Influence of infection during pregnancy on fetal development
Open accessAbstract
Infection by bacteria, viruses, and parasites may lead to fetal death, organ injury, or limited sequelae depending on the pathogen. Here, we consider the role of infection during pregnancy in fetal development including placental development and function, which can lead to fetal growth restriction. The classical group of teratogenic pathogens is referred to as ‘TORCH’ (Toxoplasma gondii, others like Treponema pallidum, rubella virus, cytomegalovirus, and herpes simplex virus) but should include a much broader group of pathogens including Parvovirus B19, Varicella zoster virus, and Plasmodium falciparum to name a few. In this review, we describe the influence of different infections in utero on fetal development and the short- and long-term outcomes for the neonate. In some cases, the mechanisms used by these pathogens to disrupt fetal development are well known. Bacterial infection of the developing fetal lungs and brain begins with an inflammatory cascade resulting in cytokine injury and oxidative stress. For some pathogens like P. falciparum, the mechanisms involve oxidative stress and apoptosis to disrupt placental and fetal growth. An in utero infection may also affect the long-term health of the infant; in many cases, a viral infection in utero increases the risk of developing type 1 diabetes in childhood. Understanding the varied mechanisms employed by these pathogens may enable therapies to attenuate changes in fetal development, decrease preterm birth, and improve survival.
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Infection of the fetus can lead to growth restriction, and hence developmental programming.
“Infection of the fetus can lead to growth restriction (3), and hence developmental programming.”
From Placental Origins of Chronic Disease (2016) · cites this paper as [3]
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- Authors
- Adams Waldorf, K. M., & McAdams, R. M.
- Affiliations
- Departments of Obstetrics and Gynecology
- University of Washington (US)
- ORCID
- McAdams, Ryan M
- Venue
- Reproduction
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-11-01
- Volume
- 146
- Issue
- 5
- Pages
- R151-R162
- ISSN
- 1470-1626 (ISSN-L)
- 1741-7899
- PMC
- PMC4060827
- OpenAlex
- W2094006394
- Cited by
- 319
- References
- 102
- Citations by year
- 2026: 12 · 2025: 16 · 2024: 22 · 2023: 34 · 2022: 41 · 2021: 33 · 2020: 35 · 2019: 29 · 2018: 19 · 2017: 25 · 2016: 28 · 2015: 11 · 2014: 13
- FWCI
- 2.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Reproduction (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- March of Dimes Foundation
- National Institute of Allergy and Infectious Diseases (R01AI100989, K08AI067910)
- National Center for Research Resources (UL1RR025014)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P30HD002274, K12HD001264)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Epidemiology › Preterm Birth and Chorioamnionitis
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Neonatal and Maternal Infections
- Keywords
- infection during pregnancy, fetal development, TORCH infections, Toxoplasma gondii, Treponema pallidum, rubella virus, cytomegalovirus, herpes simplex virus, parvovirus B19, varicella-zoster virus, Plasmodium falciparum, placental development, fetal growth restriction, teratogenicity, oxidative stress, apoptosis, type 1 diabetes, preterm birth, neonatal outcomes
- MeSH terms
- Animals, Diabetes Mellitus, Type 1, Female, Fetal Death, Fetal Growth Retardation, Humans, Placentation, Pregnancy, Pregnancy Complications, Infectious, Pregnancy Outcome, Pregnancy Complications, Parasitic, Apoptosis, Oxidative Stress, Fetal Development, Teratogenesis
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