Listeria monocytogenes strains encoding premature stop codons in inlA invade mice and guinea pig fetuses in orally dosed dams

Listeria monocytogenes is an important food-borne bacterial pathogen and listeriosis can result in abortions in pregnant women. The bacterium can colonize food-processing environments, where specific molecular subtypes can persist for years. The purpose of this study was to determine the virulence potential of a group of food-processing persistent L. monocytogenes strains encoding a premature stop codon in inlA (encoding internalin A) by using two orally dosed models, pregnant mice and pregnant guinea pigs. A food-processing persistent strain of L. monocytogenes invaded placentas (n=58; 10% positive) and fetuses (3% positive) of pregnant mice (n=9 animals per strain), similar to a genetically manipulated murinized strain, EGD-e InlA(m)* (n=61; 3 and 2%, respectively). In pregnant guinea pigs (n=9 animals per bacterial strain), a maternofetal strain (from a human fetal clinical fatal case) was isolated from 34% of placenta samples (n=50), whereas both food-processing persistent strains were found in 5 % of placenta samples (n=36 or 37). One of the food-processing persistent strains, N53-1, was found in up to 8% of guinea pig fetal liver and brain samples, whereas the maternofetal control was found in 6% of fetal tissue samples. As the food-processing persistent strains carry a premature stop codon in inlA but are invasive in orally dosed pregnant mice and guinea pigs, we hypothesize that listerial crossing of the placental barrier can occur by a mechanism that is independent of an interaction between E-cadherin and InlA.