Group B Streptococcus (GBS) or Streptococcus agalactiae is the cause of neonatal meningitis, pneumonia, and sepsis worldwide. Vaginal or rectal GBS colonization in 10–30% of pregnant women can be transmitted during delivery (ACOG, 2020). Without use of preventive intervention, 1–2% of colonized infants develop early-onset GBS disease (EOGBS) with mortality risk.
The Existing Policy: Screening and Antibiotic Prophylaxis
Screening between 35–37 weeks of pregnancy is routine in the United States and other industrialized countries. Intrapartum antibiotic prophylaxis with intravenous penicillin or ampicillin is administered if an abnormal result is obtained during labor. The 1990s policy decreased early-onset GBS disease by 80% (Verani et al., 2010, CDC).
But IAP is not exempt from late-onset GBS disease, continuing up to 3 months of life. Even mass antibiotic administration and universal screening give rise to new problems—chief among them in the sphere of antibiotic resistance and microbiome disruption.
Increased Antibiotic Resistance
GBS remains penicillin-sensitive globally, with resistance to clindamycin and erythromycin on the rise to become the drug of choice substitute for penicillin. Resistance to clindamycin in a US surveillance study went from 37% in 2011 to 43.2% in 2016 (Goins et al., 2019, JAMA Internal Medicine). The same trends are observed globally:
Resistance to clindamycin has been hovering around 40% in Korea over the past decades (Kim et al., 2025, JKMS). It was also resistant in Vietnam: 58% for clindamycin and 76% for erythromycin, and they were also commonly multidrug resistant (Vu et al., 2021, Scientific Reports). These resistance patterns restrict the available safe choices for penicillin-allergic patients and need to be rechecked on a regular basis to revisit treatment guidelines when necessary.
Influence on Neonatal Microbiome
Intrapartum antibiotic collateral damage to infant gut microbiota is an emerging issue. A number of studies have demonstrated that IAP-exposed infants have reduced colonization with normal microorganisms like Bifidobacterium and enhanced colonization with opportunistic pathogens. This type of dysbiosis can have downstream consequences, potentially promoting allergy, obesity, or autoimmune disease in the long term (Korpela et al., 2020, Nature Communications). Thus, while IAP is a very good drug for neonatal sepsis, the total biological activities of the drug have catastrophic long-term consequences on health.
Future Directions: Beyond Antibiotics
With attempts to bypass such limitations, researchers are investigating alternate ways:
Maternal GBS Vaccines – There are some candidates in clinical evaluation to induce maternal antibodies that cross the placenta and protect neonates from GBS. The vaccine would make universal antibiotic treatment unnecessary, avoid risks of resistance, and confer immunity for early- and late-onset disease (Heath, 2016, Vaccine).
Rapid Intrapartum Testing – Current culture screening is weeks before delivery, with risk of false-negative unstable colonization status. Rapid PCR intrapartum testing would provide real-time carrier detection, preventing negative women from being exposed to unnecessary antibiotics during labor (Schrag et al., 2021, Clin Infect Dis).
Microbiome-Harmonizing Interventions – There are a few experimental trials looking into probiotics or bacteriophage treatment as a way to decrease GBS colonization without antibiotics, although this is in the early stages of research.
GBS remains an important preventable cause of neonatal infection. Screening universally and intrapartum antibiotic prophylaxis were lifesavers, but at the cost of future antibiotic resistance and unintended microbiome effects necessitating more sustainable approaches. Vaccines and early diagnosis are the solution to the prevention of GBS. They offer effective prevention of the neonate in harmony with antibiotic stewardship.
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