Present address: Lauren J. Richey, Athens Diagnostic Laboratory, College of Veterinary Medicine, University of Georgia, 501 D.W. Brooks Dr., Vet Med Bldg no. 1079 Rm 229, Athens, GA 30602, USA.
Placental Lesions Caused by Experimental Infection of Sprague–Dawley Rats with Mycoplasma Pulmonis
Article first published online: 11 AUG 2003
American Journal of Reproductive Immunology
Volume 50, Issue 3, pages 254–262, September 2003
How to Cite
Peltier, M. R., Richey, L. J. and Brown, M. B. (2003), Placental Lesions Caused by Experimental Infection of Sprague–Dawley Rats with Mycoplasma Pulmonis. American Journal of Reproductive Immunology, 50: 254–262. doi: 10.1034/j.1600-0897.2003.00075.x
- Issue published online: 11 AUG 2003
- Article first published online: 11 AUG 2003
- Submitted March 5, 2002; revised June 14, 2002; accepted June 14, 2002.
- intrauterine infection;
- Mycoplasma pulmonis;
Problem: Sprague–Dawley (SD) rats infected during pregnancy with Mycoplasma pulmonis display adverse pregnancy outcomes that are similar to those observed in women with chorioamnionitis and may provide a good model system for this disease. The placental lesions caused by this microorganism, however, have not been thoroughly characterized.
Method of study: Rats were infected with 107 colony-forming units (CFU) M. pulmonis or vehicle control on gestation day (gd) 14 and were euthanized on gd 16–18. Tissues were fixed in 10% neutral buffered formalin, embedded in paraffin, sectioned at 4 μm, and stained with hematoxylin and eosin (H & E). The slides were coded and examined by a blinded pathologist using light microscopy.
Results: Infection with M. pulmonis was associated with necrosis of trophoblast giant cells at gd 18. Significantly more neutrophils were observed in the decidual region of the apex of the placenta in M. pulmonis infected animals. The vast majority of neutrophils, however, were observed in the decidua in the lateral regions of the placenta and in the adjacent endometrium.
Conclusions: Infection of SD rats with M. pulmonis resulted in histological placentitis similar to that described in deciduitis of humans and represents a good model system for investigations into the pathophysiology of intrauterine infection. The influx of neutrophils seems to migrate from the endometrium towards the lateral regions of the placenta near Reichert's membrane and the divergence of the parietal yolk sac.