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Diminishing Racial Disparities in Early-Onset Neonatal Group B Streptococcal
Disease—United States, 2000-2003
1 table, 2 figures omitted
Increased use of intrapartum antibiotics to prevent perinatal group
B streptococcal (GBS) disease during the 1990s led to substantial declines
in the incidence of GBS disease in newborns.1 Despite
this success, at the end of the 1990s, early-onset GBS disease (in infants
aged <7 days) continued to be a leading infectious cause of neonatal mortality
in the United States, and black infants remained at higher risk than white
infants.1 In 2002, CDC and the American
College of Obstetricians and Gynecologists (ACOG) revised guidelines for prevention
of early-onset GBS disease to recommend late prenatal screening of all pregnant
women and intrapartum antibiotic prophylaxis (IAP) for GBS carriers.2,3 These guidelines were expected
to result in further declines in early-onset disease.4 This
report updates early-onset incidence trends since 1999 analyzed by using population-based,
multistate data from the Active Bacterial Core surveillance (ABCs)/Emerging
Infections Program Network. The results of the analysis indicated that (1)
after a plateau in early-onset disease incidence during 1999-2002, rates declined
34% in 2003 and (2) although racial disparities in incidence persist, rates
for blacks now approach the 2010 national health objective of 0.5 cases per
1,000 live births.5 Continued implementation
of screening and prophylaxis guidelines by clinicians and public health practitioners
should lead to further declines in racial disparities.
ABCs conducts active, laboratory-based surveillance for all cases of
invasive GBS, including periodic audits to ensure completeness of case finding.
A case of early-onset GBS disease was defined as isolation of GBS from a normally
sterile site (e.g., blood or cerebrospinal fluid) in a neonate aged 0-6 days
residing in an ABCs area. Participating areas during 2000-2003 were Connecticut,
Maryland, Minnesota, and selected counties in California, Colorado (beginning
in 2001), Georgia, New York, Oregon, and Tennessee, representing a population
that produced 419,062 live births in 2001. Of the 2001 live-birth cohort,
73% were white, 20% were black, and 7% were of other races; 15% were of Hispanic
origin. The incidence of early-onset disease was calculated by using live-birth
data for 2000 and 2001 from ABCs states' vital statistics or the National
Vital Statistics Report (available at http://www.cdc.gov/nchs/data/nvsr/nvsr51/nvsr51_02.pdf). Incidence for 2002 and 2003 were calculated by using 2001 live-birth
data. Incidence of GBS disease from earlier surveillance years was derived
from data published previously1 using comparable
methods. A total of 184 (13.2%) of 1,397 cases with missing or unspecified
race data during 1996-2002 were matched with birth records to improve the
completeness of race reporting. Remaining cases of unknown race (during 1996-2002,
a total of 77 [5.5.%] of 1,397; in 2003, a total of 21 [15.7%] of 134) were
distributed on the basis of the known race distribution within each county
and included in all reported rates. To assess the impact of the August 2002
guidelines, incidence in 2003 was compared with the average incidence for
2000 and 2001; 2002 was considered a transition year.
During 2000-2003, a total of 701 cases of early-onset GBS disease were
reported in the surveillance areas (Table). Outcome was known for 676 (96.4%)
cases; the case-fatality ratio was 6.5%. A total of 150 (21.4%) infants were
born before 37 weeks' gestation; among these preterm infants, the case-fatality
ratio was 22.7%.
During 1999-2001, early-onset disease incidence remained nearly constant,
with an average of 0.47 cases per 1,000 live births. In 2003, the overall
disease incidence was 0.32 (Figure 1), representing a 34% (95% confidence
interval [CI] = 20%-46%) decline in incidence since 2000-2001. The incidence
in 2003 varied geographically, from 0.53 in Tennessee to 0.14 in Oregon (Table).
Rates in Georgia decreased significantly compared with the 2000-2001 baseline
(p<0.01), and rates in Tennessee decreased marginally (p = 0.06).
During 1999-2001, disease incidence remained stable for both black and
white populations, and rates among black infants were approximately twice
those of whites (Figure 2). In 2003, the incidence of disease was 0.26 cases
per 1,000 live births among white infants, 0.59 among black infants, and 0.16
among infants of other races; the rate among those of Hispanic origin was
0.31. Compared with disease rates in 2000 and 2001, the incidence of disease
in 2003 declined 34% among white infants and 30% among black infants. However,
black infants remained 2.2 (95% CI = 1.6-3.2) times more likely to have early-onset
GBS disease than white infants in 2003; this relative risk has not changed
significantly since 1996 (Figure 2). Compared with the pre-prevention baseline
rate in 1993, the difference in incidence between whites and blacks has declined
68% (i.e., by 0.78 cases per 1,000 births). In 1998, white neonates achieved
the 2010 national health objective5; preliminary
data from 2003 indicate that black neonates are approaching this goal.
S Brooks, MPH, M Apostol, MPH, J Nadle, MPH, A Grey, MPH, California
Emerging Infections Program, Oakland, California. N Haubert, S Burnite, T
Crume, MSPH, Emerging Infections Program, Colorado Dept of Public Health.
NL Barrett, MS, 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. L 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. G Smith, 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; AS
Craig, MD, Tennessee Dept of Health. SI McCoy, MPH, S Schrag, DPhil, A Schuchat,
MD, Div of Bacterial and Mycotic Diseases; KA Robinson, MPH, Office of Surveillance,
Active Bacterial Core surveillance/Emerging Infections Program Network, National
Center for Infectious Diseases, CDC.
CDC Editorial Note:
Although the incidence of early-onset GBS disease declined during the
incidence plateaued until 2002, when universal screening guidelines were issued.
The rate in 2003 of 0.32 cases per 1,000 live births is the lowest ever recorded
for the United States and meets the 2010 national health objective for overall
incidence,5 with all of the ABCs areas at
or below the target of 0.5 cases per 1,000 live births.
A 2002 review of a random sample of live births in ABCs areas estimated
that, under universal screening, the overall incidence of early-onset infections
would be approximately 0.3 cases per 1,000 live births4;
the data from 2003 are consistent with this prediction. These data likely
underestimate the full impact of guidelines released in the latter half of
2002, because institutions following the old risk-based guidelines were unlikely
to have completed the transition to universal screening. In addition, improved
implementation of screening through optimal prenatal specimen collection and
processing; improved communication between laboratories and providers; and
appropriate choice of prophylactic agents, particularly for penicillin-allergic
women, might lead to further declines in disease incidence. Moreover, clinical
laboratories have improved in GBS isolation and processing since the 1996
guidelines; however, opportunities to improve the implementation of recommendations
related to antimicrobial susceptibility testing and GBS bacteriuria were identified.7
Although record low rates of early-onset GBS disease were recorded for
black neonates in 2003, racial disparities persist. The reasons for higher
rates of neonatal GBS disease among blacks are multifactorial. A key factor
is substantially higher GBS colonization rates among blacks; in addition,
preterm delivery is more common in blacks and increases risk for both early-
and late-onset GBS disease.8 Increased GBS
prevention efforts during the 1990s coincided with a 75% reduction in the
difference in disease incidence between black and white infants.1 However,
starting in 1999, racial disparities in early-onset disease plateaued. Declines
in the rate of disease in black infants after release of the 2002 guidelines
and new progress towards the 2010 national health objective might indicate
that a universal screening strategy will further reduce this racial disparity.
The findings in this report are subject to at least three limitations.
First, no data on the strategy providers followed are available, so trends
cannot be directly attributed to particular prevention practices. Second,
race data were collected from the medical record rather than self-reports.
The completeness of race ascertainment was improved through the use of birth
certificate data; however, 9% of cases had unknown race reported. Finally,
live-birth data were not yet available for 2002 and 2003, so exact denominators
for incidence calculations could not be used.
To maximize prevention, correct implementation of the screening approach
is crucial. Practical tools to assist with monitoring prevention implementation
have been published9,10;
additional health communication tools have been created to assist both clinicians
and public health practitioners with GBS education and policy issues. These
resources include a recently designed website (http://www.cdc.gov/groupbstrep) with entry portals for clinicians, clinical microbiologists, the general
public, and state health departments. In addition, a new consumer education
brochure designed to reach black women is available free of charge by writing
CDC's Respiratory Diseases Branch at 1600 Clifton Road, N.E., mailstop C-23,
Atlanta, GA 30333, by faxing requests to 404-639-3970, or by ordering online
This report is based in part on contributions by P Daily, MPH, California
Emerging Infections Program, Oakland; J Mohle-Boetani, MD, California Dept
of Health Svcs. K Gershman, MD, Colorado Dept of Public Health. JL Hadler,
MD, 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. N Spina,
MPH, B Anderson, PhD, 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.
R Facklam, PhD, TH Skoff, MS, C Whitney, MD, C Wright, Div of Bacterial and
Mycotic Diseases, National Center for Infectious Diseases, CDC.
Diminishing Racial Disparities in Early-Onset Neonatal Group B Streptococcal Disease—United States, 2000-2003. JAMA. 2004;292(6):676–677. doi:10.1001/jama.292.6.676
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