Infectious causes of embryonic and fetal mortality

Givens, M. Daniel; Marley, M.S.D.

doi:10.1016/j.theriogenology.2008.04.018

Cited by 160 publications

(62 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly however, since immunity against most infections is preserved during pregnancy, these do not appear to be drastic defects in global host defense, and are instead more isolated holes that become exploited by pathogens with an established predisposition for infection during pregnancy. Furthermore, given the striking consistency in pathogens that cause prenatal infection in humans and other mammalian species (Givens and Marley 2008, Robbins and Bakardjiev 2012), these host defense defects associated with the reproductive process are apparently widely conserved.…”

Section: Infection Induced Shifts In Treg Suppression and Pregnancy Cmentioning

confidence: 99%

Regulatory T cells and the immune pathogenesis of prenatal infection

Rowe¹,

Ertelt²,

Luo³

et al. 2013

Reproduction

View full text Add to dashboard Cite

Pregnancy in placental mammals offers exceptional comprehensive benefits of in utero protection, nutrition, and elimination of metabolic waste for the developing fetus. However, these advantages also require durable strategies to mitigate maternal rejection of fetal tissue expressing foreign paternal antigens. Since the initial postulate of expanded maternal immune tolerance by Sir Peter Medawar 60 years ago, an amazingly elaborate assortment of molecular and cellular modifications acting both locally at the maternal placental interface and systemically have been shown to silence potentially detrimental maternal immune responses. In turn, simultaneously maintaining host defense against the infinite array of potential pathogens during pregnancy is equally important. Fortunately, resistance against most infections is preserved seamlessly throughout gestation. On the other hand, recent studies on pathogens with unique predisposition for prenatal infection have uncovered distinctive holes in host defense associated with the reproductive process. Using these infections to probe the response during pregnancy, the immune suppressive regulatory subset of maternal CD4 T cells has been increasingly shown to dictate the inter-workings between prenatal infection susceptibility and pathogenesis of ensuing pregnancy complications. Herein, the recent literature suggesting a necessity for maternal regulatory T cells in pregnancy induced immunological shifts that sustain fetal tolerance is reviewed. Additional discussion is focused on how expansion of maternal regulatory T cell suppression may become exploited by pathogens that cause prenatal infection, and the perilous potential of infection induced immune activation that may mitigate fetal tolerance and inadvertently inject hostility into the protective in utero environment.

show abstract

Section: Infection Induced Shifts In Treg Suppression and Pregnancy Cmentioning

confidence: 99%

Regulatory T cells and the immune pathogenesis of prenatal infection

Rowe¹,

Ertelt²,

Luo³

et al. 2013

Reproduction

View full text Add to dashboard Cite

show abstract

“…The veterinary situation is similar, and displays much overlap in pathogenic genera [4]. Viruses, bacteria and protists, they share no universal commonalities except at least partially intracellular life cycles and hematogenous systemic dissemination.…”

mentioning

confidence: 99%

Pathogens and the placental fortress

Robbins

Bakardjiev

2012

Current Opinion in Microbiology

219

242

View full text Add to dashboard Cite

Summary Placental infections are major causes of maternal and fetal disease. This review introduces a new paradigm for placental infections based on current knowledge of placental defenses and how this barrier can be breached. Transmission of pathogens from mother to fetus can occur at two sites of direct contact between maternal cells and specialized fetal cells (trophoblasts) in the human placenta: (i) maternal immune and endothelial cells juxtaposed to extravillous trophoblasts in the uterine implantation site and (ii) maternal blood surrounding the syncytiotrophoblast. Recent findings suggest that the primary vulnerability is in the implantation site. We explore evidence that the placental syncytiotrophoblast evolved as a defense against pathogens, and that inflammation-mediated spontaneous abortion may benefit mother and pathogen.

show abstract

“…Many of these are the same pathogens that cause embryonic and fetal demise in cattle, sheep, goats, and camelids. 3 All these zoonotic infections are known in the veterinary literature to be caused by intracellular organisms. Likewise every organism listed in Table 1 is able to survive in host cells.…”

Section: Beyond Torchmentioning

confidence: 99%

Intracellular Organisms as Placental Invaders

Vigliani

Bakardjiev

2014

Fet. Matern. Med. Rev.

View full text Add to dashboard Cite

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.

show abstract

Infectious causes of embryonic and fetal mortality

Cited by 160 publications

References 53 publications

Regulatory T cells and the immune pathogenesis of prenatal infection

Regulatory T cells and the immune pathogenesis of prenatal infection

Pathogens and the placental fortress

Intracellular Organisms as Placental Invaders

Contact Info

Product

Resources

About