Is neonatal group B streptococcal infection preventable
2011
Early onset group B streptococcal (EOGBS) infection causes significant neonatal morbidity and mortality. We determined the incidence of EOGBS at Galway University Hospital (GUH) and examined any âmissed opportunitiesâ for preventing neonatal infection between 2004 and 2009. Our obstetric approach is risk-based. The incidence was 0.45/1,000 live-births; one death and one with neurological sequelae. A single mother received IAP; however we could not determine any potential for reducing cases of EOGBS by improving current IAP usage. Introduction Maternal group B streptococcal colonisation is the critical determinant of neonatal acquisition and infection. 1,2 Two different approaches aimed at prevention of neonatal GBS infection exist, risk-based (Royal College of Obstetricians and Gynaecologists, UK) 3 and culture-based (Centers for Disease Control, USA). 2 Recent reports demonstrate that potentially preventable cases of EOGBS may be missed as risk-based guidelines have not resulted in significant use of intra-partum antibiotic prophylaxis (IAP). 4,5 Vergnano et al reported that if women with risk factors received adequate IAP a potential 23 of 48 cases (48%) of EOGBS may have been prevented. 4 We reviewed data for all infants (2004-2009) with culture confirmed EOGBS, delivered in GUH. Cases were reviewed with regard to âmissed opportunitiesâ for IAP use. The incidence of EOGBS from 1996 to 2002 was determined for comparison prior to the introduction of the RCOG (2003) guidelines. Methods Cases of neonatal EOGBS (birth to 7 days) were identified via the microbiology database at GUH (GBS identified from blood or cerebrospinal fluid) during the study periods. Following case identification, all case notes were reviewed for the infant-mother pair. Results Between 2004 and 2009, nine infants with EOGBS (9 bacteraemia; 1 with meningitis) were diagnosed; 20,113 live-born infants delivered with an incidence of 0.45/1,000 live-births. Most infants (67%) presented within the first 24 hours (range, 1 to 72 hours) with bacteraemia without a focus. Respiratory distress was the most frequent clinical manifestation. One infant developed meningitis and marked developmental delay; one died secondary to sepsis (case fatality rate, 11%). The table outlines potential risk factors for neonatal EOGBS. Regarding âmissed opportunitiesâ for prevention of neonatal infection we noted that a low percentage of women (1 of 9, 11%) received IAP but that only 3 mothers (33%) had one or more risk factors identified, one of which received adequate IAP. Is Neonatal Group B Streptococcal Infection Preventable? 1 Abb: +, positive; -, negative; PROM, premature rupture of membranes; GBS, group B streptococcus; IAP, intra-partum antibiotic prophylaxis; VD, vaginal delivery; EmCS, emergency cesarean section; *Meningitis, secondary hydrocephalus with severe developmental delay Of the remaining two with recognised risk factors (intra-partum pyrexia, preterm delivery and PROM) both delivered precipitously via urgent Caesarean section (without time for appropriate IAP). When compared to the RCOG recommendations we could not determine any potential for reducing our cases of EOGBS by improving current IAP usage. 4 An interesting finding however was that four of six mothers without identifiable risk factors were discovered to have vaginal GBS colonisation in the post-partum period, detected as a result of infant infection. These cases were non-urgent vaginal deliveries. In the preceding years between 1996 and 2002 the incidence of EOGBS in the unit was 0.9/1000 live births (15 infants); 83% presented within the first 24 hours (range 0 to 7 days). All infants survived. Risk factors were identified in 7 pregnancies. Antenatal swabs for GBS were performed in only 2/15 mothers, which were negative. Discussion Despite current preventative strategies, potentially preventable cases of neonatal GBS infection continue to occur. While some UK support groups advocate universal screening to reduce the incidence of GBS, a policy of screening was reviewed in depth by the UK national screening committee and was not supported, based on a relatively low incidence of disease and cost benefit analysis. 6 Another finding in our study was that 66% of mothers without identifiable risk factors were discovered to have vaginal GBS colonisation in the immediate post-partum period, and they delivered vaginally, non-urgently. Culture-based screening may have potentially detected and prevented four cases (44%) of neonatal EOGBS sepsis in our population, one with poor developmental outcome. There is disparity in the implementation or optimal use of both risk-based and universal screening guidelines. While it is clear from our study that the incidence of neonatal EOGBS has declined over the years (50% reduction), cases of EOGBS continue to occur despite an optimal risk-based strategy with potential to reduce the incidence further if a screening strategy were implemented. For 4 women without identifiable risk factors, GBS carriage was confirmed in the post-partum period. Unfortunately given the transient nature of GBS carriage, a culture-based screening approach may not necessarily have detected carriage in these 4 women at 37 weeks gestation. There is now, however, growing evidence that real-time PCR provides rapid, robust and accurate results regarding the GBS status of women during labour, which may help alleviate this difficulty in routine clinical situations. 7 Acknowledging that there is a burden of EOGBS disease despite attempts at optimal prenatal screening, 8 current risk-based approaches certainly do not prevent neonatal infection and should remain an issue of ongoing reappraisal until an effective alternative is developed most likely in the form of maternal vaccination. Acknowledgements We would like to thank the Microbiology Laboratory Staff at Galway University Hospital for their help in data acquisition. Is Neonatal Group B Streptococcal Infection Preventable? 2 Correspondence: E Moylett Department of Paediatrics, Clinical Science Institute, National University of Ireland, Galway Email: edina.moylett@nuigalway.ie References 1. Heath PT, Balfour G, Weisner AM, Efstratiou A, Lamagni TL, Tighe H, O’Connell LA, Cafferkey M, Verlander NQ, Nicoll A, McCartney AC. Group B streptococcal disease in UK and Irish Infants younger than 90 days. Lancet 2004; 363: 292-294. 2. Schrag S, Gorwitz R, Fultz-Butts K, Schuchat A. Prevention of perinatal group B streptococcal disease. Revised guidelines from CDC. MMWR Recomm Rep 2002; 51: 1-22. 3. Prevention of neonatal early onset group B streptococcal disease. RCOG Guideline No 36, 2003:1-10. London: Royal College of Obstetrics and Gynaecology. 4. Vergnano S, Embleton N, Collinson A, Menson E, Russell AB, Heath P. Missed opportunities for preventing group B streptococcus infection. Arch Dis Child Fetal Neonatal Ed 2010: 95: F72-73. 5. Cromwell D, Joffe T, Hughes R, Murphy D, Dhillon C, van der Meulen J. The local adaptation of national recommendations for preventing early-onset neonatal group B streptococcal disease in UK maternity units. J Health Serv Res Policy 2008; 13: 52-7. 6. Brocklehurst P, Kenyon S. Evaluation of antenatal screening for Group B Streptococcal (GBS) carriage against NSC Handbook Criteria. The UK NSC policy on Group B Streptococcus screening in pregnancy; October 2008 [cited from www.screening.nhs.uk/groupbstreptococcus; July 2010]. 7. Alfa MJ, Sepehri S, De Gagne P, Helawa M, Sandhu G, Harding GK. Real-time PCR assay provides reliable assessment of intrapartum carriage of group B Streptococcus. J Clin Microbiol 2010; 48: 3095-9. 8. Goins WP, Talbot TR, Schaffner W, Edwards KM, Craig AS, Schrag SJ, Van Dyke MK, Griffin MR. Adherence to perinatal group B streptococcal prevention guidelines. Obstet Gynecol 2010; 115: 1217-24. Is Neonatal Group B Streptococcal Infection Preventable? 3
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