Rat Strains Differ in Susceptibility to Maternal and Fetal Infection with Mycoplasma pulmonis
Article first published online: 12 MAR 2004
American Journal of Reproductive Immunology
Volume 51, Issue 3, pages 211–219, March 2004
How to Cite
Reyes, L., Shelton, M., Riggs, M. and Brown, M. B. (2004), Rat Strains Differ in Susceptibility to Maternal and Fetal Infection with Mycoplasma pulmonis. American Journal of Reproductive Immunology, 51: 211–219. doi: 10.1111/j.1600-0897.2004.00144.x
- Issue published online: 12 MAR 2004
- Article first published online: 12 MAR 2004
- Submitted July 14, 2003;revised September 8, 2003; accepted October 10, 2003.
- fetal infection;
- genital mycoplasmosis;
- Mycoplasma pulmonis
Problem: Vaginally infected Sprague–Dawley (SD) rats are more susceptible to adverse pregnancy outcomes than Wistar (WIS) rats. We postulated that SD rats have enhanced hematogenous spread of Mycoplasma pulmonis to fetal tissues.
Method of study: WIS and SD dams were infected intravenously with 107, 106, and 105 colony-forming units of M. pulmonis at gestation day 14. Dams and six randomly selected fetuses were cultured at days 15, 16, 17, and 18 of gestation.
Results: In the high-dose group, 100% of fetuses were colonized regardless of rat strain. Significantly higher numbers of M. pulmonis were isolated from placenta (low dose, P < 0.0001; medium dose, P < 0.024; high dose, P < 0.0001), amniotic fluid (low dose, P < 0.003; medium dose, P < 0.017), and fetuses (low dose, P < 0.0011) of SD rats. Spread of M. pulmonis to the amniotic fluid and fetus occurred 1 day earlier in SD rats.
Conclusions: The difference in susceptibility between the two rat strains cannot be explained by hematogenous spread alone. The relative resistance to adverse pregnancy outcomes in WIS rats may be a function of a more robust innate immune system. These rat strains may represent an animal model to address host resistance factors to intrauterine infection.