Intracellular Organisms as Placental Invaders

Abstract

In this article we present a novel model for how the human placenta might get infected via the hematogenous route. We present a list of diverse placental pathogens, like Listeria monocytogenes or Cytomegalovirus, which are familiar to most obstetricians, but others, like Salmonella typhi, have only been reported in case studies or small case series. Remarkably, all of these organisms on this list are either obligate or facultative intracellular organisms. These pathogens are able to enter and survive inside host immune cells for at least a portion of their life cycle. We suggest that many blood-borne pathogens might arrive at the placenta via transportation inside of maternal leukocytes that enter the decidua in early pregnancy. We discuss mechanisms by which extravillous trophoblasts could get infected in the decidua and spread infection to other layers in the placenta. We hope to raise awareness among OB/GYN clinicians that organisms not typically associated with the TORCH list might cause placental infections and pregnancy complications.

Porphyromonas gingivalisand adverse pregnancy outcome

“…Second, EVTs are susceptible to invasion by intracellular bacteria [72], unlike villous trophoblasts, which are highly resistant to microbial invasion [73]. During the first trimester of pregnancy when EVTs form anchoring villi to attach the placenta to the decidua and the uterine wall, this susceptibility affords the opportunity for vertical transmission of pathogens to the fetus [72].…”

Brucella abortus Infection of Placental Trophoblasts Triggers Endoplasmic Reticulum Stress-Mediated Cell Death and Fetal Loss via Type IV Secretion System-Dependent Activation of CHOP

“…The placenta is an important site of infections that can result in spontaneous abortion, perinatal mortality of the infant, or vertical transmission to the developing fetus (1). Colonization of the placenta is central to the pathogenesis of viral diseases caused by Zika virus and cytomegalovirus, protozoan infection caused by Toxoplasma gondii, and bacterial infections such as Q fever, listeriosis, and brucellosis (1, 2). A shared feature of several of these pathogens is their ability to replicate within host cells, specifically within fetally derived trophoblasts, which depending on the host species are termed extravillous trophoblasts in humans, trophoblast giant cells in mice, or intercotyledonary trophoblasts in ruminants (3).…”

The Neurobiology of Zika Virus: New Models, New Challenges

“…However, it is well known that the detection of biomarkers remains a challenge even in the presence of clear lesions ( Batalle et al, 2018 ), particularly for CZS that might be confounded with other TORCH (the acronym for T. gondii, rubella virus, cytomegalovirus, herpes simplex virus, and many others) ( Vigliani and Bakardjiev, 2014 ). This group of congenital infections largely overlaps CZS.…”