- Email: [email protected]
Prevention of group B streptococcal neonatal disease. A plea for a European consensus
IN SE ARCH OF EUROPE AN OPINION Prevention of group B streptococcal neonatal disease. A plea for a European consensus M. de la Rosa Fraile1, L. Cabero2, A. Andreu3 and G. G. Rao4 1 3
Microbiology Service, Hospital Virgen de las Nieves, Granada 18014, Spain, 2Obstetrics and Gynaecology Department and Microbiology Service, Hospital Vall D'Hebron, Barcelona, Spain, and 4Infection Control, Lewisham Hospital, London, UK
Group B streptococcal (GBS) early onset infection (EOGBS) is the leading cause of life-threatening bacterial neonatal infection during the ®rst week of life in the developed world, with an incidence of 1±3 per 1000 live births in USA when there is no preventive intervention [1]. The fatality rate ranges from 5 to 10% at present, but those who survive may have permanent neurological sequelae such as cognitive dysfunction, deafness or visual impairment [1,2]. In Europe the incidence (per 1000 live births) of EOGBS without preventive measures varies between the 0.2±0.3 of early reports from Denmark [3] and the more recent data of 0.76 in Finland [4], 4.5 in Rennes (France) [5], 5.4 in Vienna (Austria) [6], 1.42 in Sunderland (UK) [7], 1.15 in Luton (UK) [8], 0.4 in Oxford (UK) [9], 0.54 in Norway [10], 0.4±9 in Andalusia (Spain) [11] and 2.06 in Barcelona (Spain) (Andreu et al, personal communication, August 2000). GBS is usually a commensal bacterium that asymptomatically colonizes the vaginal or rectal areas of 10±30% of pregnant women [1]. In these women, GBS can cause preterm labor, chorioamnionitis, postpartum endometritis, postpartum wound infection and sepsis [12,13]. Invasive GBS infections also cause signi®cant morbidity and mortality in non-pregnant adults, mainly in otherwise compromised patients [1,14,15]. The most important predictive circumstance that leads to EOGBS is the exposure of the newborn to the organism in the birth canal. There are also some well-de®ned maternal risk factors that favor the development of infection in an exposed infant [16±18]. These factors include premature birth, maternal chorioamnionitis, prolonged membrane rupture (> 18 h), intrapartum fever, a previous sibling with EOGBS and GBS bacteriuria. Another factor for developing the disease is exposure to a high maternal inoculum of a virulent GBS strain. A further critical issue for a newborn to develop the disease is a low concentration in the mother's serum of antibodies to the capsular polysaccharide of the colonizing GBS strain [19]. Corresponding author and reprint requests: M. de la Rosa Fraile, Servicio de Microbiologia, Hospital Virgen de las Nieves, Granada 18014, Spain Tel: 34 958 241109 Fax: 34 988 241282 E-mail: [email protected]
Conjugate vaccines might be an excellent tool against GBS infections in mothers, infants, and even in nonpregnant adults, but they are still under investigation [20] and are not yet commercially available. Since 1979 [21], it has been known that intrapartum treatment of colonized mothers with ampicillin or penicillin reduces GBS colonization of newborns and that most cases of EOGBS can be prevented by treating colonized pregnant women with intravenous antibiotics during labor [22,23]. In the USA, the Center for Disease Control and Prevention (CDC) issued guidelines for prevention of EOGBS in 1996 [24], which were endorsed by the American College of Obstetricians and Gynecologists and the American Academy of Pediatrics [17,18]. These guidelines recommend the use of either a screening-based or a risk-based approach to identify candidates for intrapartum antibiotic prophylaxis. The riskbased approach provided intrapartum antibiotics to women who had any of the above-mentioned risk factors. The screening-based approach proposes routine prenatal GBS screening between 35 and 37 weeks' gestation, and intrapartum antibiotics are recommended for all women who are either colonized, or who presented in labor before 37 weeks' of gestation, or whose colonization status is unknown and who present risk factors. To optimize the yielding of GBS cultures the CDC recommends using selective broth media and testing vaginal and rectal specimens. The main drawback of the CDC risk-factor approach is that several studies indicate that more than 50% of cases of EOGBS appear in the absence of any known risk factor [25±27]. Since the publication of the CDC guidelines a signi®cant number of US hospitals have adopted prevention policies [2,28± 30] and there are data that suggest that the incidence of EOGBS has now dropped below 0.6/1000 live births [31]. In some US institutions the rate has fallen from 1.16 to 0.14/1000 live births [32] or from 1.7 to 0.3/1000 [33]. and now the CDC has recommended that `GBS prevention activities be integrated into all obstetric care programs' (Available at http:// www.cdc.gov/ncidod/emergplan/11obj13.htm ± retrieved on 21 August 2000). In other developed countries, an important drop in EOGBS has also taken place when a prevention policy has been set up,
ß 2001 Copyright by the European Society of Clinical Microbiology and Infectious Diseases
26 Clinical Microbiology and Infection, Volume 7 Number 1, January 2001
e.g. in Australia the incidence fell from 2 per 1000 live births in 1991±93 to 0.5 in 1995±97 [34]. It has been suggested [2,35] that prevention protocols greatly increase the proportion of women who get antibiotics during labor and delivery, and this could increase the risk of neonatal sepsis caused by resistant Enterobacteriaceae. Though some alarming reports on this issue have been published [36,37], neonatal sepsis caused by Gram-negative bacteria is more often a disease of prematurity, and the increase in Gram-negative neonatal disease seems related to situations in which the use of the CDC risk-based approach leads to a prolonged use of ampicillin. Moreover, in other studies the decline in the incidence of EOGBS after installing a screening-based prevention program has not been accompanied by an increase in Gram-negative sepsis [33,38±40]. However, the severity of resistant Escherichia coli neonatal sepsis suggests caution regarding the widespread use of ampicillin instead of penicillin for EOGBS prophylaxis [41]. In 1998 in Spain the Societies of Obstetrics and Gynaecology and of Neonatology (with the endorsement of the Societies of Infectious Diseases and Clinical Microbiology and of Chemotherapy) issued the Spanish Consensus Guidelines to Prevent EOGBS [42]. These guidelines follow in general the CDC screening-based approach using either Granada Medium [43] or the broth-enrichment technique to detect GBS-carriers at weeks 35±37 and also include recommendations on the management of newborns to GBS-carrier mothers when prophylaxis has not been used or has been incomplete. Since then a substantial number of Spanish hospitals have adopted this policy, and a considerable drop in the incidence of EOGBS has also been observed [11,44]. Thus in Catalonia the incidence dropped from 1.92/1000 live births in 1994 to 0.57/1000 in 1998 (Andreu et al, personal communication, August 2000). In other European countries in which a prevention policy has been set up a similar reduction has been noticed. In Vienna the incidence of EOGBS [6] dropped from 5.4/1000 (1992±94) to 1.1/1000 (1995±97) and in Rennes from 4.5/1000 in 1993 to 1.6/1000 in 1995 [5] after prevention programs were instituted. Now, more than 40 years after the dramatic emergence of GBS as a major cause of threatening infections in the newborn [45], and more than 20 years after the rationale of antibiotic prophylaxis was established it is clear that EOGBS disease is a very important cause of suffering for parents and newborns, and is largely preventable with currently available methods. Though it has been suggested that `when the incidence of early onset streptococcal infection is low. . ..expensive preventive measures may not be justi®ed' [34], the layperson is seriously concerned about GBS, and GBS support associations have been founded in Europe (UK Group B Strep Support, available at http:// www.gbss.org.uk/, retrieved on 22 August 2000; Dutch Foundation GBS, available at http://home.wxs.nl/sgbs/gbs.html,
retrieved on 22 August 2000) and in USA (USA Group B Strep Association, available at http://www.GroupBStrep.org/, retrieved on 22 August 2000). Quoting an American colleague [46], we can af®rm, `First and foremost, we must not ignore the problem. Neonatal Group B streptococcal infection is more prevalent than many other conditions we screen for in pregnancy, and the effect can be just as devastating'. So perhaps the time has arrived for European obstetricians, neonatologists, infectious diseases physicians and clinical microbiologists to catch up with their American colleagues and together look deeper into the issue of prevention of GBS neonatal infection. A common European consensus on prevention policies should now be established. R EFER E NCE S 1. Edwards MS, Baker CJ. Streptococcus agalactiae (Group B streptococcus). In: Mandell GL, Bennett JE, Dolin R eds. Principles and practice of infectious diseases, 5th edn. New York: Churchill Livingstone, 2000; 2156±67. 2. Schuchat A. Neonatal group B streptococcal disease: screening and prevention. N Engl J Med 2000; 343: 209±10. 3. Mayon White RT. The incidence of GBS disease in neonates in different countries. Antibiot Chemother 1985; 35: 17±27. 4. Kalliola S, Vuopio-Varkila J, Takala AK, Eskola J. Neonatal group B streptococcal disease in Finland: a ten-year nationwide study. Pediatr Infect Dis J 1999; 18: 806±10. 5. Poulain P, Betremieux P, Donnio PY, Proudhom JF, Karege G, Giraud JR. Selective intrapartum anti-bioprophylaxys of group B streptococci infection of neonates: a prospective study in 2454 subsequent deliveries. Eur J Obstet Gynecol Reprod Med 1997; 72: 137±40. 6. Hafner E, Sterniste W, Rosen A, et al. Group B streptococci during pregnancy: a comparison of two screening and treatment protocols. Am J Obstet Gynecol 1998; 179: 677±81. 7. Bignardi GE. Surveillance of neonatal group B streptococcal infection in Sunderland. Commun Dis Public Health 1999; 2: 64±5. 8. Beardsall K, Thompson MH, Mulla RJ. Neonatal group B streptococcal infection in South Bedfordshire, 1993±98. Arch Dis Child Fetal Neonatal Ed 2000; 82: F205±7. 9. Moses LM, Heath PT, Wilkinson AR, Jeffery HE, Isaacs D. Early onset group B streptococcal neonatal infection in Oxford, 1985± 96. Arch Dis Child Fetal Neonat Ed 1998; 79: F148±9. 10. Aavitsland P, Hoiby EA, Lystad A. Systemic group B streptococcal disease in neonates and young infants in Norway, 1985±94. Acta Paediatr 1996; 85: 104±5. 11. Baca M, SaÂnchez MJ, Perea-Milla E et al. Perinatal group B streptococcal infections in Andalusia (Spain) (abstract). Pren Neonat Med 2000; 5 (Suppl 2): 70. 12. Krohn MA, Hillier SL, Baker CJ. Maternal peripartum complications associated with vaginal Group B streptococci colonization. J Infect Dis 1999; 179: 1410±5. 13. Bosh J, Pericot A, Amoros M, Ros R. Endometritis puerperal: estudio de 52 casos con diagnostico microbioloÂgico y clõÂnico. Enferm Infecc Microbiol Clin 1995; 13: 203±8. 14. Gimenez M, Sopena N, VinÄado B et al. Infecciones invasivas por Streptococcus agalactiae en un hospital general universitario durante un periodo de 10 anÄos. Enferm Infecc Microbiol Clin 1996; 14: 300±3.
ß 2001 Copyright by the European Society of Clinical Microbiology and Infectious Diseases, CMI, 7, 25±27
de la Rosa Fraile et al Consensus on group B streptococcal disease
15. MunÄoz P, Llancaqueo A, Rodriguez-Creixems M, Pelaez P, Martin L, Bouza E. Group B streptococcus bacteremia in nonpregnant adults. Arch Int Med 1997; 157: 213±6. 16. Ancona RJ, Ferrieri P, Williams PP. Maternal factors that enhance the acquisition of group B streptococci by newborn infants. J Med Microbiol 1980; 13: 273±80. 17. American College of Obstetricians and Gynecologists. Prevention of early-onset group B streptococcal disease in newborns. ACOG Comm Opin 1996; 173: 1±8. 18. American Academy of Pediatrics Committee on Infectious Diseases and Committee on Fetus and Newborn. Revised guidelines for prevention of early-onset group B streptococcal (GBS) infections. Pediatrics 1997; 99: 489±96. 19. Baker CJ, Kasper DL. Correlation of maternal antibody deficiency with susceptibility to neonatal group B streptococcal infection. N Engl J Med 1976; 294: 753±6. 20. Baker CJ, Paoletti LC, Wessels MR et al. Safety and immunogenicity of capsular polysaccharide-tetanus toxoid conjugate vaccines for group B streptococcal types Ia and Ib. J Infect Dis 1999; 179: 142±50. 21. Yow MD, Mason EO, Leeds LJ, Thompson PK, Clark DJ, Gardner SE. Ampicillin prevents intrapartum transmission of group B streptococcus. JAMA 1979; 241: 1245±7. 22. Boyer KM, Gotoff SP. Prevention of early-onset neonatal group B streptococcal disease with selective intrapartum chemoprophylaxis. N Engl J Med 1986; 314: 1665±9. 23. Garland SM, Fliegner JR. Group B streptococcus (GBS) and neonatal infections: the case for intrapartum chemoprophylaxis. Aust NZ J Obstet Gynaecol 1991; 31: 119±22. 24. Centers for Disease Control and Prevention. Prevention of group B streptococcal disease: A public health perspective. Morbid Mortal Wkly Rep 1996; 45 (RR7): 1±24. 25. Andreu A, Barranco M, Bosch J et al. Prevention of perinatal Group B streptococcal disease in Europe. Scand J Infect Dis 1997; 29: 532. 26. Juncosa T, Bosch J, Dopico E et al. InfeccioÂn neonatal por Streptococcus agalactiae. Estudio multiceÂntrico en el aÂrea de Barcelona. EspanÄa Enferm Infecc Microbiol Clin 1998; 16: 312±5. 27. Towers CV, Suriano K, Asrat T. The capture rate of at risk term newborns for early onset group B streptococcal sepsis determined by a risk factor approach. Am J Obstet Gynecol 1999; 181: 1243± 91997. 28. Centers for Disease Control and Prevention. Adoption of hospital policies for prevention of perinatal group B streptococcal disease United States. Morbid Mortal Wkly Rep 1998; 47 (32): 667±70. 29. Centers for Disease Control and Prevention. Adoption of perinatal group B streptococcal disease prevention recommendations by prenatal-care providers ± Connecticut and Minnesota, 1998. Morbid Mortal Wkly Rep 2000; 49: 228±32. 30. Factor SH, Whitney CG, Zywicki SS, Schuchat A. Effects of hospital policies based on 1996 group B streptococcal disease consensus guidelines. The active bacterial core surveillance team. Obstet Gynecol 2000; 95: 377±82.
27
31. 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. 32. Brozanski BS, Jones JG, Krohn MA, Sweet RL. Effect of a screening-based prevention policy on prevalence of early onset group B streptococcal sepsis. Obstet Gynecol 2000; 95: 496±501. 33. Truong W, Yancey MK, Lentz SL. Reduction of early-onset group B streptococcal sepsis with universal screening and intrapartum antimicrobial therapy for preterm and colonized term parturients. Obstet Gynecol 2000; 95 (4 Suppl.1): S8. 34. 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. Pediatr Infect Dis J 1999; 18: 524±8. 35. McDuffie RS Jr, McGregor JA, Gibbs RS. Adverse perinatal outcome and resistant Enterobacteriaceae after antibiotic usage for premature rupture of the membranes and group B streptococcus carriage. Obstet Gynecol 1993; 82: 487±9. 36. Mercer BM, Carr TL, Beazley DD, Crouse DT, Sibai BM. Antibiotic use in pregnancy and drug-resistant infant sepsis. Am J Obstet Gynecol 1999; 181: 816±21. 37. Levine EM, Ghai V, Barton JJ, Strom CM. Intrapartum antibiotic prophylaxis increases the incidence of gram-negative neonatal sepsis. Infect Dis Obstet Gynecol 1999; 7: 210±3. 38. Isaacs D. Prevention of early onset group B streptococcal infection: screen treat or observe? Arch Dis Child Fetal Neonatal Ed 1998; 79: F81±2. 39. Main EK, Slagle T. Prevention of early onset invasive neonatal Group B streptococcal disease in a private hospital setting. The superiority of culture-based protocols. Am J Obstet Gynecol 2000; 182: 1344±54. 40. Landry L, Richardson S, Matlow A, et al. Incidence of neonatal sepsis due to gram-negative bacteria in Toronto, Canada, 1996± 1999. In: Abstracts of the 40th Interscience Conference on Antimicrobial Agents and Chemotherapy. 2000: 446. 41. Katz PF, Hibbard JU, Ranganathan D, Meadows W, Ismail M. Group B streptococcus: to culture or not to culture? J Perinatol 1999; 19: 337±42. 42. Sociedad EspanÄola de Obstetricia y GinecologõÂa. Recomendaciones para la prevencioÂn de la infeccioÂn perinatal por estreptococo grupo B. Prog Obstet Gynecol 1998; 41: 431±5. 43. Rosa-Fraile M, Rodriguez-Granger J, Cueto-Lopez M et al. Use of Granada medium to detect group B streptococcal colonization in pregnant women. J Clin Microbiol 1999; 37: 2674±7. 44. Mazon A, Salvo MS, Ezcurra R. Resultados del programa de prevencioÂn de la infeccioÂn neonatal por estreptococo del grupo B. Prog Obstet Gynecol 2000; 43: 233±6. 45. Eickhoff TC, Klein JO, Daly A, Ingall D, Finland M. Neonatal sepsis and other infections due to group B b-hemolytic streptococci. N Engl J Med 1964; 271: 1221±8. 46. Deutchman M. Thoughts on the prevention of neonatal group B streptococcal infection. Am Fam Physician 1998; 57: 2602, 2605± 07.
ß 2001 Copyright by the European Society of Clinical Microbiology and Infectious Diseases, CMI, 7, 25±27
Microbiology Service, Hospital Virgen de las Nieves, Granada 18014, Spain, 2Obstetrics and Gynaecology Department and Microbiology Service, Hospital Vall D'Hebron, Barcelona, Spain, and 4Infection Control, Lewisham Hospital, London, UK
Group B streptococcal (GBS) early onset infection (EOGBS) is the leading cause of life-threatening bacterial neonatal infection during the ®rst week of life in the developed world, with an incidence of 1±3 per 1000 live births in USA when there is no preventive intervention [1]. The fatality rate ranges from 5 to 10% at present, but those who survive may have permanent neurological sequelae such as cognitive dysfunction, deafness or visual impairment [1,2]. In Europe the incidence (per 1000 live births) of EOGBS without preventive measures varies between the 0.2±0.3 of early reports from Denmark [3] and the more recent data of 0.76 in Finland [4], 4.5 in Rennes (France) [5], 5.4 in Vienna (Austria) [6], 1.42 in Sunderland (UK) [7], 1.15 in Luton (UK) [8], 0.4 in Oxford (UK) [9], 0.54 in Norway [10], 0.4±9 in Andalusia (Spain) [11] and 2.06 in Barcelona (Spain) (Andreu et al, personal communication, August 2000). GBS is usually a commensal bacterium that asymptomatically colonizes the vaginal or rectal areas of 10±30% of pregnant women [1]. In these women, GBS can cause preterm labor, chorioamnionitis, postpartum endometritis, postpartum wound infection and sepsis [12,13]. Invasive GBS infections also cause signi®cant morbidity and mortality in non-pregnant adults, mainly in otherwise compromised patients [1,14,15]. The most important predictive circumstance that leads to EOGBS is the exposure of the newborn to the organism in the birth canal. There are also some well-de®ned maternal risk factors that favor the development of infection in an exposed infant [16±18]. These factors include premature birth, maternal chorioamnionitis, prolonged membrane rupture (> 18 h), intrapartum fever, a previous sibling with EOGBS and GBS bacteriuria. Another factor for developing the disease is exposure to a high maternal inoculum of a virulent GBS strain. A further critical issue for a newborn to develop the disease is a low concentration in the mother's serum of antibodies to the capsular polysaccharide of the colonizing GBS strain [19]. Corresponding author and reprint requests: M. de la Rosa Fraile, Servicio de Microbiologia, Hospital Virgen de las Nieves, Granada 18014, Spain Tel: 34 958 241109 Fax: 34 988 241282 E-mail: [email protected]
Conjugate vaccines might be an excellent tool against GBS infections in mothers, infants, and even in nonpregnant adults, but they are still under investigation [20] and are not yet commercially available. Since 1979 [21], it has been known that intrapartum treatment of colonized mothers with ampicillin or penicillin reduces GBS colonization of newborns and that most cases of EOGBS can be prevented by treating colonized pregnant women with intravenous antibiotics during labor [22,23]. In the USA, the Center for Disease Control and Prevention (CDC) issued guidelines for prevention of EOGBS in 1996 [24], which were endorsed by the American College of Obstetricians and Gynecologists and the American Academy of Pediatrics [17,18]. These guidelines recommend the use of either a screening-based or a risk-based approach to identify candidates for intrapartum antibiotic prophylaxis. The riskbased approach provided intrapartum antibiotics to women who had any of the above-mentioned risk factors. The screening-based approach proposes routine prenatal GBS screening between 35 and 37 weeks' gestation, and intrapartum antibiotics are recommended for all women who are either colonized, or who presented in labor before 37 weeks' of gestation, or whose colonization status is unknown and who present risk factors. To optimize the yielding of GBS cultures the CDC recommends using selective broth media and testing vaginal and rectal specimens. The main drawback of the CDC risk-factor approach is that several studies indicate that more than 50% of cases of EOGBS appear in the absence of any known risk factor [25±27]. Since the publication of the CDC guidelines a signi®cant number of US hospitals have adopted prevention policies [2,28± 30] and there are data that suggest that the incidence of EOGBS has now dropped below 0.6/1000 live births [31]. In some US institutions the rate has fallen from 1.16 to 0.14/1000 live births [32] or from 1.7 to 0.3/1000 [33]. and now the CDC has recommended that `GBS prevention activities be integrated into all obstetric care programs' (Available at http:// www.cdc.gov/ncidod/emergplan/11obj13.htm ± retrieved on 21 August 2000). In other developed countries, an important drop in EOGBS has also taken place when a prevention policy has been set up,
ß 2001 Copyright by the European Society of Clinical Microbiology and Infectious Diseases
26 Clinical Microbiology and Infection, Volume 7 Number 1, January 2001
e.g. in Australia the incidence fell from 2 per 1000 live births in 1991±93 to 0.5 in 1995±97 [34]. It has been suggested [2,35] that prevention protocols greatly increase the proportion of women who get antibiotics during labor and delivery, and this could increase the risk of neonatal sepsis caused by resistant Enterobacteriaceae. Though some alarming reports on this issue have been published [36,37], neonatal sepsis caused by Gram-negative bacteria is more often a disease of prematurity, and the increase in Gram-negative neonatal disease seems related to situations in which the use of the CDC risk-based approach leads to a prolonged use of ampicillin. Moreover, in other studies the decline in the incidence of EOGBS after installing a screening-based prevention program has not been accompanied by an increase in Gram-negative sepsis [33,38±40]. However, the severity of resistant Escherichia coli neonatal sepsis suggests caution regarding the widespread use of ampicillin instead of penicillin for EOGBS prophylaxis [41]. In 1998 in Spain the Societies of Obstetrics and Gynaecology and of Neonatology (with the endorsement of the Societies of Infectious Diseases and Clinical Microbiology and of Chemotherapy) issued the Spanish Consensus Guidelines to Prevent EOGBS [42]. These guidelines follow in general the CDC screening-based approach using either Granada Medium [43] or the broth-enrichment technique to detect GBS-carriers at weeks 35±37 and also include recommendations on the management of newborns to GBS-carrier mothers when prophylaxis has not been used or has been incomplete. Since then a substantial number of Spanish hospitals have adopted this policy, and a considerable drop in the incidence of EOGBS has also been observed [11,44]. Thus in Catalonia the incidence dropped from 1.92/1000 live births in 1994 to 0.57/1000 in 1998 (Andreu et al, personal communication, August 2000). In other European countries in which a prevention policy has been set up a similar reduction has been noticed. In Vienna the incidence of EOGBS [6] dropped from 5.4/1000 (1992±94) to 1.1/1000 (1995±97) and in Rennes from 4.5/1000 in 1993 to 1.6/1000 in 1995 [5] after prevention programs were instituted. Now, more than 40 years after the dramatic emergence of GBS as a major cause of threatening infections in the newborn [45], and more than 20 years after the rationale of antibiotic prophylaxis was established it is clear that EOGBS disease is a very important cause of suffering for parents and newborns, and is largely preventable with currently available methods. Though it has been suggested that `when the incidence of early onset streptococcal infection is low. . ..expensive preventive measures may not be justi®ed' [34], the layperson is seriously concerned about GBS, and GBS support associations have been founded in Europe (UK Group B Strep Support, available at http:// www.gbss.org.uk/, retrieved on 22 August 2000; Dutch Foundation GBS, available at http://home.wxs.nl/sgbs/gbs.html,
retrieved on 22 August 2000) and in USA (USA Group B Strep Association, available at http://www.GroupBStrep.org/, retrieved on 22 August 2000). Quoting an American colleague [46], we can af®rm, `First and foremost, we must not ignore the problem. Neonatal Group B streptococcal infection is more prevalent than many other conditions we screen for in pregnancy, and the effect can be just as devastating'. So perhaps the time has arrived for European obstetricians, neonatologists, infectious diseases physicians and clinical microbiologists to catch up with their American colleagues and together look deeper into the issue of prevention of GBS neonatal infection. A common European consensus on prevention policies should now be established. R EFER E NCE S 1. Edwards MS, Baker CJ. Streptococcus agalactiae (Group B streptococcus). In: Mandell GL, Bennett JE, Dolin R eds. Principles and practice of infectious diseases, 5th edn. New York: Churchill Livingstone, 2000; 2156±67. 2. Schuchat A. Neonatal group B streptococcal disease: screening and prevention. N Engl J Med 2000; 343: 209±10. 3. Mayon White RT. The incidence of GBS disease in neonates in different countries. Antibiot Chemother 1985; 35: 17±27. 4. Kalliola S, Vuopio-Varkila J, Takala AK, Eskola J. Neonatal group B streptococcal disease in Finland: a ten-year nationwide study. Pediatr Infect Dis J 1999; 18: 806±10. 5. Poulain P, Betremieux P, Donnio PY, Proudhom JF, Karege G, Giraud JR. Selective intrapartum anti-bioprophylaxys of group B streptococci infection of neonates: a prospective study in 2454 subsequent deliveries. Eur J Obstet Gynecol Reprod Med 1997; 72: 137±40. 6. Hafner E, Sterniste W, Rosen A, et al. Group B streptococci during pregnancy: a comparison of two screening and treatment protocols. Am J Obstet Gynecol 1998; 179: 677±81. 7. Bignardi GE. Surveillance of neonatal group B streptococcal infection in Sunderland. Commun Dis Public Health 1999; 2: 64±5. 8. Beardsall K, Thompson MH, Mulla RJ. Neonatal group B streptococcal infection in South Bedfordshire, 1993±98. Arch Dis Child Fetal Neonatal Ed 2000; 82: F205±7. 9. Moses LM, Heath PT, Wilkinson AR, Jeffery HE, Isaacs D. Early onset group B streptococcal neonatal infection in Oxford, 1985± 96. Arch Dis Child Fetal Neonat Ed 1998; 79: F148±9. 10. Aavitsland P, Hoiby EA, Lystad A. Systemic group B streptococcal disease in neonates and young infants in Norway, 1985±94. Acta Paediatr 1996; 85: 104±5. 11. Baca M, SaÂnchez MJ, Perea-Milla E et al. Perinatal group B streptococcal infections in Andalusia (Spain) (abstract). Pren Neonat Med 2000; 5 (Suppl 2): 70. 12. Krohn MA, Hillier SL, Baker CJ. Maternal peripartum complications associated with vaginal Group B streptococci colonization. J Infect Dis 1999; 179: 1410±5. 13. Bosh J, Pericot A, Amoros M, Ros R. Endometritis puerperal: estudio de 52 casos con diagnostico microbioloÂgico y clõÂnico. Enferm Infecc Microbiol Clin 1995; 13: 203±8. 14. Gimenez M, Sopena N, VinÄado B et al. Infecciones invasivas por Streptococcus agalactiae en un hospital general universitario durante un periodo de 10 anÄos. Enferm Infecc Microbiol Clin 1996; 14: 300±3.
ß 2001 Copyright by the European Society of Clinical Microbiology and Infectious Diseases, CMI, 7, 25±27
de la Rosa Fraile et al Consensus on group B streptococcal disease
15. MunÄoz P, Llancaqueo A, Rodriguez-Creixems M, Pelaez P, Martin L, Bouza E. Group B streptococcus bacteremia in nonpregnant adults. Arch Int Med 1997; 157: 213±6. 16. Ancona RJ, Ferrieri P, Williams PP. Maternal factors that enhance the acquisition of group B streptococci by newborn infants. J Med Microbiol 1980; 13: 273±80. 17. American College of Obstetricians and Gynecologists. Prevention of early-onset group B streptococcal disease in newborns. ACOG Comm Opin 1996; 173: 1±8. 18. American Academy of Pediatrics Committee on Infectious Diseases and Committee on Fetus and Newborn. Revised guidelines for prevention of early-onset group B streptococcal (GBS) infections. Pediatrics 1997; 99: 489±96. 19. Baker CJ, Kasper DL. Correlation of maternal antibody deficiency with susceptibility to neonatal group B streptococcal infection. N Engl J Med 1976; 294: 753±6. 20. Baker CJ, Paoletti LC, Wessels MR et al. Safety and immunogenicity of capsular polysaccharide-tetanus toxoid conjugate vaccines for group B streptococcal types Ia and Ib. J Infect Dis 1999; 179: 142±50. 21. Yow MD, Mason EO, Leeds LJ, Thompson PK, Clark DJ, Gardner SE. Ampicillin prevents intrapartum transmission of group B streptococcus. JAMA 1979; 241: 1245±7. 22. Boyer KM, Gotoff SP. Prevention of early-onset neonatal group B streptococcal disease with selective intrapartum chemoprophylaxis. N Engl J Med 1986; 314: 1665±9. 23. Garland SM, Fliegner JR. Group B streptococcus (GBS) and neonatal infections: the case for intrapartum chemoprophylaxis. Aust NZ J Obstet Gynaecol 1991; 31: 119±22. 24. Centers for Disease Control and Prevention. Prevention of group B streptococcal disease: A public health perspective. Morbid Mortal Wkly Rep 1996; 45 (RR7): 1±24. 25. Andreu A, Barranco M, Bosch J et al. Prevention of perinatal Group B streptococcal disease in Europe. Scand J Infect Dis 1997; 29: 532. 26. Juncosa T, Bosch J, Dopico E et al. InfeccioÂn neonatal por Streptococcus agalactiae. Estudio multiceÂntrico en el aÂrea de Barcelona. EspanÄa Enferm Infecc Microbiol Clin 1998; 16: 312±5. 27. Towers CV, Suriano K, Asrat T. The capture rate of at risk term newborns for early onset group B streptococcal sepsis determined by a risk factor approach. Am J Obstet Gynecol 1999; 181: 1243± 91997. 28. Centers for Disease Control and Prevention. Adoption of hospital policies for prevention of perinatal group B streptococcal disease United States. Morbid Mortal Wkly Rep 1998; 47 (32): 667±70. 29. Centers for Disease Control and Prevention. Adoption of perinatal group B streptococcal disease prevention recommendations by prenatal-care providers ± Connecticut and Minnesota, 1998. Morbid Mortal Wkly Rep 2000; 49: 228±32. 30. Factor SH, Whitney CG, Zywicki SS, Schuchat A. Effects of hospital policies based on 1996 group B streptococcal disease consensus guidelines. The active bacterial core surveillance team. Obstet Gynecol 2000; 95: 377±82.
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