Hematogenous infection of Sprague-Dawley rats with Mycoplasma pulmonis: development of a model for maternal and fetal infection.

OBJECTIVES

The specific objective of this study was to conduct a dose response experiment with Mycoplasma pulmonis in Sprague-Dawley rats to develop a reproducible animal model of maternal and fetal infection that would provide a versatile mechanism to address the innate fetal immune response during intrauterine infection.

STUDY DESIGN

Pregnant rats were infected intravenously at gestation day 14 with 0 (control), 10(1), 10(3), 10(5), and 10(7) colony forming units of M. pulmonis and necropsied at gestational day 18. Quantitative culture of maternal and fetal tissues as well as histopathologic examination of the placenta were performed.

RESULTS

We have characterized a rat model of maternal and fetal infection that can be manipulated by alteration of infectious dose. Colonization of Sprague-Dawley rat dam and fetal tissues by M. pulmonis occurred in a dose-dependent manner after intravenous inoculation (P < .001). Placental lesion severity increased with infection dose (P = .0001). The minimum threshold dose required to establish infection of the dam and fetus was at least 10(3) colony forming units, with consistent colonization of maternal and fetal tissues achieved only with 10(7) colony forming units. In some instances, rat fetal tissues could be colonized in the absence of concomitant amniotic fluid colonization. Interestingly, there appeared to be a predilection for colonization of the reproductive tissues.

CONCLUSIONS

In the Sprague-Dawley rat, the infection rate of both the dam and fetus can be controlled by the inoculum dose. Our data support the concept that hematogenous spread of M. pulmonis to the rat fetus can occur without amniotic fluid infection and suggest that the fetus itself can potentially seed the amniotic fluid with microorganisms. Importantly, manipulation of both the route of infection as well as infection dose provide a reproducible way to study both maternal and fetal immune response to infection during pregnancy.