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Respiratory and genital mycoplasmosis of laboratory rodents: implications for biomedical research
Abstract:
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.
Insights
Murine respiratory mycoplasmosis, caused by Mycoplasma pulmonis, is influenced by genetics, ammonia, and other infections. Heredity is a key factor in this chronic respiratory disease in mice.
Area of Science:
- Veterinary Pathology
- Microbiology
- Immunology
Background:
- Murine respiratory mycoplasmosis is a chronic disease caused by Mycoplasma pulmonis.
- Environmental factors like ammonia and co-infections significantly impact disease severity.
Purpose of the Study:
- To elucidate the multifactorial nature of Mycoplasma pulmonis-induced respiratory disease in mice.
- To investigate the roles of environmental factors, co-infections, and heredity in disease pathogenesis.
- To explore transmission routes and potential as a model for human diseases.
Main Methods:
- Experimental induction of Mycoplasma pulmonis infection in mice.
- Controlled exposure to ammonia and co-infection with Sendai virus.
- Comparative analysis of disease incidence, severity, and progression.
- Investigation of transmission routes, including aerosol and in utero.
Main Results:
- High ammonia levels (25-250 ppm) exacerbate disease incidence, severity, and progression.
- Co-infection with Sendai virus potentiates Mycoplasma pulmonis disease.
- Heredity is identified as a critical determinant of disease susceptibility.
- Evidence suggests both aerosol and in utero transmission of Mycoplasma pulmonis.
Conclusions:
- Mycoplasma pulmonis infection is a complex disease influenced by genetics, environment, and other pathogens.
- The experimental models are valuable for studying chronic pulmonary inflammation and reproductive failure in humans.
- Understanding these factors is crucial for managing the disease in research animals and modeling human conditions.