Introduction

Lancefield Group B Streptococci (GBS) have become a leading cause of perinatal morbidity and mortality within the past 30 years. Maternal colonisation rates for GBS are from 5% to 40%.^1-4 Neonatal GBS disease presents as an early (0-7 days) fulminant and often lethal disease with an incidence of 1.3-3.0 per 1000, or a later less fulminant disease with an incidence of 0.8-1.7 per 1000, often complicated by meningitis.^5,6

Numerous trials have demonstrated a reduction in vertical transmission of GBS with reduction in subsequent mortality and morbidity when prophylactic intrapartum antibiotics are used.^7,8 The aims of this study were to identify GBS colonisation and GBS serotype distribution rates for a typical Irish pregnant population. 

Methods

There are 6000-7000 deliveries per annum in the National Maternity Hospital. This comprises about 12% of the deliveries nationwide each year. Women attending the hospital for private and public care attend weekly after 36 weeks gestation and were invited to enrol in the study. Enrolment was continued until the number of subjects required for the results to be statistically valid by power studies (500) were obtained. Each woman had a perianal and a low-vaginal swab taken by clinic staff at one of their visits between 36 and 40 weeks. The swabs were incubated overnight at 37C in Todd Hewitt broth containing 5% sheep blood and colistin sulphate 10 micrograms per millilitre (mg/ml) and oxalinic acid 5 g/ml. Each swab was then subcultured onto Columbia blood agar plates (aerobic) and neomycin agar plates (anaerobic) as GBS is a facultative organism. Possible GBS was identified using the Oxoid streptococcal grouping kit which identifies group B specific antigen. Where possible, the results were made available before labour. Any isolates identified as GBS were forwarded to the Central Public Health Laboratory, London for serotyping using previously described methods.¹⁵

When possible, GBS positive women received 1 gram of ampicillin intravenously in labour (or erythromycin if allergic to penicillin). Infants of GBS carriers had a full blood count, C-reactive protein and blood culture performed within 8 hours of birth. They were then treated prophylactically with penicillin, regardless of presence or absence of risk factors other than maternal GBS colonisation. Demographic data including maternal age, parity, marital status and attendance at public or private clinics were recorded. Presence of risk factors for transmission of GBS and perinatal complications were also noted. 

Results

Five hundred and four women were enrolled in the study. 129 (25.6%) of the women were colonised by GBS. 74 (14.7%) had both swabs positive for GBS, 26 (5.2%) only cultured GBS on low-vaginal swab, 26 (5.2%) had GBS on perianal swab alone and 3 (0.6%) had a single swab from unspecified site identifying GBS (Table 1). 17 (3.4%) of women were identified as carriers on anaerobic culture media only. The serotype distribution is shown in Table 2.

The predominant GBS serotypes were Ia/c, III/R and II/R. GBS carriage was not significantly related to age, parity, attendance at private clinic, marital status or prolonged rupture of membranes greater than 18 hours. Two non-carriers developed a pyrexia in labour of 38C or greater (Table 3). The total cost per GBS swab including all materials and laboratory personnel costs was 6.48 (Irish punts). Although the intention of this study was to treat all carriers and their infants with prophylactic antibiotics, only 63% of GBS mothers and 82% of their infants were treated. The partial septic screens revealed no markers for sepsis in these infants. The failure to follow the protocol for prophylaxis in the study was primarily due to unavailability of culture results when the women presented in labour.

Table 1. Number of GBS positive women and site of positive culture.

Table 2. Polysaccharide serotype distribution of GBS cultures.

Table 3. Demographic and pregnancy details.

Discussion

This study demonstrates that the GBS colonisation rate for the population in this unit is 25.6%. We believe this to be an accurate representation of the probable carriage rate in the country as this unit manages 12% of the population and the socio-economic profile of our group was representative of the hospital population. For an accurate estimate of GBS colonisation rates it is known that both the perianal and low vaginal areas must be cultured, bearing in mind that GBS is a commensal organism in the gastrointestinal tract.^3,9 Culture of the vaginal site alone would have led to 5% of our population not being identified as carriers. The use of selective culture media is essential for the successful identification of this organism.¹⁰ Todd Hewitt broth with gentamycin or colistin and nalidixic acid are most useful in culturing GBS. Cultures performed at 36 weeks gestation or later, as in this study, have been shown to accurately predict GBS colonisation at parturition.¹ Earlier cultures are not predictive⁶ and treatment antenatally does not eradicate the organism.^2,11 An important limitation within this study was the failure of 37% GBS positive women to receive intrapartum antibiotics. This resulted principally from delays with culture results reaching the chart so that appropriate information about a positive GBS culture was not available to the labour ward staff. This was clearly a major weakness in the study and highlights the fact that labour ward staff must be able to access information routinely and easily for all women in labour if GBS protocols are to be correctly followed. The GBS serotype distribution in this study (Table 2) corresponds with recent documentation in the literature.^3,12 Types Ib and III appear to be common isolates in neonatal GBS sepsis.¹³

The virulent effect of type III seems to be restricted to young infants. Two newly designated serotypes, IV and V, have recently been described^4-15 and neonatal sepsis due to type V has been described.¹⁶ Our data shows the prevalence of types IV and V in similar proportions to those described by Rench et al.¹⁷Both Obstetricians and Paediatricians recognise the need for a strategy which will decrease the occurrence of perinatal morbidity and mortality resulting from GBS colonisation and infection.¹⁸

There are three possible strategies:(i) Screen all pregnant women for GBS and treat carriers in labour with intrapartum antibiotics; (ii) Screen all pregnant women antenatally and treat only those with risk factors in addition to GBS sepsis, such as prematurity or pyrexia in labour; (iii) Do not screen but treat women with risk factors for GBS vertical transmission (e.g. prematurity, prolonged rupture of membranes) with intrapartum antibiotics. ^19,20,21,22The first protocol is very effective in eradicating GBS infection but will result in very large numbers of women receiving antibiotics. The third option is cost effective and simple, but less effective in eradicating GBS infection.²³In our estimate of cost, based on a screening based approach and treating positive women in labour, GBS screening costs 6.48 per negative culture and 32.40 per positive swab. The cost per neonatal GBS illness prevented, based on an incidence of 2 per 1000 new-born is 3,240 which compares favourably with a cost of 2000 per positive test in the National Neonatal Screening Program. This may be considered an acceptable price to pay when the mortality and severe morbidity of the disease is considered. The development of a rapid bacteriological surveillance method may be the key to screening in order to identify carriers in labour, however, attempts to develop rapid antigen tests have been disappointing so far.²⁴

Penicillin G remains the antibiotic of choice for the treatment of neonatal and adult GBS sepsis. Other penicillins are equally active against the organism.²⁵Multivalent vaccine development is currently being researched vigorously and may be the ultimate solution for the prevention of neonatal GBS sepsis.²⁶This study confirms a high colonisation rate with GBS in our patient population which may well reflect carriage in Ireland in pregnancy. Our screening confirms the need for dual site screening (perianal and low-vaginal). It is likely that the use of selective culture media increased the sensitivity of the screening. The serotype distribution reflects that reported by other papers. 

Correspondence:

Dr Winifred Gorman,

Consultant Neonatologist,
National Maternity Hospital,
Holles Street,
Dublin 2.

References

1. American College of Obstetricians and Gynecologists. Group B streptococcal infections in pregnancy. ACOG Bulletin no. 170. Washington DC: American College of Obstetricians and Gynecologists, 1992. 
2. Gardener SE, Yow MD, Leeds LJ, Thompson PK, Mason EO Jr, Clark DJ. Failure of penicillin to eradicate group B streptococcal colonisation in pregnant women. A couple study. Am J Obstet Gynecol 1979;135:1062-65. 
3. Anthony BF, Eisenstadt RT, Carter J, Kim KS, Hobel CJ. Genital and intestinal carriage of group B streptococci during pregnancy. J Infect Dis 1981;143:761-66. 
4. Vaginal Infections and Prematurity Study Group. Regan JA, Klebanhoff MA, Nugent RP. The epidemiology of group B streptococcus in pregnancy. Obstet Gynecol 1991;77:604-10. 
5. Dillon HC Jr, Khare S, Gray BM. Group B streptococcal carriage and disease: a 6-year prospective study. J Pediatr 1987;110:31-36. 
6. Mercer BM, Ramsey RD, Sibai BM. Prenatal screening for group B streptococcus. II. Impact of antepartum screening and prophylaxis on neonatal care. Am J Obstet Gynecol 1986; 155: 979-83. 
7. Allen UD, Navas L, King SM. Effectiveness of intrapartum penicillin prophylaxis in preventing early onset group B streptococcal infection: results of a meta analysis. Can Med Assoc J 1993;149:1659-65. 
8. Pylipow M, Gaddis M, Kinney JS. Selective intrapartum prophylaxis for group B streptococcus colonisation: management and outcome of new-borns. Pediatrics 1994,93:631-35. 
9. Dillon HC, Gray E, Pass MA, Gray BM. Anorectal and vaginal carriage of group B streptococci in pregnancy. J Infect Dis 1982;145:794-99. 
10. Silver HM, Struminsky J. A comparison of the yield of positive antenatal group B streptococcus cultures with direct inoculation in selective growth media versus primary inoculation in transport medium followed by delayed inoculation in selective growth medium. Am J Obstet Gynecol 1996;175:155-57. 
11. Thomsen AC, Morup CL, Hansen KB. Antibiotic elimination of group B streptococcus in urine in prevention of preterm labour. Lancet 1987;i:591-93. 
12. Kvam AI, Efstratiou A, Bevanger L, et al. Distribution of serovarients of group B streptococci from England and Norway. J Med Microbiol 1995;42:246-50. 
13. Baker CJ, Edwards MS. Group B streptococcal infections. In: Remington JS, Klein JO (eds). Infectious disease of the fetus and newborn infant. 3rd edn. Philadelphia: WB Saunders Company, 1990:742-80. 
14. Motlova J, Wagner M, Jelinkova J. A search for new group B streptococcal serotypes. J Med Microbiol 1986;22:101-105. 
15. Wessels MR, Benedi VJ, Jennings HJ, Michon F, DiFabio JL, Kasper DL. Isolation and characterisation of type IV group B streptococcus capsular polysaccharide. Infect Immun 1989;57:1089-94. 
16. Wessels MR, DiFabio JL, Benedi VJ, et al. Structure determination and immunochemical characterisation of the type V group B streptococcus capsular polysaccharide. J Biol Chem 1991; 266:6714-19. 
17. Rench MA, Baker CJ. Neonatal sepsis caused by a new group B streptococcal serotype. J Pediatrics 1993;122:638-640. 
18. Philipson EH, Herson VC. Intrapartum chemoprophylaxis for group B streptococcus infection to prevent neonatal disease: who should be treated? Am J Perinatol 1996;13:487-90. 
19.  Jeffrey HE, McIntosh ED. Antepartum screening and non-selective intrapartum chemoprophylaxis for group B streptococcus. Aust N Z J Obstet Gynecol 1994;34:14-19. 
20. American Academy of Pediatrics. Guidelines for prevention of group B streptococcal infection by chemoprophylaxis. Pediatrics 1992;90:775-778. 
21. Garland SM, Kelly N. Early onset group B streptococcal sepsis: economics of various prevention strategies. Med J Aust 1995;162:413-17. 
22. McDuffie RS, McGregor JA, Gibbs RS. Adverse perinatal outcome and resistant enterobacteriae after antibiotic usage for premature rupture of membranes and group B streptococcus carriage. Obstet Gynecol 1993;82:487-89 
23. Centres for Disease Control and Prevention. Prevention of group B streptococcal disease: a public health perspective. MMWlR 1996;45:1-24. 
24. Baker CJ. Inadequacy of rapid immunoassays for intrapartum detection of group B streptococcal carriers. Obstet Gynecol 1996;88:51-55. 
25. Meyn LA, Hillier SL. Ampicillin susceptibilities of vaginal and placental isolates of group B streptococcus and Escherichia coli obtained between 1992 and 1994. Antimicrob Agents Chemother 1997;41:1173-4. 
26. Kasper DL. Designer vaccines to prevent infections due to group B streptococcus. Proct Assoc Am Physicians 1995;107:369-73.