A Vaccine in Pregnancy Against the Bacterium That Still Causes Newborn Sepsis

Two studies — one measuring how much protection a baby needs, one testing whether a vaccine can provide it — bring a group B strep vaccine closer

Group B Streptococcus is a common bacterium that lives harmlessly in about one in five pregnancies but can cause life-threatening infection in a newborn. Antibiotics given during labour prevent much of the early illness, but they do nothing for infections that appear in the weeks after birth, and in many parts of the world they are simply not available. Two studies published within nine months of each other bring a vaccine given during pregnancy meaningfully closer.

Why this bacterium is such a stubborn problem

Group B Streptococcus — often shortened to "group B strep" or GBS — is not an exotic organism. It lives in the bowel and genital tract of a large minority of healthy adults, causes no symptoms, and comes and goes. But if a baby is exposed to it around the time of birth, or picks it up in the weeks afterwards, it can cause sepsis (a whole-body infection), pneumonia, or meningitis (infection of the lining around the brain).

Worldwide, this adds up to an estimated 231,800 cases of infection in the first week of life and 162,200 cases in the weeks that follow, with roughly 91,900 infant deaths each year and lasting difficulties with development in some of the children who survive [1]. Doctors divide the illness into "early-onset" disease, appearing in the first six days, and "late-onset" disease, appearing from day seven to about three months. Although many varieties of the bacterium exist, six of them cause more than 97% of infections in babies [2] — a fact that turns out to be the reason a vaccine is possible at all.

How the current approach came about, and where it stops

For most of the twentieth century there was no prevention at all; group B strep infection was something that either happened or did not. That changed in the 1990s, when hospitals in a number of countries began testing pregnant women for the bacterium late in pregnancy and giving antibiotics through a drip during labour to those who tested positive. In the United States this became universal third-trimester screening [3]; the United Kingdom and others instead give antibiotics to women with particular risk factors. Either way, it works: careful reviews comparing the different strategies confirm that antibiotics in labour reduce early infection [4].

But this approach has two limits that no amount of refinement can fix. The first is timing. The antibiotics protect the baby only while they are circulating in the mother's bloodstream during labour; once the baby is born, the protection stops. That is why late-onset infection — which a baby usually catches afterwards from close contact with a colonised adult — is untouched by the strategy. The second limit is practical. Screening every pregnancy and delivering four hours of intravenous antibiotics before birth requires laboratories, drips, staff and records. A review of policies around the world found that many countries outside the wealthiest regions have no such programme [5], even though careful studies in South Asia and Africa show that the bacterium is just as common there [6]. The babies at highest risk are, as so often, the ones least able to reach the existing solution.

Vaccinating the mother has been the obvious way past both limits since the 1980s. The idea is simple and already familiar: when a pregnant woman is vaccinated, her body makes antibodies, and those antibodies cross the placenta into the baby before birth. This is exactly how tetanus, whooping cough, influenza and — more recently — respiratory syncytial virus are prevented in newborns. Several group B strep vaccines were tried over the decades, and they were safe and did transfer antibodies. None was ever licensed. The obstacle was not the vaccine; it was the mathematics of proving it works. Because the infection, while devastating, is uncommon, a conventional trial would need tens of thousands of pregnancies to show a difference in the number of babies who fall ill — a study so large and expensive that it has never been run.

A different way to prove a vaccine works

The alternative is to prove it indirectly. If researchers can establish how much antibody a newborn needs in order to be at substantially lower risk, then a vaccine trial only needs to show that vaccinated mothers' babies reach that level. Regulators have signalled openness to this approach, but it depends entirely on having a trustworthy number to aim for.

That is what the first of the two studies set out to provide [7]. Researchers working with a United States disease surveillance network compared 643 babies who had developed invasive group B strep infection with 2,801 babies who had not, all of them born to mothers known to carry the bacterium. Ingeniously, they measured antibody levels using the leftover dried blood spots that are already collected from every newborn's heel for routine screening — meaning no baby had to have an extra blood test. The blood spots came from eight regions across California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New York and Oregon, and nearly nine in ten were collected within the first 48 hours of life.

Their central finding was that there is no single magic number. The antibody level associated with an 80% reduction in risk ranged from 0.52 to 2.49 micrograms per millilitre for early infection, but only 0.02 to 0.14 micrograms per millilitre for late infection [7]. In plain terms: protecting a baby against infection in the first days of life takes considerably more antibody than protecting against infection in the following weeks. That makes biological sense — a baby passing through the birth canal of a colonised mother meets an enormous quantity of bacteria all at once, while later exposure, from a kiss or a cuddle, is far smaller. It also carries a hopeful implication. The kind of infection that current antibiotics cannot prevent appears to be the kind that a modest amount of antibody can.

What the vaccine trial found

The second study tested an investigational vaccine called GBS6, designed to cover the six bacterial varieties that cause almost all infant disease [8]. It was run in three stages: the first two in South Africa, and the third in South Africa, the United States and the United Kingdom.

In that third stage, 216 pregnant women were randomly assigned to receive either the vaccine or a dummy injection between 24 and 36 weeks of pregnancy, and 209 babies were born. Neither the women nor the staff assessing them knew which they had received. Side effects were mild. Soreness at the injection site was the only local reaction, affecting 30% of vaccinated women compared with 18% of those given the placebo. Tiredness and headache were reported almost identically in both groups — 42% versus 43%, and 37% versus 38% — which is the pattern you would expect if pregnancy itself, rather than the vaccine, is responsible.

Outcomes for the pregnancies and the babies were similar in both groups. Around nine in ten babies in each group were born at full term. There were no major birth defects and no confirmed group B strep infections in either group. Two babies died of sepsis, one in each group, on day 11 and day 7 of life; investigators judged that neither death was related to the vaccine [8].

The antibody results were the point of the study, and they were substantial. Vaccinated mothers had antibody levels at delivery between 0.5 and 22.5 micrograms per millilitre, compared with 0.01 to 0.05 in the placebo group — a difference of tens to hundreds of times. Their babies were born with levels between 0.28 and 16.1 micrograms per millilitre. Roughly 60% to 80% of the mother's antibody reached the baby, and the antibody was functional, meaning it actively helped immune cells destroy the bacteria in laboratory testing.

Reading the two studies together

Set the trial's results against the threshold study's targets and a picture emerges, with one honest caveat. The antibody levels these babies were born with are comfortably above every threshold identified for late-onset infection — the form of the disease that antibiotics in labour cannot prevent. Against the higher thresholds for early infection the picture is genuinely mixed, and the two studies cannot yet be matched variety by variety from the published figures alone. What makes the comparison worth making at all is that both studies measured antibodies using the same standardised laboratory test [9], so they are speaking the same language.

There are real limitations. The trial deliberately excluded higher-risk pregnancies — women who had previously delivered early, or who had high blood pressure or pre-eclampsia — and those are exactly the pregnancies in which antibody transfer is least reliable and infection risk is highest. Most participants were recruited in South Africa, and few Asian women took part, even though Asia carries a large share of the global burden [1]. The threshold study drew entirely on a United States population where antibiotics in labour are widely used.

What happens next, and what it would mean for families

This vaccine is not available, and nothing about a family's care changes today. A larger trial in pregnancy is under way, along with a separate study in pregnant women with and without HIV — an important group in the regions carrying most of the disease [10]. Researchers are also working out how a group B strep vaccine would fit alongside the whooping cough, influenza and respiratory syncytial virus vaccines already offered in pregnancy [11], which In[Neo]Sight has covered in its article on RSV vaccination during pregnancy. Earlier stages of this same vaccine programme, including work in non-pregnant volunteers, laid the groundwork for the pregnancy studies [12], [13].

If such a vaccine is eventually approved, it is worth knowing what it would and would not do. It would not replace testing and antibiotics in labour, at least not at first — a baby born very soon after the mother is vaccinated, or born prematurely, will have received less antibody. What it would add is protection that continues after birth, which no current measure provides; and in the many places where screening and intravenous antibiotics have never been achievable, it would be the first prevention available at all. For families, the honest summary today is that the science has moved from "this ought to work" to "here is what it would take, and here is a vaccine that appears to deliver it."

References

  1. Gonçalves BP, Procter SR, Paul P, et al. Group B streptococcus infection during pregnancy and infancy: estimates of regional and global burden. The Lancet Global Health. 2022;10(6):e807–e819. doi:10.1016/S2214-109X(22)00093-600093-6) ↩
  2. Madrid L, Seale AC, Kohli-Lynch M, et al. Infant group B streptococcal disease incidence and serotypes worldwide: systematic review and meta-analyses. Clinical Infectious Diseases. 2017;65(suppl_2):S160–S172. doi:10.1093/cid/cix656 ↩
  3. American College of Obstetricians and Gynecologists. Prevention of group B streptococcal early-onset disease in newborns: ACOG Committee Opinion, Number 797. Obstetrics & Gynecology. 2020;135(2):e51–e72. doi:10.1097/AOG.0000000000003668 ↩
  4. Panneflek TJR, Hasperhoven GF, Chimwaza Y, et al. Intrapartum antibiotic prophylaxis to prevent Group B streptococcal infections in newborn infants: a systematic review and meta-analysis comparing various strategies. eClinicalMedicine. 2024;74:102748. doi:10.1016/j.eclinm.2024.102748 ↩
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  7. Rhodes JC, Kahn R, Bolcen S, et al. A US case-control study to estimate infant group B streptococcal disease serological thresholds of risk-reduction. Nature Communications. 2025;16(1):9381. doi:10.1038/s41467-025-64324-y ↩
  8. Madhi SA, Snaggs H, Skogeby Z, et al. Maternal 6-valent group B Streptococcus vaccine in non-pregnant and pregnant females: a randomized phase 1/2 trial. Nature Medicine. 2026;32(8):3048–3059. doi:10.1038/s41591-026-04558-5 ↩
  9. Gaylord MA, Larrier M, Giordano-Schmidt D, et al. Development and validation of a 6-plex Luminex-based assay for measuring human serum antibodies to group B streptococcus capsular polysaccharides. Human Vaccines & Immunotherapeutics. 2024;20(1):2311480. doi:10.1080/21645515.2024.2311480 ↩
  10. Thorn N, Karampatsas K, Le Doare K, Heath PT. Progress towards a Group B streptococcal vaccine – where are we now? Vaccine. 2025;62:127575. doi:10.1016/j.vaccine.2025.127575 ↩
  11. Kampmann B, Madhi SA, Munjal I, et al. Bivalent prefusion F vaccine in pregnancy to prevent RSV illness in infants. New England Journal of Medicine. 2023;388(16):1451–1464. doi:10.1056/NEJMoa2216480 ↩
  12. Absalon J, Segall N, Block SL, et al. Safety and immunogenicity of a novel hexavalent group B streptococcus conjugate vaccine in healthy, non-pregnant adults: a phase 1/2, randomised, placebo-controlled, observer-blinded, dose-escalation trial. The Lancet Infectious Diseases. 2021;21(2):263–274. doi:10.1016/S1473-3099(20)30478-330478-3) ↩
  13. Madhi SA, Anderson AS, Absalon J, et al. Potential for maternally administered vaccine for infant group B Streptococcus. New England Journal of Medicine. 2023;389(3):215–227. doi:10.1056/NEJMoa2116045 ↩