Prevention of perinatal group B streptococcal disease: screening practice in public hospitals in Victoria

In Australia, the prevalence of GBS vaginal carriage has been estimated at 12%-15%,^3-5 and about 1%-2% of infants born to women carrying GBS develop EOGBSD, with about 6% of cases being fatal.^2,5-7The risks of EOGBSD and death are particularly high in preterm infants.² However, antibiotic prophylaxis given to "at risk" women during labour has been shown to significantly reduce the incidence of EOGBSD, and is an important and worthwhile public health measure.^2,7-9

While the value of prophylactic antibiotic intervention in at-risk women is now widely agreed, the best means of targeting these women is perhaps less clear. Comprehensive reviews of the available evidence have been published both in Australia^1,5,10 and overseas.^2,11-13 There are two broad approaches to targeting prophylaxis -- identification of GBS carriers by bacteriological screening or treating by clinical risk factors.

No trials have compared the efficacy of the two approaches. It is therefore perhaps not surprising that, anecdotally, GBS intervention practices differ greatly between public hospitals across the State of Victoria. However, no objective data are available to assess the extent of these differences and the appropriateness of current practice.

We surveyed all public maternity hospitals in Victoria to explore what GBS intervention programs were in place and, in particular, to assess whether practice was in line with currently available evidence.

Data on deliveries in 1996 were supplied by the Victorian Perinatal Data Collection Unit. Statistical analyses were performed using Statview 4.1.¹⁴ Significance was taken as P < 0.05.

Of the 64 hospitals, 62 (97%) reported undertaking procedures that would identify and treat at least some women with a baby at risk of EOGBSD; 48 hospitals (75%) undertook routine antenatal screening for maternal GBS carriage, including 45 which also offered antibiotic prophylaxis on the basis of risk factors. Another 14 hospitals (22%) used the latter approach alone.

Of the 48 hospitals that undertook screening, 20 had a unified hospital screening protocol, with the remainder using individual-doctor protocols. The 20 with a unified protocol comprised nine of the 16 metropolitan hospitals and 11 of the 32 rural hospitals (P = 0.22, Fisher's exact test).

Characteristics of the screening protocols among these 20 hospitals are shown in Box 1. Most protocols (65%) were less than five years old, and 40% were less than two years old. The most common approach to bacteriological screening was to perform a low vaginal swab only (15 of 20 hospitals), or, less commonly, a high vaginal swab only (four hospitals). Only one hospital performed a low vaginal swab combined with an anal swab. All but one hospital screened only once in the pregnancy, either before 30 weeks' gestation (12 hospitals) or between 30 and 34 weeks' gestation (seven). The hospital that screened more than once did not specify gestations. All hospitals that performed bacteriological screening administered intrapartum antibiotics to all women who were GBS-positive.

With regard to the antibiotic used as chemoprophylaxis, 14 of the 20 hospitals with a unified protocol used penicillin, four amoxycillin and two ampicillin. The 14 hospitals using penicillin all had different treatment regimens. Of the hospitals that lacked a unified protocol, only four reported the antibiotic regimen used -- penicillin in three and amoxycillin in one.

Current evidence suggests that the optimum approach to reduce EOGBSD is to offer intrapartum chemoprophylaxis, using penicillin (or erythromycin in women allergic to penicillin) to at-risk mother-infant pairs. These at-risk pairs are identified by bacteriological screening, involving a low vaginal and anal swab performed at 36-38 weeks' gestation and/or by clinical risk factors (Box 3).^2,10

In our survey, most hospitals reported targeting prophylaxis through bacteriological screening. However, the varied approaches to this screening revealed that current practice may not be as effective as possible. In addition, while most hospitals undertook screening, only 20 had a unified protocol, while the remaining 28 reported that protocols differed between doctors. This, together with the variable practice for private patients, suggests that it may be useful to develop more uniform Australian guidelines. Indeed, that only two hospitals (3% of respondents) reported a current protocol that would be expected to maximally prevent EOGBSD (targeting prophylaxis by bacteriological screening and by all risk factors shown in Box 3) suggests that the introduction of uniform practice guidelines would be worthwhile.

The most common differences between the reported screening protocols and an approach expected to minimise EOGBSD were the maternal sites sampled and the timing of screening. GBS carriage within individuals is not constant. Consequently, bacteriological swabs taken at 28 weeks' gestation have only a 50%-70% positive predictive value for carriage at delivery, while about 5%-10% of women who are GBS-positive at delivery are negative at 28 weeks.^3,13,16 Therefore, the closer to delivery that bacteriological screening is undertaken, the greater its utility, both as sensitivity and specificity are increased,^2,10,16 and as the costs of screening are saved for the 5% of pregnant women who deliver preterm (and should receive prophylaxis irrespective of the screening result.^2,11). Thus, bacteriological screening is probably best undertaken at 36-38 weeks' rather than at less than 30 weeks' gestation, the most popular time in our survey.

Nevertheless, despite these theoretical considerations, a significant reduction in the incidence of EOGBSD was recently reported by King George V Hospital, Sydney, where screening is performed at 28 weeks' gestation.¹⁷ This result emphasises that bacteriological screening at 28 weeks' gestation is preferable to no screening at all.

Detection of GBS is increased by 5%-25% if an anal swab is collected in addition to a vaginal swab.^16,18,19 Only one hospital in our survey reported collecting both swabs; most took only a low vaginal swab. It has been suggested that Australian women would find collection of anal swabs unacceptable,²⁰ but no objective evidence has been presented for this. Furthermore, most United States centres surveyed by the Centers for Disease Control took anal swabs,²¹ suggesting that the practice may be more acceptable than is assumed. It would certainly be worthwhile asking Australian women, and reappraising the method of screening most appropriate for our population. Collection of high vaginal swabs, reported by four hospitals in our survey, is inappropriate for GBS screening.

The most cost-effective approach to preventing EOGBSD is to offer antibiotic prophylaxis to women with identified risk factors, without bacteriological screening.¹⁵ This approach has been recommended by some Australian groups (Professor James King, Mater Perinatal Epidemiology Unit, Mater Misericordiae Mothers' Hospital, Brisbane, Qld, personal communication). Most hospitals surveyed (92%) offered prophylaxis on the basis of risk factors, but only four (6%) used all recognised risk factors appropriately (Box 3). As the relative risk of EOGBSD is significantly greater in preterm neonates than in babies born at term,⁷ any EOGBSD prevention program should ideally include intrapartum prophylaxis for any woman labouring before 37 weeks' gestation, irrespective of whether she was screened earlier in pregnancy or of the result of that screening.^2,11 It was disappointing that only a minority of the hospitals surveyed had such a policy, particularly as infection per se is a major recognised cause of preterm labour. That no rural hospital had such a policy may reflect that these hospitals transfer such women for level 3 neonatal care, and that preparation for transfer focuses more on tocolytic therapy and corticosteroid prophylaxis. If so, then an educational campaign to encourage early antibiotic treatment instituted at the referring hospital might be worthwhile.

We were also surprised that only a few hospitals offered antibiotic prophylaxis to women who had had a previous baby with EOGBSD. Neonatal EOGBSD is a devastating infection, and, in our experience, parents who have had an infected child usually seek interventions to prevent infection in a future delivery. That most clinicians and hospitals do not routinely offer prophylaxis in this situation suggests a lack of awareness that this history is an important risk factor. Similarly, the variable responses to the other accepted risk factors suggest that a significant proportion of health providers are either unaware of the epidemiology of EOGBSD or do not perceive EOGBSD as an important clinical problem.

Our survey of Victorian public hospitals showed that, while most are clearly aware of EOGBSD, only a minority currently have a strategy that maximises prevention of EOGBSD and represents most cost-effective practice. However, very minor changes in practice would be expected to improve EOGBSD prevention and significantly reduce costs,¹⁵ for both screening and treatment. Accordingly, our data support the case for a comprehensive, statewide, or possibly national, education program, and for the development and introduction of uniform consensus practice guidelines.

Disclosure: We are not aware of any conflict of interest arising from performing or reporting this work.

1. Vigneswaran R, O'Loughlin JA, McDonald HM. Group B streptococcus and pregnancy. Aust N Z J Obstet Gynaecol 1995; 35: 117-119.
2. Prevention of perinatal group B streptococcal disease: a public health perspective. Centers for Disease Control and Prevention. MMWR Morb Mortal Wkly Rep 1996; 45 (RR-7): 1-24.
3. McDonald H, Vigneswaran R, O'Loughlin JA. Group B streptococcal colonization and preterm labour. Aust N Z J Obstet Gynaecol 1989; 29: 291-293.
4. Australasian Study Group for Neonatal Infections. Early-onset group B streptococcal infections in Aboriginal and non-Aboriginal infants. Med J Aust 1995; 163: 302-306.
5. Jefferey HE, McIntosh ED. Antepartum screening and non-selective intrapartum chemoprophylaxis for group B streptococcus. Aust N Z J Obstet Gynaecol 1994; 34: 14-19.
6. Garland SM, Fleigner JR. Group B streptococcus (GBS) and neonatal infections: the case for intrapartum chemoprophylaxis. Aust N Z J Obstet Gynaecol 1991; 31: 119-122.
7. Zangwill KM, Schuchat A, Wenger JD. Group G streptococcal disease in the United States, 1990: report from a multistate active surveillance system. Morb Mortal Wkly Rep CDC Surveill Summ 1992; 41: 25-32.
8. Smaill F. Intrapartum antibiotics for Group B streptococcal colonisation (Cochrane review). The Cochrane Library, 1999: 3. Oxford: Update Software.
9. Schrag SJ, Zywicki S, Farley MM, et al. Group B streptococcal disease in the era of intrapartum antibiotic prophylaxis. N Engl J Med 2000; 342: 15-20.
10. Gilbert GL, Isaacs D, Burgess MA, et al. Prevention of neonatal group B streptococcal sepsis: is routine antenatal screening appropriate. Aust N Z J Obstet Gynaecol 1995; 35: 120-126.
11. Schuchat A. Group B streptococcus. Lancet 1999; 353: 51-56.
12. Rouse DJ, Goldenberg RL, Cliver SP, et al. Strategies for the prevention of early-onset neonatal group B streptococcal sepsis: a decision analysis. Obstet Gynecol 1994; 83: 483-494.
13. Regan JA, Klebanoff MA, Nugent RP, et al, VIP Study Group. Colonization with group B streptococci in pregnancy and adverse outcome. Am J Obstet Gynecol 1996; 174: 1354-1360.
14. Statview 4.1. Berkeley, CA: Abacus, 1994.
15. Garland SM, Kelly N. Early-onset group B streptococcal sepsis: economics of various prevention strategies. Med J Aust 1995; 162: 413-417.
16. Boyer KM, Gadzala CA, Kelly PD, et al. Selective intrapartum chemoprophylaxis of neonatal group B streptococcal early-onset disease. II. Predictive value of prenatal cultures. J Infect Dis 1983; 148: 802-809.
17. Jefferey HE, Lahra MM. Eight-year outcome of universal screening and intrapartum antibiotics for maternal group B streptococcal carriers. Pediatrics 1998; 101: E2.
18. Badri MS, Zawaneh S, Cruz AC, et al. Rectal colonisation with group B streptococcus: relation to vaginal colonisation of pregnant women. J Infect Dis 1977; 135: 308-312.
19. Dillon HC, Gray E, Pass MA, Gray BM. Anorectal and vaginal carriage of group B streptococci during pregnancy. J Infect Dis 1982; 145: 794-799.
20. Prevention of neonatal group B streptococcal sepsis: is routine antenatal screening appropriate? [editorial comment]. Aust N Z J Obstet Gynaecol 1995; 35: 120.
21. Adoption of hospital policies for prevention of perinatal group B streptococcal disease -- United States, 1997. MMWR Morb Mortal Wkly Rep 1998; 47: 665-670.

Reprints: Dr E M Wallace, Department of Obstetrics and Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168.
euan.wallaceATmed.monash.edu.au

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