The War on Group B Strep

Group B Streptococcus (GBS) are bacteria that live inside (or colonise) the gastrointestinal tract, bladder and / or throat of many people, including pregnant and labouring women.

Estimates of the prevalence of colonisation range from 5% to 80% of the population (which shows, if nothing else, the difficulty with have with deducing some of these numbers).

GBS is generally benign in adults, only posing a danger to people with compromised immune systems. It is also benign in most of the babies who pick up these bacteria during their birth, but can occasionally cause serious harm to others.

Because of this, pregnant women may be offered screening and intervention – yet another pond of uncertainty to have to swim in, which is beset with complex numbers, difficult decisions and tiny chances of very serious conditions.

This is the introduction to an article that was first written in 2003 and, while some of the issues remain the same, some of the statistics have now changed. For instance, neonatal care has improved and the chance of a baby dying from GBS disease is lower than when this article was written. I know that older articles are still of interest to people and some of what it in here is still relevant, but I have now edited this article to remove the information that is no longer accurate. The latest data are included and discussed in my book on this topic and you may also like to search this site for other GBS-related resources on my website.

Group B Strep Explained

Group B Strep Explained; the updated second edition of a popular book which helps parents, professionals and others to understand the issues and the evidence relating to the screening and prophylactic measures offered in the hope of preventing early-onset group B strep (EOGBS) disease.


The approaches to screening

For several years, most areas in the UK have taken a “risk-based” approach to GBS screening, where practitioners attempt to identify the babies who are at increased risk of becoming infected with GBS.

Risk factors (which vary between hospitals) include premature labour (before 37 weeks of pregnancy), a woman with a high temperature during labour or a woman whose waters have been broken for 18-24 hours (1).

Where such a risk factor is identified, the woman will be offered intravenous antibiotics in labour. In these situations, swabs may be taken to see if the woman has GBS (or other bacteria), but it takes a while to perform the testing, so the results are usually only available after the birth. As a consequence of this, the woman is making a decision based on the possibility that, IF she has GBS, her baby might be more at risk of becoming infected, rather than knowing (from screening tests) THAT she has GBS.

By contrast, pregnant women in the USA, Australia and some other countries are offered routine screening for GBS at the end of pregnancy (2), and are offered intravenous antibiotics in labour if they are found to have GBS in their vagina or rectum.

Some people have mooted the idea of replacing the UK’s current “risk-based approach” with the approach used in the US, termed “culture-based screening” (3).

With culture-based screening, some of the women who have risk factors but not GBS may escape having unnecessary antibiotics (although some practitioners may recommend them anyway, in case other pathogens are present). However, hospitals will instead offer antibiotics to all of the 10-30% of women whose vaginas and rectums are colonised with GBS (4), even though only a tiny proportion of these babies will be affected with GBS disease (5,6).


GBS disease

GBS disease itself comes in two timeframes; early onset and late onset.

Early onset GBS disease occurs within the first week of life; three quarters of babies who develop GBS disease will do so at this stage. Problems usually become apparent within a few hours of birth and can include generalised infection (sepsis), pneumonia or meningitis.

GBS disease is termed “late onset” when it occurs between one week and a few months of age. Not all cases of late onset will occur because the baby’s mother transmitted GBS during birth; some will occur from other (but usually unknown) sources. The impact of late-onset disease is usually less severe. Babies found to have GBS disease are treated with antibiotics and given whatever other support they need in Special Care Units.

As above, culture based screening would identify the 10 to 30% of pregnant women whose vaginas or rectums are colonised with GBS (4). The screening test involves taking swabs of the inside of a woman’s vagina and rectum – not a particularly pleasant procedure, but not as invasive as some. Yet only 1 or 2 in every thousand of the women who have a positive result if we screen this way will have a baby who ends up with GBS disease (5,6).

It may be that, while policymakers are debating which of the two approaches to use, women might be better served by research which looked at the outcomes where the two were combined. Even this means that many more women would have antibiotics than needed them, but at least we are getting a bit more specific for the women who would prefer to take them if they were at risk.


What else is important?

Perhaps we could also see whether there are other factors that could help us be even more specific about who is at risk. While this might not be deemed cost-effective on a population basis, it may be more helpful for the women who want to avoid unnecessary intervention.

There are, inevitably, a number of reasons why women may not want antibiotics in labour unless they are truly necessary. Apart from the side effects, and the discomfort of having movement hindered by an intravenous cannula in labour, there are more serious ramifications of policies advocating mass antibiotic cover. While penicillin (8) and ampicillin (9) are currently effective for treating GBS disease in babies, since antibiotics have been used to treat large numbers of women whose babies are deemed at risk of GBS disease (whether this is on a risk-based or culture-based policy), the rate of Escherichia coli infections in premature babies has more than doubled. Around 85 percent of the E. coli infections in one study were resistant to the drugs prescribed to treat GBS (10).

There is a huge debate about antibiotic resistant bacteria generally, and these policies involve giving antibiotics to a lot of women, which may have ramifications for the population as a whole. It has also been suggested that giving antibiotics while babies are still in their mother’s uterus might delay the baby’s gut being colonised with normal, “good” bacteria and allow dangerous penicillin-resistant bacteria to become established there instead (11).


Do antibiotics work?

There is also a need to find out whether giving antibiotics actually makes a difference to the outcome.

The assumption that this is the case has long been just that – an assumption.

Cochrane reviewers (12) who looked at the trials comparing women who had been given antibiotics with women who had not been given antibiotics found that, although antibiotics reduced the incidence of GBS infection in babies, there was no significant difference in the numbers of babies who died. They found the few trials that had looked at this area to be of poor quality, and called for further research – something which surely needs to be done before even more women receive unnecessary drugs in labour.

Having said that, there is plenty of research to support the fact that midwifery and medical interventions in labour, such as vaginal examination, can increase the rate of infection (13-17), yet there is no evidence to suggest that hospitals are making attempts to limit these interventions. Added to the suggestion, from an American review of laboratory procedures (18), that these may not always be effective at detecting GBS in cultures, the decision can become fraught for some women.

Women looking for information about GBS on the Internet are likely to come across some of the most emotive websites in existence. Some are named for babies who died from GBS disease or who continue to suffer from the effects. While I have enormous sympathy for these families, this is only one side of the picture. The other, I hope, can be seen by looking at the actual risks and the wider picture, and this is why I explain the issues in such depth in my book. The available data show that there is no simple answer to this issue, and no way of screening for GBS in babies that doesn’t lead to thousands of women having antibiotics they don’t need.


Sledgehammers and nuts

It is appealing to want to reduce the rate of GBS infection; it is the commonest cause of infectious disease in babies, and it can be fatal.

Yet, as with the issue of haemorrhagic disease, we are often using sledgehammers to crack nuts, potentially at the expense of future health.

Antibiotics have been a marvellous and life-saving discovery. When used appropriately, they are truly useful to humanity. We are already suffering some consequences of our over-use of antibiotics, which is surely something we need to temper. GBS is increasingly seen as a public health issue.

However, one’s position on GBS (and many other birth interventions) really depends on two things. It depends on whether you are happy to be gathered together with all of the other Ms. Publics and be told what is best for your health (and that of your children), or whether you want to make the decisions that suit you as an individual.

And, perhaps more importantly, it depends on how you define health, on whether you are happy to accept the potential costs of medical technology, and how comfortable you are with the very unfashionable idea that nothing in life is certain.



        1. Boyer KM, Gotoff SP. Strategies for chemoprophylaxis of GBS early-onset infections. Antibiotic Chemotherapy 1985; 35: 267-80.
        2. Schrag SJ, Zell ER, Lynfield R and others. (2002) A Population-Based Comparison of Strategies to Prevent Early-Onset Group B Streptococcal Disease in Neonates. New England Journal of Medicine, July 25, 2002. 347: 4, 233-239.
        3. Schrag S, Gorwitz R, Fultz-Butts K and others. (2002)  Prevention of Perinatal Group B Streptococcal Disease.  Revised Guidelines from CDC.  August 16, 2002 / 51 (RR11); 1-22.
        4. Regan JA, Klebanoff MA, Nugent RP, Vaginal Infections and Prematurity Study Group. The epidemiology of group B streptococcal colonization in pregnancy. Obstetrics and Gynecology 1991; 77: 604-10.
        5. Gilbert GL, Garland SM. Perinatal group B streptococcal infections. Medical Journal of Australia 1983; 1: 566-571.
        6. Isaacs D, Royle JA. Intrapartum antibiotics and early onset neonatal sepsis caused by group B Streptococcus and by other organisms in Australia. Australasian Study Group for Neonatal Infections. Pediatric Infectious Diseases Journal 1999; 18: 524-528.
        7. Oddie S Embleton ND. Risk factors for early onset neonatal group B streptococcal sepsis: case-control study British Medical Journal 2002; 325: 308.
        8. Garland SM, Fliegner JR. Group B streptococcus (GBS) and neonatal infections: the case for intrapartum chemoprophylaxis. Australian and New Zealand Journal of Obstetrics and Gynaecology 1991; 31: 119-22.
        9. Boyer KM, Gotoff SP. Prevention of early-onset neonatal group B streptococcal disease with selective intrapartum chemoprophylaxis. New England Journal of Medicine 1986; 314: 1665-9.
        10. Stoll BJ, Hansen N, Fanaroff AA. Changes in Pathogens Causing Early-Onset Sepsis in Very-Low-Birth-Weight Infants New England Journal of Medicine  347: 4; 240-47.
        11. Gilbert GL Preventing perinatal group B streptococcal infection: the jury is still out (Editorial)  Medical Journal of Australia2002: 178: 5; 199-200
        12. Smaill F. Intrapartum antibiotics for Group B streptococcal colonisation (Cochrane Review). In: The Cochrane Library, Issue 4, 2003. Chichester, UK: John Wiley & Sons, Ltd
        13. Yancey MK, Duff P, Clark P et al. Peripartum infection associated with vaginal group B streptococcal colonization. Obstetrics and Gynecology 1994; 84: 816-9.
        14. Schuchat A, Zywicki S, Dinsmoor MJ, et al. Risk factors and opportunities for prevention of early-onset neonatal sepsis: a multicenter case-control study. Pediatrics 2000; 105: 21-6.
        15. Gibbs RS, Jones PM, Wilder CJY. Internal fetal monitoring and maternal infection following cesarean section: a prospective study. Obstetrics and Gynecology 1978; 52: 193–7.
        16. Soper DE, Mayhall CG, Froggatt JW. Characterization and control of intraamniotic infection in an urban teaching hospital. American Journal of Obstetrics and Gynecology 1996; 175: 304-10.
        17. Seaward P, Gareth MB, Hannah ME, et al. International multicentre term prelabor rupture of membranes study: evaluation of predictors of clinical chorioamnionitis and postpartum fever in patients with prelabor rupture of membranes at term. American Journal of Obstetrics and Gynecology 1997; 177: 1024-29.
        18. CD Laboratory Practices for prenatal group B streptococcal screening and reporting – Connecticut, Georgia and Minnesota. 1997-1998.  MMWR 1999; 48: 426-8.
A version of this article was first published as Wickham S (2003). The War on Group B Strep. AIMS Journal 15(4): 7-9.