations that lower lymphocyte GSH content with age would increase susceptibility to oxidative stress.

Obesity in male and female rhesus monkeys: fat distribution, glucoregulation, and serum androgen levels.

Obese (n = 8) and nonobese (n = 6) adult rhesus monkeys (Macaca mulatta) were assessed in terms of body size and distribution of body fat, glucose tolerance, and serum lipid, insulin, and androgen levels. The weights of the obese monkeys were more than 2 SD above the mean for their sex, while the nonobese monkeys averaged less than 0.25 SD from the mean. Obese males and females had excess body fat located predominantly in the abdominal region; abdominal circumference was highly correlated with total body fat, as estimated by the isotope dilution method (r = 0.98; P less than 0.001). Obese monkeys of both sexes had fasting hyperinsulinemia, greater insulin response to iv glucose administration, and marginally impaired glucose tolerance. Obese males had delayed maximal insulin response to glucose administration. Fasting serum triglycerides also were elevated in the obese monkeys (0.95 +/- 0.08 vs. 0.47 +/- 0.05 mmol/L; P less than 0.001). Obese males had lower serum dihydrotestosterone levels than nonobese males (3.1 +/- 0.7 vs. 5.6 +/- 0.4 nmol/L; P less than 0.01). Nonobese females had approximately 2-fold higher serum dehydroepiandrosterone sulfate levels than the other groups. We conclude that obese male and female rhesus monkeys have patterns of fat distribution and glucoregulatory abnormalities similar to those of humans with upper body obesity. The contribution of differences in androgen metabolism to the development of obesity and its complications in rhesus monkeys remain to be defined.