Myriam Bélanger

Genome Sequence ofPorphyromonas gingivalisStrain A7A1-28

ABSTRACT Porphyromonas gingivalis is an oral opportunistic pathogen. Sequenced P. gingivalis laboratory strains display limited diversity in antigens that modulate host responses. Here, we present the genome sequence of A7A1-28, a strain possessing atypical fimbrillin and capsule types, with a single contig of 2,249,024 bp and a G+C content of 48.58%.

1141681087 An animal model for maternal and fetal infection with Porphyromonas gingivalis

In recent years, a growing body of epidemiological evidence strongly suggests that Porphyromonas gingivalis (Pg) a causative agent of periodontitis, may have an important role in prematurity and low birth weight. This study was designed to evaluate the effect of intravenous inoculation of Pg on intrauterine infection in rats. Pregnant SD rats were intravenously inoculated with sterile PBS or 105, 106, or 109 CFU of Pg strains ATCC33277, W83 or A7436 at gestation day (GD) 14. Animals were sacrificed at GD 18, and dam uterus, vagina and fetal‐placental units (placenta, amniotic fluid, and fetus) were cultured for Pg. Placental sections were also evaluated by histopathology. Of the three strains, Pg A7436 produced the highest rates of infection in the maternal genital tract as well as in fetal tissues (P < 0.0001). For all three strains, 109 CFU produced the highest degree of placental and fetal infection (Pg A7436 at 90%, ATCC33277 at 30%, and W83 at 8.3%). Endometritis with extensive infiltration of degenerated polymorphonuclear cells with vasculitis and hyaline degeneration of maternal vessel were observed in uteroplacental tissues from dams infected with Pg A7436. The inflammatory infiltrate and cellular necrosis was also present at the placental edge, and hemorrhage and necrosis extended into the labyrinth layer. An unexpected finding was the epithelial hyperplasia, cellular necrosis and inflammatory infiltrate present in the chorioallantois. Based on our studies intravenously administered Pg could induce intrauterine infection, chorioamnionitis, and fetal infection in SD rats. Taken together, this data supports the use of the SD rat as an animal model to elucidate the mechanisms by which Pg can induce adverse pregnancy outcome.