Respiratory and genital mycoplasmosis of laboratory rodents: implications for biomedical research.

Murine respiratory mycoplasmosis (formerly murine chronic respiratory disease) has been conclusively shown to be due to Mycoplasma pulmonis. Based upon experimental studies, it is clear that the disease is an insidious, protracted process involving a variety of interrelated factors. Intracage NH3 (25 to 250 ppm) greatly increases disease incidence, severity and progression. In mice, the presence of other infectious agents, like Sendai virus, also potentiates disease. However, comparisons of animals matched for age, sex, microbial, and environmental factors indicate that heredity is one of the most critical determinants of disease. M. pulmonis is generally thought to be transmitted via aerosol, but recent evidence indicates that in utero transmission is also possible. M. pulmonis can colonize and produce disease in all parts of the female genital tract. While the natural occurrence of both respiratory and genital mycoplasmoses seriously restricts the usefulness of rats and mice for other research purposes, the experimental diseases represent useful models for the study of human disease, particularly mechanisms involved in chronic pulmonary inflammation and reproductive failure.