Skip Navigation LinksSkip Navigation Links
Centers for Disease Control and Prevention
Safer Healthier People
Blue White
Blue White
bottom curve
CDC Home Search Health Topics A-Z spacer spacer
Blue curve MMWR spacer

Decreasing Incidence of Perinatal Group B Streptococcal Disease -- United States, 1993-1995

Group B streptococcal (GBS) infections are the leading cause of bacterial disease and death among newborns in the United States and an important cause of morbidity among peripartum women and nonpregnant adults with chronic medical conditions. Disease in infants usually presents as sepsis, pneumonia, or meningitis but also may include cellulitis or osteomyelitis (1). In 1990, GBS infections caused an estimated 7600 serious illnesses and 310 deaths among U.S. infants aged less than or equal to 90 days; infections among infants aged less than 7 days (i.e., early-onset disease) accounted for approximately 80% of these illnesses (2). To determine the incidence of GBS disease during 1993-1995, CDC conducted surveillance for this disease in an aggregate population of 12.5 million persons with 190,000 annual live-born infants. This report summarizes the findings of surveillance in this population, which indicate that a statistically significant decline in the incidence of early-onset GBS disease occurred in some surveillance areas.

Surveillance was conducted in the three-county San Francisco Bay area, California; four urban counties in Tennessee; the eight-county metropolitan area of Atlanta, Georgia; and the entire state of Maryland. At biweekly intervals, surveillance personnel requested standardized reports of cases of invasive GBS disease from contacts in each laboratory that served acute-care hospitals within specified surveillance areas. Periodic audits of all laboratories were conducted to validate completeness of reporting. A case of invasive GBS disease was defined as isolation of group B streptococci from a normally sterile site (e.g., blood or cerebrospinal fluid) from a resident of an area under surveillance. Cases were categorized as early-onset and late-onset (illness onset at age 7-90 days). To calculate the incidence of neonatal GBS disease for the surveillance areas, the number of live-born infants for 1993-1995 was obtained from the respective state health departments or from CDC's National Center for Health Statistics. Race-specific data are presented only for blacks and whites because numbers for other racial/ethnic groups were too small for meaningful analysis.

During 1993-1995, a total of 3023 cases of invasive GBS disease were reported from the surveillance areas; 1071 (35%) cases occurred among newborns aged less than 90 days. Of the 1071 cases among newborns, 520 (49%) occurred among blacks and 478 (45%), among whites. Approximately three fourths (822 {77%}) of cases were early-onset disease. Bacteremia (89%) and meningitis with or without bacteremia (10%) were the most common types of neonatal disease.

The case-fatality rates were 4.0% for neonatal disease, 4.5% for early-onset disease, and 2.4% for late-onset disease. Of the 708 (66%) infants for whom data about gestational age were available; 85 (12%) were born at less than 34 weeks' gestation; 65 (9%), at 34-36 weeks' gestation; and 558 (79%), at greater than or equal to 37 weeks. In comparison, of all infants born in the United States in 1993, 89% were born at greater than or equal to 37 weeks (3). Preterm infants were more likely to die than those born at greater than or equal to 37 weeks (23 {16%} of 148 versus 11 {2%} of 553).

During 1993-1995, the overall annual incidence of early-onset GBS disease in the surveillance areas declined 24%, from 1.7 cases per 1000 live-born infants in 1993 to 1.3 per 1000 in 1995 (Figure_1). The race-specific incidence rate declined 27% for black newborns and 18% for white newborns. The decline in the overall incidence primarily reflected changes in rates for newborns in Maryland and San Francisco: in both of these sites, the rate of early-onset GBS disease decreased 43%, from 1.4 per 1000 in 1993 to 0.8 per 1000 in 1995. No significant decline occurred in Tennessee or Atlanta during this period. In 1995, the rate varied by geographic location, ranging from 0.8 (Maryland and San Francisco) to 1.9 (Atlanta), and race-specific rates were higher for black newborns (1.8) than for white newborns (1.2). During this same period, the rates of late-onset neonatal GBS disease (0.5 in 1993 and in 1995) and of GBS disease for adults remained stable.

Reported by: G Rothrock, MPH, N Mukerjee, MPH, P Daily, MPH, L Gelling, MPH, A Reingold, MD, Emerging Infections Program; DJ Vugia, MD, S Waterman, MD, State Epidemiologist, California State Dept of Health Svcs. M Rados, B Barnes, L Lefkowitz, MD, Vanderbilt Medical Center, Nashville, Tennessee. W Baughman, MSPH, M Farley, MD, D Stephens, MD, Veterans Administration Medical Svcs and Emory Univ School of Medicine, Atlanta, Georgia. L Billmann, MPH, L Harrison, MD, Johns Hopkins Univ, Baltimore; DM Dwyer, MD, State Epidemiologist, Maryland State Dept of Health and Mental Hygiene. Childhood and Respiratory Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Since the mid-1980s, multiple studies have demonstrated consistently that early-onset GBS disease can be prevented by targeted use of antimicrobial prophylaxis after onset of labor or membrane rupture (4). The overall incidence of early-onset GBS disease remained relatively constant during 1991-1993 (5); however, findings in this report of more recent surveillance indicate that, during 1993-1995, the incidence declined significantly in some areas. The recent decline may reflect the impact of adopting measures to prevent early-onset neonatal GBS infections and improved implementation of existing clinical and laboratory policies during 1994 and early 1995. For example, in mid-1993, the proportion of obstetric-care providers in Georgia who reported using optimal techniques for detecting GBS carriage was limited -- only 9% of those who performed prenatal screening cultures for GBS collected swabs from recommended sites (both the vagina and rectum), and only 4% of laboratories used the optimal method (selective broth media) for isolating GBS (6,7). In comparison, a survey conducted during mid-1994 (including three of the sites in this report) indicated that 38% of hospital obstetric programs had adopted a formal strategy for preventing perinatal GBS disease and only 12% had written policies (7); however, of those programs without prevention policies at the time of the survey, approximately two thirds reported they were considering or developing such policies.

In addition to adoption of prevention measures for early-onset GBS, other factors probably contributed to the recent decline in early-onset GBS disease. First, during 1992, the American College of Obstetricians and Gynecologists (ACOG) and the American Academy of Pediatrics (AAP) issued statements about preventing early-onset GBS disease (4). Second, during 1994, state legislatures in California and Florida considered bills that would have mandated development and implementation of practice guidelines for preventing GBS. Although the proposed legislation was not enacted, the issues were widely publicized and resulted in state-sponsored prevention activities. Third, in 1994, CDC issued draft prevention guidelines for public comment (8) and, in 1995, provided educational materials to clinicians who had participated in previous surveys.

Because of the geographical variation in the incidence rates of GBS disease, the decline in early-onset GBS disease documented in the surveillance sites in this report may not represent national trends. However, the changes probably are not the result of surveillance artifacts because the incidence of early-onset disease declined while rates for late-onset and adult GBS disease remained stable, and because audits of microbiology laboratories have been routinely conducted in all surveillance areas. These findings are consistent with the effect of prevention efforts that can interrupt mother-to-infant transmission, rather than a change in virulence of circulating GBS strains or decreasing prevalences of GBS carriage among all age groups. Ongoing surveillance in these and additional sites is assessing whether the decline in early-onset GBS disease will continue and become more widespread.

The greater risk for early-onset GBS disease among black newborns than among white newborns may be multifactorial, although GBS carriage rates among pregnant women who are black have been higher than those among women in other racial groups (1,4), and rates of GBS disease have been higher among blacks of all age groups (2,5). More cases of early-onset GBS disease occur in hospitals with higher proportions of deliveries to black women or women without prenatal care. These associations are independent of the frequency of low birthweight (less than 5 lbs 8 oz {less than 2500 g}) or patients receiving medical assistance (7).

In collaboration with ACOG, AAP, and a multidisciplinary panel of experts, CDC has developed two strategies (a screening approach and a nonscreening approach) for preventing perinatal GBS disease (4,9,10). The screening approach specifies that all pregnant women should be screened at 35-37 weeks' gestation for GBS carriage, and all identified carriers and women who deliver preterm before availability of a culture result should be offered intrapartum antimicrobial prophylaxis. The nonscreening approach specifies that intrapartum antimicrobial agents should be offered to women with risk factors (e.g., those with elevated intrapartum temperature, membrane rupture greater than or equal to 18 hours, or premature onset of labor or rupture of membranes at less than 37 weeks). Copies of the guidelines and educational materials for prenatal patients are available from CDC's Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, Mailstop C-23, 1600 Clifton Road NE, Atlanta, GA 30333, or from the World-Wide Web at


  1. Baker CJ, Edwards MS. Group B streptococcal infections. In: Remington J, Klein JO, eds. Infectious diseases of the fetus and newborn infant. 4th ed. Philadelphia, Pennsylvania: WB Saunders, 1995:980-1054.

  2. Zangwill KM, Schuchat A, Wenger JD. Group B streptococcal disease in the United States, 1990: report from a multistate active surveillance system. In: CDC surveillance summaries (November). MMWR 1992;41(no. SS-6):25-32.

  3. Ventura SJ, Martin JA, Taffel SM, et al. Advance report of final natality statistics, 1993. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, National Center for Health Statistics, 1995. (Monthly vital statistics report; vol 44, no. 3, suppl).

  4. CDC. Prevention of perinatal group B streptococcal disease: a public health perspective. MMWR 1996;45(no. RR-7).

  5. Whitney CG, Deaver K, Plikaytis BS, Wenger JD, Schuchat A. Perinatal group B streptococcal infections: United States, 1991-1993 {Abstra Conference on Antimicrobial Agents and Chemotherapy. Washington, DC: American Society for Microbiology, 1995.

  6. Jafari HS, Schuchat A, Hilsdon R, Whitney CG, Toomey KE, Wenger JD. Barriers to prevention of perinatal group B streptococcal disease. Pediatr Infect Dis J 1995;14:662-7.

  7. Whitney CG, Plikaytis BD, Gozansky WS, Wenger JD, Schuchat A. Prevention practices for group B streptococcal disease: a multi-state surveillance analysis. Obstet Gynecol 1997;89: 28-32.

  8. CDC. Prevention of group B streptococcal disease: a public health perspective. Federal Register 1994;59:64764-73.

  9. Committee on Obstetric Practice, American College of Obstetricians and Gynecologists. Prevention of early-onset group B streptococcal disease in newborns. Washington, DC: American College of Obstetricians and Gynecologists, 1996; ACOG committee opinion no. 173.

  10. Committee on Infectious Diseases/Committee on Fetus and Newborn, American Academy of Pediatrics. Revised guidelines for prevention of early-onset group B streptococcal (GBS) infection. Pediatrics 1997;99:489-96.


    Return to top.


Return to top.

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

Page converted: 09/19/98


Safer, Healthier People

Morbidity and Mortality Weekly Report
Centers for Disease Control and Prevention
1600 Clifton Rd, MailStop E-90, Atlanta, GA 30333, U.S.A


Department of Health
and Human Services

This page last reviewed 5/2/01