ArticleFrontiers in immunology2017
Neonatal Group B Streptococcal Disease in Otherwise Healthy Infants: Failure of Specific Neonatal Immune Responses.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- High prevalence of penicillin-resistant group B Streptococcus among pregnant women in Northwest Ethiopia.Scientific reports · 2025Article
- Antimicrobial Resistance Profile of Group BMicroorganisms · 2024Article
- Neonatal Late-Onset Meningitis Caused by Serotype III CC17 Group BInfection and drug resistance · 2023Article
- Single-Cell Mapping of Progressive Fetal-to-Adult Transition in Human Naive T Cells.Cell reports · 2021Article
- Breast Milk: A Meal Worth Having.Frontiers in nutrition · 2021Review
- Stratified Management for Bacterial Infections in Late Preterm and Term Neonates: Current Strategies and Future Opportunities Toward Precision Medicine.Frontiers in pediatrics · 2021Review
- Group B streptococcal disease in the mother and newborn-A review.European journal of obstetrics, gynecology, and reproductive biology · 2020Article
- Susceptibility to infection in early life: a growing role for human genetics.Human genetics · 2020Review
- Article
- Group B streptococcal colonization in mothers and infants in western China: prevalences and risk factors.BMC infectious diseases · 2018Article
- Codevelopment of Microbiota and Innate Immunity and the Risk for Group B Streptococcal Disease.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Only a small proportion of newborn infants exposed to a pathogenic microorganism develop overt infection. Susceptibility to infection in preterm infants and infants with known comorbidities has a likely multifactorial origin and can be often attributed to the concurrence of iatrogenic factors, environmental determinants, underlying pathogenic processes, and probably genetic predisposition. Conversely, infection occurring in otherwise healthy full-term newborn infants is unexplained in most cases. Microbial virulence factors and the unique characteristics of the neonatal immune system only partially account for the interindividual variability in the neonatal immune responses to pathogens. We here suggest that neonatal infection occurring in otherwise healthy infants is caused by a failure of the specific protective immunity to the microorganism. To explain infection in term and preterm infants, we propose an extension of the previously proposed model of the genetic architecture of infectious diseases in humans. We then focus on group B streptococcus (GBS) disease, the best characterized neonatal infection, and outline the potential molecular mechanisms underlying the selective failure of the immune responses against GBS. In light of the recent discoveries of pathogen-specific primary immunodeficiencies and of the role of anticytokine autoantibodies in increasing susceptibility to specific infections, we hypothesize that GBS disease occurring in otherwise healthy infants could reflect an immunodeficiency caused either by rare genetic defects in the infant or by transmitted maternal neutralizing antibodies. These hypotheses are consistent with available epidemiological data, with clinical and epidemiological observations, and with the state of the art of neonatal physiology and disease. Studies should now be designed to comprehensively search for genetic or immunological factors involved in susceptibility to severe neonatal infections.
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