Neonatal meningitis and recurrent bacteremia with group B Streptococcus transmitted by own mother’s milk: A case report and review of previous cases

Abstract

This article reports a case of neonatal meningitis and recurrent bacteremia caused by group B Streptococcus (GBS) transmitted via the mother's milk. A 3-day-old neonate suffered early-onset meningitis due to GBS, from which he recovered after antibiotic treatment for 4 weeks. GBS was not detected in the vaginal or stool cultures of the neonate's mother before delivery. However, 4days after treatment of GBS meningitis, the neonate developed GBS bacteremia. As the mother repeatedly showed signs of mastitis after the delivery, bacterial culture tests were performed on her breast milk, in addition to vaginal and stool culture tests. GBS was exclusively detected in the mother's breast milk. The GBS strains detected in the cerebrospinal fluid of the neonate and the mother's breast milk were both serotype III, and were confirmed to be identical through pulsed-field gel electrophoresis analysis. As horizontal GBS transmission between the mother and neonate was indicated, breastfeeding was ceased and replaced with formula milk. No recurrence of bacterial meningitis or bacteremia due to GBS was observed thereafter. Physicians need to consider culturing breast milk in cases of recurrent neonatal GBS infections, even in mothers without prior detection of GBS in conventional vaginal or stool cultures before delivery.

The Diverse Antimicrobial Activities of Human Milk Oligosaccharides against Group B Streptococcus

“…One example is that breast milk has been demonstrated to be a vehicle of transmission of GBS infection [14] . GBS can cause invasive infections of mammary tissues that lead to mastitis, and consequently, GBS can be transmitted from mother to infant via ingestion of GBS‐contaminated breastmilk [14] …”

“…Although the protective properties of human milk and breastfeeding are well‐supported, [10] there are also risks associated with breast feeding. One example is that breast milk has been demonstrated to be a vehicle of transmission of GBS infection [14] . GBS can cause invasive infections of mammary tissues that lead to mastitis, and consequently, GBS can be transmitted from mother to infant via ingestion of GBS‐contaminated breastmilk [14] …”

“…[14] GBS can cause invasive infections of mammary tissues that lead to mastitis, and consequently, GBS can be transmitted from mother to infant via ingestion of GBScontaminated breastmilk. [14]…”

Recurrent neonatal sepsis and progressive white matter injury in a premature newborn culture-positive for group B Streptococcus

“…Postnatal exogenous acquisition from nursery personnel, household, and community or nosocomial sources has been implicated in late-onset disease [5] . Recurrence may occur in 0.5% to 4.5% of infected infants, [6] frequently preterm babies, due to original or unrelated strains via the following estimated mechanisms: subclinical persistent mucosal colonization related to various factors including insufficient host immunity, inadequate treatment dosage or duration, and microbial hypervirulence and resistance and repetitive exposure to the exogenous sources including GBS-contaminated breast milk which is linked to high recurrence rates and severe presentation [7,8] …”

“…[5] Recurrence may occur in 0.5% to 4.5% of infected infants, [6] frequently preterm babies, due to original or unrelated strains via the following estimated mechanisms: subclinical persistent mucosal colonization related to various factors including insufficient host immunity, inadequate treatment dosage or duration, and microbial hypervirulence and resistance and repetitive exposure to the exogenous sources including GBScontaminated breast milk which is linked to high recurrence rates and severe presentation. [7,8] Cerebral white matter injury (WMI) includes focal necrosis (severe form) causing preoligodendrocyte death that evolves into macroscopic cysts (grade II-IV periventricular leukomalacia [PVL]) or microcysts and diffuse non-necrotic lesions (predominant form) leading to aberrant preoligodendrocyte maturation, both resulting in myelination disturbance. [9] Premature infants may be at the greatest risk for WMI associated with a developmental window of 23 to 32 gestational weeks characterized by immature white matter features of poor vascularization with impaired cerebral flow autoregulation and maturationdependent vulnerability of oligodendrocyte progenitors to various insults.…”