Streptococcus agalactiae (Lancefield Group B Streptococcus; GBS) is now recognized as a leading cause of early neonatal sepsis.1
Late-onset GBS infection has been related to case reports of transmission via infected breast milk. Early-onset GBS infection (introducing in the first six days of postnatal age) represents 60–70% of all GSB infections.
GBS serotypes Ia, Ib, II, III, and V are the most associated with early onset infection, whereas serotype III predominates in late onset infection.2
GBS in raw breast milk
A study of cases reported that the percentage of GBS associated with infants infected by breast milk was up to 2% when enteral feeding was raw breast milk samples, and up to 1.4% for pasteurized breast milk sample.3 The GBS count in breast milk samples ranged between 103 and >109 colony-forming units (CFU)/mL after late onset infection.3
GBS in pasteurized donor milk
Pasteurization can eliminate a part of bacteria in breast milk but also reduces the immune components (immunoglobulins, including secretory (IgA).4 The reduction of breast milk immune components promotes the growth of pathogenic bacteria.5
Breast milk antibodies
High levels of antibodies in breast milk could protect neonates via neutralizing antibodies specific to GBS.
IgA, IgM, and IgG specific to capsular polysaccharide (CPS) of type III GBS were identified in breast milk samples at different levels.6,7 The correlation between GBS-antibody levels in breast milk and infant colonization/infection by GBS remains to be determined. However, GBS-positive breast milk was associated with heavy infant colonization.8
Human milk studies and outcomes
Dinger et al. 2002 study
Blood and gastric juice cultures of the infant were taken before the initiation of antibiotic therapy and were positive for GBS (Table 1). Freshly expressed breast milk samples contained >106 CFU/mL, but mothers did not show clinical evidence of mastitis (such as clogged breast, redness and pain in breast, fever/fatigue/rash). The transmission of GBS was confirmed to be from her breast milk. The GBS strains of mother and infant were not serotyped. The infant survived after treated with antibiotics for 19 days, while the mother was treated with oral amoxicillin for 10 days.9 Cultures of breast milk after antibiotics were negative, but breastfeeding was not reintroduced for other unknown reasons.
Bertini et al. 2008
Sixteen hours after the infant started to breastfeed, she developed severe sepsis. Infant blood culture was positive for GBS, while spinal fluid was negative (Table 1). The mother was colonized with GBS in her vagina and rectum and received 10 days of amoxicillin. The GBS isolated from the mother was the identical serotype III isolated from the infant. A single culture of breast milk before starting the antibiotic.10 The breast milk culture was negative, while the real-time polymerase chain reaction (RT-PCR) assay with primers identified the GBS serotype III (10). The PCR assay is the most sensible method and allows identifying the GBS subtypes that are more virulent (III). The presence of GBS in breast milk could originate from lymphatic circulation to the colon and the mammary glands.10
Olver et al. 2000
Female triplets (T1, T2, and T3, Table 1) had negative blood cultures before the enteral feeding expressed breast milk in the first week.11 The triplets developed GBS infection after different days and had a second episode of GBS disease. Expressed breast milk was cultured and detected a high population of viable GBS (>105 CFU/mL), but there was no clinical evidence of mastitis. Isolates from each baby and the mother were all shown to be serotype III. Breast milk feeding was not reintroduced, and the triplets were discharged from NICU at 3 months of age. The source of infection in these triplets was the mother’s expressed milk.11
Conclusions
The transmission of GBS through breast milk may be under-reported. The culture and RT-PCR of the left and right expressed breast milk samples should be carried out to identify the cause of neonatal sepsis.
Looking for more on this topic? Read Holder Pasteurization for NICU Donor Milk: Does it Eliminate Pathogenic Bacterial Spores?
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References
1. Le Doare, Kampmann B. Breast milk and Group B streptococcal infection: vector of transmission or vehicle for protection? Vaccine. 2014;32(26):3128-3132.
2. Phares CR, Lynfield R, Farley MM, et al. Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005. Jama 2008;299(17):2056-2065.
3. Filleron A, Lombard F, Jacquot A, et al. Group B streptococci in milk and late neonatal infections: an analysis of cases in the literature. Arch Dise Childhood-Fetal Neonatal Ed 2014;99:F41-F47.
4. Ewaschuk JB, Unger S, O'connor DL, et al. Effect of pasteurization on selected immune components of donated human breast milk. J Perinatol 2011;31(9):593-598.
5. Christen L, Lai CT, Hartmann B, et al. The effect of UV-C pasteurization on bacteriostatic properties and immunological proteins of donor human milk. PLoS One 2019;8(12):e85867.
6. Lagergård T, Thiringer K, Wassen L, et al. Isotype composition of antibodies to streptococcus group B type III polysaccharide and to tetanus toxoid in maternal, cord blood sera and in breast milk. Eur J Pediatr 1992;151(2):98-102.
7. Edwards MS, Munoz FM, Baker CJ. Antibodies to type III group B streptococcal polysaccharide in breast milk. Pediatr Infect Dis J 2004;23(10):961-963.
8. Berardi A, Rossi C, Creti R, et al. Group B streptococcal colonization in 160 mother-baby pairs: a prospective cohort study. J Pediatr 2013;163(4):1099-1104.
9. Dinger J, Müller D, Pargac N, Schwarze R. Breast milk transmission of group B streptococcal infection. Pediatr Infect Dis J 2002;21(6):567-8.
10. Bertini G, Dani C. Group B streptococcal late-onset sepsis with submandibular phlegmon in a premature infant after beginning of breast-feeding. J Maternal-Fetal Neonat Med 2008;21(3):213-215.
11. Olver WJ, Bond DW, Boswell TC, Watkin SL. Neonatal group B streptococcal disease associated with infected breast milk. Arch Dis Childhood-Fetal Neonat Ed 2000;83(1):F48-49.
About the Author
Dr. Veronique Demers-Mathieu is the Senior Research Scientist in the department of Neonatal Immunology and Microbiology at Medolac Laboratories. She did 3-years of postdoctoral training in Neonatal Nutrition under Dr. Dallas at Oregon State University and earned her Ph.D. in Food Microbiology at Laval University. Her expertise focuses on the immune components (including antibodies, immune cells, cytokines, and bioactive proteins) from human milk that protect infants against infectious diseases.