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 10(7), 10(6), and 10(5) 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.
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 10(7), 10(6), and 10(5) 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.