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Updated: Aug 8, 2026
A Murine Model of Group B Streptococcus Vaginal Colonization
Published on: November 16, 2016
Hypervirulent Streptococcus agalactiae septicemia in twin ex-premature infants transmitted by breast milk: report of
Edward P C Ager1, Eric D Steele2, Lindsey E Nielsen2
1Department of Clinical Investigations, Brooke Army Medical Center, San Antonio, TX, USA. Edward.p.ager.mil@mail.mil.
Insights
Group B Streptococcus (GBS) caused late-onset septicemia in premature twins, with breast milk identified as the infection source. This case highlights a novel transmission route for the hypervirulent ST-452 GBS strain.
Area of Science:
- Neonatal infectious diseases
- Bacterial pathogenesis
- Molecular epidemiology
Background:
- Group B Streptococcus (GBS) is a primary cause of neonatal meningitis and sepsis.
- Early-onset GBS infections are linked to perinatal transmission, but late-onset sources remain less understood.
- This report details a case of late-onset GBS septicemia in premature twins.
Background:
Group B Streptococcus (GBS) infections caused by Streptococcus agalactiae is a leading cause of meningitis and sepsis in neonates, with early-onset GBS symptoms emerging during the first week of life and late-onset occurring thereafter. Perinatal transmission of GBS to the neonate through the birth canal is the main factor associated with early-onset neonate infections, while less is understood about the source of late-onset infections.
Methods:
In this report we describe a case of twin ex-premature infants who presented one month after birth with GBS septicemia. The mother had been appropriately screened at gestational age 35-37 weeks and laboratory methods failed to detect GBS colonization by culture or clinical molecular methods. In attempts to identify and isolate the source of GBS infection, additional surveillance swabs were collected from the mother at the time of neonate admission. Culture and a commercially available, FDA-cleared molecular PCR assay were performed.
Results:
No GBS was detected from swabs collected from the perianal, thigh/groin or axillary areas. However, expressed breast milk and swabs from the breastmilk pump were positive by both methods. Since simultaneous culture and molecular methods which used breastmilk as a source were performed, investigators ascertained the limit of detection for GBS in breastmilk. The limit of detection was determined to be tenfold lower than that of LIM-broth enriched cultures-the FDA-approved source. Subsequent whole genome sequencing (WGS) analysis of isolates recovered from breastmilk and blood cultures from the infants demonstrated all strains were related and characterized as ST-452. Both infants responded very well to treatment and continued to have no related events or concerns at the two-year follow up appointment.
Conclusions:
Strain type 452 (capsular type IV) has recently emerged as a hypervirulent strain and has previously been documented as causing GBS infections in elderly populations. Antibiotic therapy resolved both mother and infant infections. Subsequent testing for the presence of GBS in breastmilk samples also showed an absence of bacteria. This is the first report of infant twins late-onset GBS infections caused by the hypervirulent S. agalactiae ST-452 with breastmilk as the source.
