Growth of Listeria monocytogenes in the guinea pig placenta and role of cell-to-cell spread in fetal infection

Abstract

Listeria monocytogenes causes foodborne outbreaks that lead to infection in human and other mammalian fetuses. To elucidate the molecular and cellular mechanisms involved in transplacental transmission, we characterized placental-fetal infection in pregnant guinea pigs inoculated with wild-type (wt) or mutant L. monocytogenes strains. The wt strain increased in number in the placenta by >1000-fold during the first 24 h after inoculation--an increase that was unparalleled in other maternal organs. The ActA- mutant, which is impaired in cell-to-cell spread and attenuated in maternal organs, increased in the placenta by a similar amount, although, in fetal infection, the number of ActA- mutant bacteria was 100-fold lower, compared with that of the wt strain. Furthermore, a mutant impaired in vacuolar escape was rapidly eliminated from maternal organs but persisted in the placenta. We concluded that cell-to-cell spread facilitates maternal-to-fetal transmission. Furthermore, the placenta provides a protective niche for growth of L. monocytogenes.