Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: email@example.com. Type 508 Accommodation and the title of the report in the subject line of e-mail.
Early-Onset and Late-Onset Neonatal Group B Streptococcal Disease --- United States, 1996--2004
In 2002, CDC, the American College of Obstetricians and Gynecologists (ACOG), and the American Academy of Pediatrics (AAP) issued revised guidelines for prevention of perinatal invasive group B streptococcal (GBS) disease (1,2). These guidelines recommend universal screening of pregnant women for rectovaginal GBS colonization at 35--37 weeks' gestation and administering intrapartum antimicrobial prophylaxis to carriers. To assess the impact of the guidelines on multistate trends in neonatal GBS disease incidence, CDC analyzed data from the Active Bacterial Core surveillance (ABCs) system from 1996--2004. This report summarizes the results of that analysis, which determined that incidence of GBS disease in infants aged 0--6 days (i.e., early-onset disease) in 2004 had decreased by 31% from 2000--2001, the period immediately before universal screening was implemented. Incidence of GBS disease in infants aged 7--89 days (i.e., late-onset disease) remained unchanged during the 9-year period reviewed. Continued monitoring is needed to assess the impact of the 2002 guidelines on early-onset disease and the long-term effect of widespread intrapartum use of antimicrobial agents on neonatal GBS disease.
ABCs, part of CDC's Emerging Infections Program (EIP) Network, conducts active, population-based surveillance for invasive GBS disease, defined as isolation of GBS from a normally sterile site. The surveillance areas represented approximately 337,000 live births in 1996 and approximately 427,000 live births in 2004.* ABCs collects data from standardized case-report forms that capture demographic, obstetric, and neonatal data from medical records. For this analysis, infants were classified by race and by Hispanic ethnicity independently. Where race or ethnicity was missing from the case-report form, race or ethnicity as recorded on the birth certificate was used. Otherwise, race was imputed (for 15% of cases) using a multiple imputation method (3). To calculate annual incidence, natality data reported by state vital records or national vital statistics reports (4) were used as denominators. Incidence for 2004 was calculated using 2003 natality data in the denominator. The Cochran-Armitage chi-square test was conducted to determine trend significance.
In 2004, a total of 308 cases of neonatal GBS disease were reported in EIP surveillance areas participating since 2001, including 146 (47%) early-onset cases and 162 (53%) late-onset cases. By race, 55% of infants with neonatal disease (early-onset and late-onset) were white, 42% were black, and 3% were of other races; by ethnicity, 19% were Hispanic, 48% were non-Hispanic, and 33% were of unknown ethnicity. Overall, 51% of the infants were female. Among early-onset cases with complete data, the proportion born at <37 weeks' gestation increased significantly from 20% (40 of 204) in 2000 to 29% (41 of 141) in 2004 (p<0.01). Among late-onset cases with complete data in 2004, 55% (81 of 147) were born preterm. Among both early-onset and late-onset cases, case-fatality ratios remained highest for preterm infants, at 23% (nine of 40) and 9% (seven of 80) for early-onset and late-onset cases, respectively. Among term infants, the case-fatality ratio was 4% (four of 100) for early-onset cases, and no deaths were reported for 66 late-onset cases.
Incidence of early-onset disease remained stable during 1999--2001, averaging 0.47 cases per 1,000 live births (5); incidence declined to 0.32 in 2003 and was stable at 0.34 in 2004 (Figure 1). During 1996--2004, late-onset disease incidence varied little, averaging 0.35 per 1,000 live births, with annual rates ranging from 0.29--0.39 per 1,000 live births (Figure 1). The rate of late-onset disease surpassed that of early-onset disease for the first time in 2003, a trend that continued in 2004. Incidence of both early-onset and late-onset disease varied by site (Table).
Compared with the pre-prevention era baseline rate in 1993, the absolute difference in early-onset disease incidence between blacks and whites had declined by 68% in 2003 (5). However, racial disparities in the incidence of both early-onset and late-onset GBS disease persist (Figure 2). In 2004, the rates per 1,000 live births for early-onset disease were 0.73 for black infants, 0.26 for white infants, and 0.15 for infants of other races. The rates per 1,000 live births for late-onset disease were 0.83 for blacks, 0.28 for whites, and 0.19 for infants of other races.
Reported by: S Brooks, MPH, M Apostol, MPH, J Nadle, MPH, K Wymore, MPH, California Emerging Infections Program, Oakland, California. N Haubert, S Burnite, A Daniels, MSPH, Emerging Infections Program, Colorado Dept of Public Health. JL Hadler, MD, Emerging Infections Program, Connecticut Dept of Public Health. MM Farley, MD, P Martell-Cleary, MSW, Georgia Emerging Infections Program, Veterans Affairs Medical Center and Emory Univ School of Medicine, Atlanta, Georgia. LH Harrison, MD, LT Sanza, Maryland Emerging Infections Program, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. C Morin, MPH, R Lynfield, MD, Minnesota Dept of Health. B Albanese, MD, J Bareta, MS, Emerging Infections Program, New Mexico Dept of Health. B Anderson, PhD, Emerging Infections Program, New York State Dept of Health. P Cieslak, MD, K Stefonek, MPH, Oregon Dept of Human Svcs. B Barnes, Vanderbilt Univ School of Medicine, Nashville, Tennessee; AS Craig, MD, Tennessee Dept of Health. SJ Schrag, DPhil, E Zell, MStat, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases; CR Phares, PhD, EIS Officer, CDC.
Invasive GBS disease emerged in the 1970s as a leading cause of neonatal morbidity and mortality in the United States. In the mid-1980s, clinical trials demonstrated that administering antimicrobials intrapartum to GBS carriers protected their newborns from early-onset disease. In 1996, CDC, in collaboration with ACOG and AAP, formally recommended intrapartum antimicrobial prophylaxis for women with late antenatal GBS colonization or, as an alternative to screening for colonization, for those women with obstetrical risk factors for transmitting infection (6). A large, population-based cohort study of deliveries during 1998--1999 demonstrated that routine screening and prophylaxis for carriers prevented more cases of early-onset disease than the risk-based method (7). In response to this finding, in 2002, CDC, ACOG, and AAP endorsed revised guidelines that discarded the risk-based approach in favor of universal screening of pregnant women for GBS carriage and administering prophylaxis to carriers (1,2).
Multistate ABCs data indicated a 65% decline in the incidence of early-onset disease from 1993 to 1998, coinciding with increased use of intrapartum prophylaxis, followed by a plateau during 1999--2001 (5,8). Adoption of the 2002 guidelines was expected to result in further reductions in early-onset disease, and a subsequent decline was observed during 2003--2004. Whether the maximum benefit provided by the current prevention strategy has been achieved is unknown. A multistate retrospective cohort study had predicted that universal screening would achieve an incidence of 0.32 per 1,000 live births for early-onset disease, nearly equal to the incidence of 0.34 recorded by ABCs in 2004 (7). However, improved implementation of the screening strategy by clinicians and laboratorians and potential use of a polymerase chain reaction test (approved in 2002) for women whose GBS status is unknown at the time of labor might produce additional gains.
No strategies exist to prevent late-onset disease, although more than half of reported cases of neonatal GBS disease now occur during the late-onset period. In addition, concern continues among health officials that widespread intrapartum antimicrobial use might delay, rather than prevent, GBS disease onset, resulting in increased rates of late-onset disease. No evidence exists to suggest an increase; however, careful monitoring of disease trends remains a priority.
Black infants remain at highest risk for both early-onset and late-onset GBS disease. Although white infants achieved the Healthy People 2010 target of fewer than 0.5 early-onset cases per 1,000 live births in 1998, the incidence of early-onset disease among black infants remains above the target. This disparity might be associated with less access to prenatal care among black mothers, higher rates of preterm birth (a risk factor for both early-onset and late-onset disease) among black infants, and higher GBS colonization rates among black mothers (9).
The findings in this report are subject to at least two limitations. First, although incidence trends enable tracking of the effects of prevention measures, these data cannot be directly linked to changes in provider practices. Second, although racial disparities in disease incidence are monitored, the data do not permit evaluation of why these disparities exist.
To characterize provider practices, CDC is collaborating with the EIP Network to abstract a large, population-based sample of maternal labor and delivery records for live births during 2003--2004 in 10 states that participate in ABCs. This effort will 1) provide data on provider adherence to the revised prevention guidelines, 2) identify barriers to adherence, 3) detect missed opportunities for prevention, and 4) increase understanding of racial disparities.
Information for patients, providers, and public health practitioners regarding GBS is available from CDC at http://www.cdc.gov/groupbstrep. Brochures explaining GBS testing and prevention are available in both English and Spanish by telephone at 404-639-2215; bulk orders can be placed through the CDC Foundation by telephone at 877-252-1200.
This report is based in part on contributions by P Daily, MPH, G Rothrock, MPH, California Emerging Infections Program, Oakland, California; J Mohle-Boetani, MD, California Dept of Health Svcs. K Gershman, MD, Colorado Dept of Public Health. NL Barrett, MS, S Petit, MPH, MZ Fraser, Emerging Infections Program, Connecticut Dept of Public Health. W Baughman, MSPH, Emerging Infections Program, Veterans Affairs Medical Center, Atlanta, Georgia. Maryland Active Bacterial Core surveillance, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. L Triden, B Jewell, J Rainbow, MPH, R Danila, PhD, Minnesota Dept of Health. K Angeles, MPH, L Butler, K Johnson, MPH, J Keefe, MPH, Emerging Infections Program, Univ of New Mexico, Albuquerque; New Mexico Dept of Health. N Spina, MPH, G Smith, Emerging Infections Program, New York State Dept of Health. M Dragoon, A Zeigler, Multnomah County Health Dept, Portland, Oregon. W Schaffner, MD, Vanderbilt Univ School of Medicine, Nashville, Tennessee. TH Skoff, MS, A Roberson, MS, C Wright, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC.
* In 1996, the ABCs system included surveillance areas in California (three-county San Francisco Bay area), Connecticut, Georgia (eight-county Atlanta area), Maryland, Minnesota (seven-county Minneapolis-St. Paul area), Oregon (three-county Portland area), and Tennessee (five urban counties). By 2000, surveillance had expanded to include 12 additional counties in the Atlanta area of Georgia, all of Minnesota, seven counties in the Rochester area and eight counties in the Albany area of New York, and six additional urban counties in Tennessee. The five-county Denver area of Colorado was added in 2001, and the state of New Mexico joined in 2004.
In this report, infants classified as white, black, or of other races include both those classified as Hispanic and non-Hispanic. Conversely, infants classified as Hispanic or non-Hispanic include infants from all racial classifications.
Disclaimer All MMWR HTML versions of articles are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the electronic PDF version and/or the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.**Questions or messages regarding errors in formatting should be addressed to firstname.lastname@example.org.
Date last reviewed: 12/1/2005