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Influence of infection during pregnancy on fetal development
Reproduction (Cambridge, England), 2013-11, Vol.146 (5), p.R151-R162
[Peer Reviewed Journal]
2013 Society for Reproduction and Fertility ;ISSN: 1470-1626 ;EISSN: 1741-7899 ;DOI: 10.1530/REP-13-0232 ;PMID: 23884862
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Title:
Influence of infection during pregnancy on fetal development
Author:
Adams Waldorf, Kristina M
;
McAdams, Ryan M
Subjects:
Animals
;
Apoptosis
;
Diabetes Mellitus, Type 1 - etiology
;
Female
;
Fetal Death - etiology
;
Fetal Development
;
Fetal Growth Retardation - etiology
;
Humans
;
Oxidative Stress
;
Placentation
;
Pregnancy
;
Pregnancy Complications, Infectious - microbiology
;
Pregnancy Complications, Infectious - physiopathology
;
Pregnancy Complications, Infectious - virology
;
Pregnancy Complications, Parasitic - parasitology
;
Pregnancy Complications, Parasitic - physiopathology
;
Pregnancy Outcome
;
Reviews
;
Teratogenesis
Is Part Of:
Reproduction (Cambridge, England), 2013-11, Vol.146 (5), p.R151-R162
Description:
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.
Publisher:
England: BioScientifica
Language:
English
Identifier:
ISSN: 1470-1626
EISSN: 1741-7899
DOI: 10.1530/REP-13-0232
PMID: 23884862
Source:
MEDLINE
Alma/SFX Local Collection
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