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Perinatal Group B Streptococcal Disease After Universal Screening Recommendations --- United States, 2003--2005

Group B streptococcus (GBS) is a leading cause of neonatal morbidity and mortality in the United States. In 2002, CDC, the American College of Obstetricians and Gynecologists (ACOG), and the American Academy of Pediatrics (AAP) issued revised guidelines for the prevention of perinatal GBS disease. These guidelines recommend universal screening of pregnant women by culture for rectovaginal GBS colonization at 35--37 weeks' gestation and the use of intrapartum antibiotic prophylaxis for GBS carriers (1). To examine rates of neonatal and pregnancy-associated GBS disease after the revised guidelines were issued, CDC analyzed surveillance data from the Active Bacterial Core surveillance (ABCs) system from the period 2003--2005 and compared them with data from 2000--2001, the period immediately preceding the universal screening recommendations. This report describes the results of that analysis, which indicated that annual incidence of early onset GBS disease (i.e., in infants aged 0--6 days) was 33% lower during 2003--2005 than during 2000--2001. However, although incidence among white infants decreased steadily during 2003--2005, incidence increased 70% among black infants. Incidence of GBS disease among infants aged 7--89 days (i.e., late-onset disease) and pregnant women remained stable after revised universal screening guidelines were issued. Continued surveillance is needed to monitor the impact of the guidelines on perinatal GBS disease and trends in racial disparities and to guide interventions to reduce disparities.

ABCs, part of CDC's Emerging Infections Program (EIP) network, conducts active, laboratory- and population-based surveillance in selected counties of 10 states for invasive GBS disease,* defined as isolation of GBS from a normally sterile site or from the placenta or amniotic fluid in cases of fetal death. In 2004, the surveillance area represented approximately 455,000 live births; 72% of the infants were white, 19% were black, and 9% were of other race. Surveillance areas used standardized case-report forms to collect demographic, neonatal, and obstetric data from medical records. Race and ethnicity were determined from medical records or birth certificates. Multiple imputations were used to account for missing race data (2). Live-birth data from state vital records and national vital statistics reports were used as denominators for incidence calculations. Incidence for 2005 was calculated using 2004 natality data. The Cochran-Armitage test was conducted to determine linear trend significance. Average incidence during 2000--2001, designated as the baseline period, was compared with incidence during 2003--2005.

During 2000--2005, a total of 1,020 cases of early-onset GBS disease (EOD) were reported from the surveillance areas (202 in 2000, 193 in 2001, 175 in 2002, 131 in 2003, 152 in 2004, and 167 in 2005). The number of surveillance areas was stable during 2000--2005; however, surveillance started in Colorado in 2001 and in New Mexico in 2004. New Mexico cases are not included in comparison of incidence over time.

Average EOD incidence during 2003--2005 (0.33 cases per 1,000 live births), after the revised guidelines were issued, was 33% lower than during the baseline period (0.49). Incidence after the revised guidelines was 0.31 cases per 1,000 live births in 2003 and increased to 0.35 in 2005. Stratified by race, rates increased significantly (p<0.05) from 2003 to 2005 among black infants (0.52 to 0.89 cases per 1,000 live births) and decreased among white infants (0.26 to 0.22 cases per 1,000 live births) (Figure 1). When further stratified by gestational age, incidence increased among full-term (i.e., >37 weeks' gestation) black infants from 2003 to 2005 (0.31 to 0.50 per 1,000 live births), but incidence decreased among full-term white infants during the same period. Incidence among preterm infants, although higher among black infants, fluctuated in both racial groups and demonstrated no trend (Figure 2).

A total of 167 EOD cases were reported for 2005, the year when racial disparities were largest. Incidence of EOD in 2005 was 0.37 cases per 1,000 live births and varied by surveillance area (Table). By race, 44% were white, 39% were black, 4% were of other race, and 12% were of unknown race. Of GBS isolates from EOD cases, 97.6% were from blood only, 1.8% were from blood and cerebrospinal fluid (CSF), and 0.6% were from CSF only. The case-fatality ratio was 5%. Among EOD cases for which gestational age data were available (164 of 167), 29% occurred in infants born preterm (i.e., at <37 weeks' gestation). Among black infants with EOD, 40% of cases occurred in infants born preterm, compared with 24% of cases in white infants (p=0.05, by chi-square test). Among cases in preterm infants, 60% of cases in white infants were in those born at 35--36 weeks' gestation, and 40% were in those born at <35 weeks, compared with 16% of cases in black infants born at 35--36 weeks and 84% born at <35 weeks. Approximately 88% of cases in white infants born full term and 81% of cases in black infants born full term were in infants born to mothers who received prenatal GBS screening.

A total of 165 cases of late-onset GBS disease (LOD) were reported from the surveillance areas in 2005, resulting in an incidence of 0.36 per 1,000 live births. Incidence of LOD varied by surveillance area (Table). Rates of LOD were similar before and after the revised guidelines (0.36 per 1,000 live births for the baseline period, compared with 0.38 cases per 1,000 live births for 2003--2005).

During 2003--2005, the annual incidence of GBS infection among pregnant women remained stable (averaging 0.12 cases per 1,000 live births) and was similar to the baseline incidence (0.15 cases per 1,000 live births). In 2005, a total of 53 cases of pregnancy-associated GBS invasive infections in women were reported. Incidence varied by surveillance area (Table). Of those pregnancies with known outcomes (50 of 53), 31 (62%) resulted in abortion or stillbirth, 15 (30%) resulted in delivery of healthy infants, one (2%) resulted in delivery of an infant who had clinical infection but survived, and three (6%) resulted in neonatal death.

Reported by: A Reingold, MD, School of Public Health, Univ of California at Berkeley. K Gershman, MD, Colorado Dept of Public Health. S Petit, MPH, Emerging Infections Program, Connecticut Dept of Public Health. K Arnold, MD, Emerging Infections Program, Div of Public Health, Georgia Dept of Human Resources. L Harrison, MD, Maryland Emerging Infections Program. R Lynfield, MD, Minnesota Dept of Health. B Albanese, MD, New Mexico Dept of Health. S Zansky, PhD, Emerging Infections Program, New York State Dept of Health. A Thomas, Oregon Public Health Div. A Craig, MD, Tennessee Dept of Health. SJ Schrag, DPhil, ER Zell, MStat, P Lewis, Div of Bacterial Diseases, National Center for Immunization and Respiratory Diseases; RM Patel, MD, EIS Officer, CDC.

Editorial Note:

Clinical trials conducted in the 1980s demonstrated that intrapartum antibiotic prophylaxis (IAP) was effective at preventing EOD by interrupting transmission of GBS from mothers who are colonized with the bacteria to their newborns (3). However, IAP use was not widely adopted, and national standards for IAP administration were not implemented until 1996, when ACOG, AAP, and CDC issued consensus guidelines recommending that health-care providers use either risk-based or culture-based screening to identify candidates for IAP (4). In 2002, a population-based study, demonstrating that routine screening of all pregnant women at 35--37 weeks' gestation and IAP for carriers prevented more cases of EOD than the risk-based approach, led to the universal prenatal screening recommendation in 2002 (5). The study predicted that universal screening could decrease incidence of EOD in the United States to 0.32 cases per 1,000 live births. Although this level was achieved in 2003, the rate of overall EOD increased during 2003--2005, reflecting increases in incidence among black infants. This report highlights the need for strategies to reduce the rate of neonatal GBS disease among black infants, to evaluate missed opportunities for prevention, and to continue monitoring disease trends.

Disparities between black and white infants in incidence of GBS disease have been observed since the disease emerged as a leading cause of neonatal sepsis (6). Factors that might contribute to this disparity include higher maternal colonization rates in blacks (7), higher rates of preterm deliveries (a risk factor for neonatal GBS disease) among blacks, and less access to prenatal care among black women compared with white women. However, a study that controlled for these factors indicated that black race remained an independent risk factor for disease (8). Healthy People 2010 objectives include achieving rates of EOD below 0.5 cases per 1,000 live births for all racial populations. Rates of EOD among white infants reached this target in 1998 and have remained below this level since the universal screening recommendations were issued. In 2003, the year after the recommendations were issued, incidence among black infants reached a record low (0.52 per 1,000 live births) and suggested that national health objectives might also be met for black infants (9; CDC, unpublished data, 2007). However, during the following 2 years, incidence of EOD among black infants returned to levels observed before the recommendations were issued. Continued surveillance is needed to determine whether this trend persists and to identify possible barriers to universal screening for pregnant black women.

The findings in this report are subject to at least two limitations. First, although the surveillance system describes trends in disease, these results alone are not sufficient to determine causes of increases or decreases in GBS disease rates. Second, these results alone do not measure health-care--provider compliance with the guidelines; therefore, changes in incidence of GBS cannot be attributed directly to compliance with prevention guidelines. Although increases in rates of EOD among black infants were reported, whether these increases are attributed to barriers in implementation of the guidelines is not known. To overcome these two limitations, CDC is collaborating with the EIP network to conduct Birthnet, a review of maternal labor and delivery records of live births in 10 ABCs states during 2003--2004. The purpose of the study is to characterize provider compliance to universal screening guidelines, identify barriers to implementation, detect missed prevention opportunities, and increase understanding of racial disparities.

Universal screening and IAP are the most effective measures available for EOD prevention. Rates of EOD were lower after the universal screening recommendations were issued, compared with the baseline period. However, even optimal implementation of the recommendations is unlikely to eliminate EOD because neither screening for GBS carriers nor IAP is 100% effective. When the guidelines were issued, the potential impact of screening and IAP on LOD was unknown; the exact modes of transmission for LOD were not well understood, and vertical transmission might have only a limited role. This report indicates minimal change in rates of LOD and infections in pregnancy since the universal screening recommendations were issued.

The use of a GBS vaccine could be effective in preventing perinatal GBS disease, possibly also preventing stillbirths and premature deliveries attributed to GBS. Vaccination might also help reduce racial disparities in disease. Several potential vaccines are under consideration, some of which have completed Phase II trials (10).

Information for patients, health-care providers, and public health practitioners regarding GBS is available from CDC at http://www.cdc.gov/groupbstrep. Brochures are available in both English and Spanish by telephone (404-639-2215); information regarding bulk orders is available through the CDC Foundation by telephone (877-252-1200).

Acknowledgments

This report is based, in part, on contributions by S Burnite, N Comstock, A Daniels, Colorado Dept of Public Health; JL Hadler, MD, MZ Fraser, Emerging Infections Program, Connecticut Dept of Public Health; P Martell-Cleary, MSW, MM Farley, MD, Emerging Infections Program, Div of Public Health, Georgia Dept of Human Resources; Maryland Active Bacterial Core Surveillance, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; C Morin, MPH, J Rainbow, MPH, B Jewell, L Triden, Minnesota Dept of Health; J Bareta, MS, K Angeles, MPH, J Keefe, MPH, K Johnson, MS, L Butler, New Mexico Dept of Health; N Spina, MPH, G Smith, B Anderson, PhD, Emerging Infections Program, New York State Dept of Health; M Barber, L Duke, Oregon Public Health Div; B Barnes, W Schaffner, MD, Vanderbilt Univ School of Medicine; and TH Skoff, MS, C Wright, Div of Bacterial Diseases, National Center for Immunization and Respiratory Diseases, CDC.

References

  1. CDC. Prevention of perinatal group B streptococcal disease: revised recommendations from CDC. MMWR 2002;51(No. RR-11).
  2. Little RJ, Rubin DB. Statistical analysis with missing data. 2nd ed. Wiley series in probability and statistics. Hoboken, NJ: Wiley & Sons; 2002.
  3. 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.
  4. CDC. Prevention of perinatal group B streptococcal disease: a public health perspective. MMWR 1996;45(No. RR-7).
  5. Schrag SJ, Zell ER, Lynfield R, et al. A population-based comparison of strategies to prevent early-onset group B streptococcal disease in neonates. N Engl J Med 2002;347:233--9.
  6. 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.
  7. Stapleton RD, Kahn JM, Evans LE, et al. Risk factors for group B streptococcal genitourinary tract colonization in pregnant women. Obstet Gynecol 2005;106:1246--52.
  8. Schuchat A, Oxtoby M, Cochi S, et al. Population-based risk factors for neonatal group B streptococcal disease: results of a cohort study in metropolitan Atlanta. J Infect Dis 1990;162:672--7.
  9. CDC. Diminishing racial disparities in early-onset neonatal group B streptococcal disease---United States, 2002--2003. MMWR 2004;53: 502--5.
  10. Heath PT, Feldman RG. Vaccination against group B streptococcus. Expert Rev Vaccines 2005;4:207--18.

* Information available at http://www.cdc.gov/ncidod/dbmd/abcs/index.htm.

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Date last reviewed: 7/18/2007

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