Abstract

Invasive Group-B streptococcal (GBS) disease is a leading cause of infant mortality and morbidity worldwide. GBS colonises the maternal rectum and vagina and transmission of bacteria from a colonized mother to her infant at birth is an important risk factor for GBS disease. GBS disease has also been associated with case reports of transmission via infected breast milk raising questions about mode of acquisition and transmission of this enteric pathogen and the development of neonatal disease. However, most breastfed infants remain unaffected by GBS in breast milk. Mechanisms associated with transmission of GBS in breast milk and potential factors that may protect the infant from transmission remain poorly understood. Understanding factors involved in protection or transmission of GBS infection via breast milk is important both for premature infants who are a high-risk group and for infants in the developing world where breastfeeding is the only sustainable infant feeding option. In this review we discuss the proposed mechanisms for GBS colonization in breast milk on one hand and its immune factors that may protect from transmission of GBS from mother to infant on the other. Innate and adaptive immune factors, including serotype-specific antibody and their significance in the prevention of infant disease are presented. We further report on the role of human oligosaccharides in protection from invasive GBS disease. Advances in our knowledge about breast milk and immunity in GBS disease are needed to fully appreciate what might mitigate transmission from mother to infant and protect neonates from this devastating disease and to contribute to the development of novel prevention strategies, including maternal immunization to prevent infant disease.

Highlights

  • Streptococcus agalactiae (Lancefield Group B streptococcus; Group-B streptococcal (GBS)) was first described as a cause of bovine mastitis by Nocard and Mollereau in 1887 [1]

  • In this review we focus on the peculiarities of GBS that may aid transmission in breast milk and the role of immune parameters such as antibody in breast milk on the other hand that may help protect the breastfed infant from GBS disease

  • secretory IgA (SIgA) production is enhanced by Interleukin-6 (IL-6) whilst the production of secretory components is enhanced by TNF-␣ and transforming growth factor (TGF)-␤ causes class switching towards B cells producing IgA [47], all of which are present in breast milk

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Summary

Introduction

Streptococcus agalactiae (Lancefield Group B streptococcus; GBS) was first described as a cause of bovine mastitis by Nocard and Mollereau in 1887 [1]. By the early 1980s GBS had become the most common cause of neonatal sepsis and meningitis in a number of developed countries [6,7,8]. Via infected breast milk [9] raising questions about mode of acquisition and transmission of this enteric pathogen and the development of neonatal disease. There appears to be a dichotomy between cases of LO disease through infected breast milk and the potential benefits of the components of breast milk which protect the majority of infants from invasive disease. In this review we focus on the peculiarities of GBS that may aid transmission in breast milk and the role of immune parameters such as antibody in breast milk on the other hand that may help protect the breastfed infant from GBS disease

Breast milk as vector of transmission of GBS
Proposed methods of acquisition
Breast milk as vehicle of protection from GBS infection
Innate and adaptive immune properties of breast milk
Antibody in breast milk
The role of SIgA in breast milk
Group B Streptococcal antibody in breast milk
Human oligosaccharides
Findings
Conclusion
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