What Is Streptococcus agalactiae (Group B Strep)?

Streptococcus agalactiae, commonly called Group B Streptococcus or GBS, is a bacterium that harmlessly colonizes the gastrointestinal and genital tracts of a large proportion of healthy adults but can cause serious infections in newborns, pregnant women, and older adults with chronic health conditions. Roughly one in four pregnant women carry GBS at any given time without symptoms, yet the bacterium is the leading infectious cause of sepsis and meningitis in newborns during their first week of life. The gap between “harmless passenger” and “dangerous pathogen” is what makes GBS one of the most important organisms in perinatal medicine and, increasingly, in adult infectious disease.

A Quiet Resident of the Human Body

GBS is a gram-positive bacterium first identified as a cause of udder infections in cattle, and it was only in the 1960s and 1970s that clinicians recognized it as a human pathogen. It belongs to the Lancefield Group B classification, a system that sorts streptococcal species by their surface carbohydrates. The bacterium lives primarily in the lower gastrointestinal tract and often migrates to the vaginal and rectal areas. Colonization is typically transient or intermittent, meaning a person might test positive one month and negative the next.

The vaginal microbiome plays a role in whether GBS takes hold. Research has found that women whose vaginal flora is dominated by Lactobacillus crispatus are significantly less likely to carry GBS. In one study, the presence of L. crispatus cut the odds of GBS colonization roughly in half.¹ Conversely, a study of pregnant women at 35 to 37 weeks found that those who carried GBS tended to have higher levels of bacteria associated with bacterial vaginosis, such as Prevotella and Gardnerella, in their vaginal microbiome.² This suggests the balance of the microbial community matters, though researchers are still working out whether an altered microbiome invites GBS or GBS disrupts the existing community.

Why GBS Matters Most During Pregnancy and Birth

For the pregnant woman herself, GBS colonization usually causes no symptoms and no harm. The danger is to the baby. During labor and delivery, as the infant passes through the birth canal, GBS can be transmitted to the newborn’s skin, mouth, and respiratory tract. If the bacterium enters the bloodstream or lungs, it can cause life-threatening infections including sepsis, pneumonia, and meningitis.

Doctors divide neonatal GBS disease into two categories based on timing. Early-onset disease (EOD) appears within the first six days of life, most often in the first 24 to 48 hours. It typically presents as sepsis or pneumonia. In a study tracking over a hundred cases, about 80% of newborns with early-onset GBS disease showed symptoms, while roughly 20% had positive blood cultures but appeared well for the first 72 hours.³ That second group is unsettling because it means some infected babies initially look perfectly healthy.

Late-onset disease (LOD) occurs from 7 through 89 days of life and more often manifests as meningitis. The routes of transmission are broader and less well understood. Maternal colonization remains the dominant source, but breast milk, hospital environments, and community contacts can all be involved.⁴ Established risk factors for LOD include preterm birth, very young maternal age, HIV exposure, and African ethnicity. Importantly, the antibiotics given during labor to prevent early-onset disease do reduce GBS colonization at birth, but a significant number of these newborns still pick up the bacterium at mucosal sites in the weeks that follow.⁴

Among the most devastating consequences of neonatal GBS is meningitis. Survivors face a meaningful risk of long-term neurological problems, including developmental delays, hearing loss, and seizures.⁵ The exact mechanisms by which GBS crosses the blood-brain barrier and damages developing neural tissue remain an active research question.

How Pregnant Women Are Screened

Screening for GBS colonization in pregnant women is recommended at 35 to 37 weeks of gestation in many countries, including the United States.⁶ A healthcare provider collects a swab from both the vaginal and rectal areas, because GBS often lives in the gut and migrates to the vagina. The standard method is bacterial culture, where the swab is placed in an enrichment broth and then plated on selective media. Results typically take one to two days.

Molecular testing using PCR technology offers a faster alternative and can detect GBS that culture misses. In one head-to-head comparison, PCR detected roughly 10 to 16% more positive cases than culture alone, depending on whether swabs were collected by a healthcare worker or by the woman herself.⁷ Another study found PCR sensitivity of 97% and specificity of about 96% when compared against intrapartum culture.⁸ Self-collection by the woman herself showed a trend toward even better detection than healthcare-worker collection, an encouraging result because self-swabbing is often preferred by patients and easier to implement in resource-limited settings.⁷

Because colonization can be intermittent, a positive result at 36 weeks does not guarantee the bacterium will still be present at delivery, and a negative result does not guarantee the woman has not acquired it since. This is one reason some researchers advocate for rapid intrapartum PCR testing at the time of labor rather than relying solely on prenatal culture.

Intrapartum Antibiotics and How Well They Work

The primary prevention strategy for early-onset GBS disease is intrapartum antibiotic prophylaxis, or IAP. This means giving the mother intravenous antibiotics, usually penicillin or ampicillin, during labor. The goal is to reduce the concentration of GBS in the birth canal before the baby passes through. Two broad approaches exist for deciding which women receive IAP: a “universal screening” strategy, where everyone is tested and those who are positive get antibiotics, and a “risk-based” strategy, where antibiotics are given based on clinical risk factors like fever during labor or preterm delivery, without routine culture screening.

Both approaches reduce early-onset GBS infections compared to doing nothing. A large meta-analysis found that any IAP strategy cut rates of early-onset disease by more than half, but universal screening-based strategies were more effective than risk-based approaches, reducing the risk by about 63% versus 35%.⁹ When screening and risk-based strategies were directly compared in the same analysis, universal strategies performed significantly better. One earlier study estimated that IAP was roughly 84% effective at interrupting mother-to-newborn GBS transmission overall.¹⁰

Still, IAP has limits. A Cochrane review noted that while the evidence points toward benefit, the underlying randomized trials had significant risk of bias, and no fully rigorous trial has been completed that would eliminate all doubt.¹¹ Conducting a placebo-controlled trial today would be ethically difficult, since withholding antibiotics from colonized women has become unacceptable in many settings where IAP is standard care. Penicillin and ampicillin remain effective against GBS, with no resistance to these first-line agents detected across multiple surveillance studies.⁹ For women with penicillin allergies, however, alternatives like clindamycin and erythromycin are sometimes needed, and resistance to those drugs is a growing concern.

The Antibiotic Resistance Picture

GBS has remained remarkably susceptible to penicillin and ampicillin, which is the good news. The worrying trend involves second-line drugs. Erythromycin resistance was found in about 22% of isolates in one U.S. study, and clindamycin resistance tracked alongside it because the resistance genes often overlap.¹² A global systematic review confirmed that resistance to clindamycin, erythromycin, and several other antibiotic classes has risen significantly over time.¹³

This matters practically because the alternative drugs are exactly the ones prescribed to penicillin-allergic women during labor. If you are allergic to penicillin and carry GBS, your doctor should request antibiotic susceptibility testing on your culture to confirm that clindamycin will actually work before prescribing it. Vancomycin is the typical fallback if it will not.

GBS Is Not Just a Newborn Problem

While the perinatal context gets the most attention, GBS has been quietly increasing as a cause of invasive infections in non-pregnant adults, particularly older people and those with chronic conditions. U.S. surveillance data from 2008 to 2016 showed that 95% of adults with invasive GBS disease had at least one underlying health condition, with obesity and diabetes being the most common.¹⁴ Roughly 27% of those admitted required intensive care, and about 6% died.¹⁴

The infections in adults look different from those in newborns. Skin and soft tissue infections account for about a third of cases. Bloodstream infection without a clear source is another common presentation. Bone and joint infections, pneumonia, and urinary tract infections round out the list.¹⁵ European surveillance data tell a similar story: diabetes, obesity, cancer, kidney disease, and age over 65 were the most frequent risk factors among adults with invasive GBS in Brussels.¹⁶ Meningitis and endocarditis are rarer in adults than in newborns but carry higher morbidity when they do occur.¹⁵

The aging population in high-income countries and rising rates of diabetes and obesity are likely contributing to this upward trend. No routine screening or prophylaxis program exists for non-pregnant adults; treatment is reactive, usually with penicillin-class antibiotics once the infection is identified.

The Serotype Landscape

GBS is not a single uniform entity. Different strains produce different polysaccharide capsules, and these capsules define the bacterium’s serotype. Ten serotypes are currently recognized, designated Ia, Ib, and II through IX. The most recent, serotype IX, was proposed after researchers found isolates that did not react with any of the nine previously known antisera.¹⁷ Serotypes Ia, Ib, II, III, and V account for the vast majority of human disease globally. Serotype III is especially associated with late-onset disease and meningitis in newborns.

The capsule is the bacterium’s primary shield against the immune system. It helps GBS evade being engulfed and killed by white blood cells. Research in fish has demonstrated this directly: deleting the gene responsible for capsule formation made GBS dramatically less virulent, while a separate virulence factor, a toxin called hemolysin, contributed less to the bacterium’s ability to survive and spread inside a host.¹⁸ Serotype distribution matters for vaccine development, because a vaccine designed to target one capsule type may offer no protection against another.

Why a Vaccine Does Not Exist Yet

Given the effectiveness of IAP in reducing early-onset disease, it is reasonable to wonder why a maternal vaccine has not replaced the need for antibiotics. A vaccine given during pregnancy could stimulate the mother’s immune system to produce antibodies that cross the placenta and protect the baby from birth onward, potentially covering both early and late-onset disease. Research supports this concept: a study found that when mothers had high levels of capsule-specific antibodies at delivery, the risk of early-onset GBS disease dropped by about 90% for the most common serotypes.¹⁹

Several candidates are in development. One vaccine under clinical development targets a family of surface proteins found across GBS strains, aiming to generate antibodies that cross the placenta and protect infants for the first months of life.²⁰ Phase I and II trials of various candidates are ongoing, but a fundamental challenge has slowed progress: because invasive GBS disease, while devastating, occurs at a relatively low rate, a traditional phase III efficacy trial would need enormous numbers of participants to detect a statistically meaningful difference between vaccinated and unvaccinated groups.²¹ Researchers have proposed that regulators consider alternative pathways to licensure, such as approving a vaccine based on an agreed-upon antibody level that serves as a proxy for protection rather than requiring a massive efficacy trial. That antibody threshold work is ongoing.

The Global Burden Is Uneven

The impact of GBS falls disproportionately on low- and middle-income countries, particularly in sub-Saharan Africa. Estimates for 2020 found that nearly half of all global GBS-related infant deaths occurred in sub-Saharan Africa, driven by high colonization rates, minimal adoption of intrapartum antibiotic prophylaxis, and a case fatality rate reaching about 23%.²² Asia also carries a large absolute burden. In these settings, culture-based screening is often impractical due to limited laboratory infrastructure, making the case for rapid PCR tests or a vaccine even more urgent.

In high-income countries, the economics of prevention have been studied extensively. One U.S. analysis estimated that intrapartum antibiotic prophylaxis of high-risk women identified through screening could prevent roughly 3,300 cases of neonatal disease annually and save approximately $16 million in direct medical costs.²³ A Dutch analysis compared strategies and found that risk-based prophylaxis was relatively cost-effective, while universal screening yielded the largest reduction in cases but at a substantially higher cost per quality-adjusted life year gained.²⁴ These economic trade-offs explain why countries adopt different strategies and why the debate between universal screening and risk-based approaches continues.

GBS in Animals and Aquaculture

Streptococcus agalactiae is not exclusively a human problem. It was first recognized as a pathogen in dairy cattle, where it remains a major cause of mastitis, the inflammation of udder tissue that reduces milk yield and causes significant economic losses for farmers.²⁵ In cattle, GBS is classified as a contagious mastitis pathogen, meaning it spreads cow-to-cow primarily during milking.²⁶

More recently, GBS has emerged as a serious threat in aquaculture, particularly in warm-water fish farming. Nile tilapia, one of the most widely farmed fish species in the world, is highly susceptible to GBS infection, which can cause mass die-offs in crowded pond or cage environments.²⁷ The fish strains of GBS are not identical to the ones that primarily infect humans, but there is genuine concern about zoonotic transmission. Fish handlers who work with infected stock may be at risk of acquiring GBS through skin wounds, and some genomic studies have identified closely related strains circulating in both fish and human populations.²⁷ Research into live-attenuated fish vaccines, using GBS strains with their capsule and hemolysin genes deleted, is one avenue being explored to manage outbreaks in aquaculture without relying on antibiotics.¹⁸

1
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2
PubMed Central. Comparative Characterization of Vaginal and Gut Microbiota in Late-Pregnancy Women with or Without Group B Streptococcus Colonization
3
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4
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8
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10
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11
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12
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13
PubMed Central. Global patterns of antibiotic resistance in group B Streptococcus: a systematic review and meta-analysis
14
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15
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16
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17
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18
PubMed. Streptococcus agalactiae 1a capsule (cpsE) and hemolysin (cylE) deletion mutants display attenuated virulence in Nile tilapia (Oreochromis niloticus)
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The Journal of Infectious Diseases. Maternal Antibody at Delivery Protects Neonates From Early Onset Group B Streptococcal Disease
20
PubMed. Preclinical development of a novel Group B Streptococcus vaccine candidate for maternal immunization based upon the alpha-like protein family of GBS surface proteins (Alp)
21
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22
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23
JAMA. Comparison of Prevention Strategies for Neonatal Group B Streptococcal Infection: A Population-Based Economic Analysis
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PubMed Central. Streptococcus agalactiae Infection in Nile Tilapia (Oreochromis niloticus): A Review