Group B Streptococcal Disease in the Era of Intrapartum Antibiotic Prophylaxis
Stephanie J. Schrag, D.Phil., Sara Zywicki, M.P.H., Monica M. Farley, M.D., Arthur L. Reingold, M.D., Lee H. Harrison, M.D., Lewis B. Lefkowitz, M.D., James L. Hadler, M.D., Richard Danila, M.D., Paul R. Cieslak, M.D., and Anne Schuchat, M.D.
Background Group B streptococcal infections are a leading causeof neonatal mortality, and they also affect pregnant women andthe elderly. Many cases of the disease in newborns can be preventedby the administration of prophylactic intrapartum antibiotics.In the 1990s, prevention efforts increased. In 1996, consensusguidelines recommended use of either a risk-based or a screening-basedapproach to identify candidates for intrapartum antibiotics.To assess the effects of the preventive efforts, we analyzedtrends in the incidence of group B streptococcal disease from1993 to 1998.
Methods Active, population-based surveillance was conductedin selected counties of eight states. A case was defined bythe isolation of group B streptococci from a normally sterilesite. Census and live-birth data were used to calculate therace-specific incidence of disease; national projections wereadjusted for race.
Results Disease in infants less than seven days old accountedfor 20 percent of all 7867 group B streptococcal infections.The incidence of early-onset neonatal infections decreased by65 percent, from 1.7 per 1000 live births in 1993 to 0.6 per1000 in 1998. The excess incidence of early-onset disease inblack infants, as compared with white infants, decreased by75 percent. Projecting our findings to the entire United States,we estimate that 3900 early-onset infections and 200 neonataldeaths were prevented in 1998 by the use of intrapartum antibiotics.Among pregnant girls and women, the incidence of invasive groupB streptococcal disease declined by 21 percent. The incidenceamong nonpregnant adults did not decline.
Conclusions Over a six-year period, there has been a substantialdecline in the incidence of group B streptococcal disease innewborns, including a major reduction in the excess incidenceof these infections in black infants. These improvements coincidewith the efforts to prevent perinatal disease by the wider useof prophylactic intrapartum antibiotics.
Invasive group B streptococcal disease emerged in the 1970sas a leading cause of neonatal morbidity and mortality in theUnited States.1,2,3,4 In the 1990s, 4 to 6 percent of affectednewborns died from the infection.5,6 Surviving infants oftenhave developmental disabilities, including mental retardationand hearing or vision loss. The incidence of group B streptococcaldisease is also high among pregnant women and the elderly.7
Clinical trials in the mid-1980s demonstrated that antibioticprophylaxis administered during labor to mothers colonized withgroup B streptococci was highly effective in preventing diseasein newborns.8 However, the medical community was slow to incorporateintrapartum prophylaxis into routine practice. In 1989 the Centersfor Disease Control (CDC) established active multistate surveillancefor group B streptococcal disease. In the early 1990s, the costeffectiveness of alternative prevention strategies was evaluated,9,10,11,12and a national advocacy group was formed by parents of infantswith group B streptococcal disease (Group B Strep Association,which can be contacted on the Internet at www.groupbstrep.org).In 1996 consensus guidelines for the prevention of perinatalgroup B streptococcal disease were issued by the American Academyof Pediatrics,13 the American College of Obstetricians and Gynecologists,14and the CDC.15 These guidelines recommend the use of a risk-basedor screening-based approach to identify candidates for intrapartumprophylaxis. According to the risk-based approach, women whopresent at the time of labor with risk factors for disease transmission(fever, prolonged rupture of the membranes, or imminent pretermdelivery) are offered intrapartum chemoprophylaxis. Accordingto the screening-based approach, all women are screened forcarriage of group B streptococci between 35 and 37 weeks ofgestation, and intrapartum chemoprophylaxis is offered to carriers.
We analyzed data from a program of active surveillance for invasivegroup B streptococcal disease in selected areas of the UnitedStates to determine how efforts at prevention affected the incidenceof disease from 1993 to 1998. This surveillance system, whichwas designed to identify all cases of invasive disease in apopulation ranging from 12 million (in 1993) to more than 20million (in 1998), provides data on national trends in the incidenceof invasive group B streptococcal disease in the era of perinataldisease prevention.
Methods
Active, laboratory-based surveillance for invasive group B streptococcalinfection from 1993 to 1998 was conducted by previously describedmethods.5 Project personnel communicated at least twice a monthwith contacts in all participating microbiology laboratoriesserving acute care hospitals in the following areas: Maryland,all counties from 1993; California, 3 counties (Alameda, ContraCosta, and San Francisco) from 1993; Georgia, 8 counties (Cobb,Clayton, Dekalb, Douglas, Fulton, Gwinnett, Newton, and Rockdale)from 1993, and 12 additional counties in the Atlanta area from1997; Tennessee, 4 counties (Davidson, Hamilton, Knox, and Shelby)from 1993, and Williamson County from 1995; Connecticut, allcounties from 1995; Minnesota, 7 counties (Anoka, Carver, Dakota,Hennepin, Ramsey, Scott, and Washington) from 1995; Oregon,3 counties (Clackamas, Multnomah, and Washington) from 1995;and New York, 7 counties (Genesee, Livingston, Monroe, Ontario,Orleans, Wayne, and Yates) from 1997.
A case was defined by the isolation of group B streptococcifrom a normally sterile site (e.g., blood or cerebrospinal fluid)in a resident within a surveillance area; cases identified onthe basis of isolation of group B streptococci from amnioticfluid, placenta, or urine alone were not included. Periodicaudits were conducted in each area. Any cases newly identifiedby audits were included in the surveillance data base.
We defined early-onset neonatal disease as that occurring ininfants less than 7 days old, late-onset disease as that occurringin infants 7 to 89 days old, childhood disease as that occurringin children from 90 days to 14 years old, and adult diseaseas that occurring in persons 15 years of age or older.5 Pregnantgirls and women, including those under 14 years of age, wereanalyzed as a separate category from nonpregnant adults andchildren. Because the samples were small after stratificationaccording to race, we reduced this variable to three categories— black, white, and other — on the basis of previousobservations that invasive group B streptococcal disease ismore common among blacks than in other groups.5 The racial distributionin the population under surveillance ranged from 24 percentblack and 69 percent white in 1993 to 19 percent black and 75percent white in 1997. Data on ethnic background were availablefor 61 percent of the patients with group B streptococcal disease.Of these, 367 (8 percent) were Hispanic, 56 percent of whomidentified themselves as white Hispanics.
To describe epidemiologic characteristics of persons with invasivedisease, we analyzed data from all participating surveillanceareas between 1993 and 1998. However, we limited our analysisof changes in the incidence of disease over time to sites wheresurveillance data were available for the entire period (1993through 1998 in Georgia, California, Maryland, and Tennessee).To place the trends from 1993 to 1998 in a broader context,in Figure 1 we show data from 1990 to 1998 for the three surveillanceareas (California, Georgia, and Tennessee) where continuousdata were available. Estimates of age- and race-specific incidencefor these surveillance areas were calculated by using populationdata from the U.S. Bureau of the Census and data on live birthsfrom the National Center for Health Statistics. For 1998, live-birthfigures for the year 1997, obtained directly from the statehealth departments and Census data, were used as denominators.
Figure 1. Incidence of Early- and Late-Onset Invasive Group B Streptococcal Disease in Three Active Surveillance Areas (California, Georgia, and Tennessee), 1990 through 1998, and Activities for the Prevention of Group B Streptococcal Disease.
Live births for 1998 were approximated on the basis of 1997 data. Arrows designate the dates when prevention activities occurred. ACOG denotes the American College of Obstetricians and Gynecologists, and AAP the American Academy of Pediatrics.
National estimates of the incidence of group B streptococcaldisease were calculated by multiplying age- and race-specificincidence in the aggregate surveillance areas by the appropriatelive-birth and population figures for the United States. Whencalculating the incidence of disease and projecting it to thetotal U.S. population, we assigned patients of unknown raceto one of the three categories (white, black, and other) onthe basis of the proportion of known cases occurring in eachracial group. Changes in incidence over time were analyzed byPoisson regression with the PROC GENMOD procedure (SAS, version6.12, SAS, Cary, N.C.). Ninety-five percent confidence intervalsare reported throughout.
Results
From 1993 through 1998, the active surveillance system identified7867 cases of invasive group B streptococcal disease in thesurveillance areas. Eighty-four percent of isolates were obtainedfrom blood, 4 percent from cerebrospinal fluid, 4 percent fromsynovial fluid, and the remainder from the following normallysterile sites: bone (2 percent), peritoneal fluid (2 percent),surgical specimens (2 percent), pleural fluid (1 percent), andother sites (1 percent).
Of the cases that were identified, 2196 (28 percent) occurredin infants less than three months old. The majority of neonatalcases (1584 of 2196, or 72 percent) presented as early-onsetneonatal disease and were identified on the day of birth (1140of 1584, or 72 percent of early-onset cases). The percentageof early-onset cases identified on the day of birth declinedfrom 76 percent in 1993 to 71 percent in 1998, but this declinewas not statistically significant (2 for linear trend=1.7, P=0.19).Early-onset neonatal disease presented primarily as bacteremia(80 percent), meningitis (6 percent), or pneumonia (7 percent).The case fatality rate associated with each of these presentationswas 4 percent. Preterm infants (those with a gestational ageof less than 37 weeks) who had early- onset disease had a higherrisk of dying than did term infants with similar disease (relativerisk, 6.7; 95 percent confidence interval, 4.5 to 10.0) (Table 1).
Table 1. Number of Cases of Early-Onset Neonatal Invasive Group B Streptococcal Disease and Case Fatality Rates According to Gestational Age in Selected Counties in the United States, 1993 to 1998.
Late-onset disease presented primarily as bacteremia (63 percent),meningitis (24 percent), or pneumonia (2 percent). Late-onsetdisease was more likely than early-onset disease to presentas meningitis (relative risk, 4.3; 95 percent confidence interval,3.4 to 5.5; P<0.001). The overall case fatality rate forlate-onset disease was 2.8 percent (Table 2), which was onlymarginally lower than that for early-onset disease (2 with Yates'correction=3.51, P=0.06).
Table 2. Number of Cases of Invasive Group B Streptococcal Disease and Case Fatality Rates According to Age at Disease Onset in Selected Counties in the United States, 1993 through 1998.
Changes in the Incidence of Disease in Young Infants
The incidence of early-onset neonatal disease remained fairlystable between 1990 and 1993 and then declined from 1993 to1998 (Figure 1). A steep decline coincided with the releaseof the consensus guidelines in 1996 (Figure 1). In the fourareas with continuous active surveillance, the incidence ofearly-onset disease declined by 65 percent, from 1.7 per 1000live births in 1993 to 0.6 per 1000 live births in 1998 (slope=–0.19,2=121.0, P<0.001). In California and Maryland, the largestdecline in incidence (28 percent and 34 percent, respectively)in a one-year period occurred between 1993 and 1994, whereasin Tennessee the largest decline (45 percent) occurred between1997 and 1998.
The incidence of early-onset disease declined more steeply amongblack neonates than among white neonates during this period,and the difference between blacks and whites in the incidenceof early-onset disease was reduced by 75 percent (Figure 2).In 1998 the rate of early-onset disease in both black neonates(0.8 per 1000 live births) and white neonates (0.5 per 1000live births) already approached the Healthy People 2010 objective16of a reduction in the incidence of early-onset disease to 0.5case per 1000 live births for all races (Figure 2).
Figure 2. Incidence of Early-Onset Invasive Group B Streptococcal Disease in Black Neonates and White Neonates in Four Active Surveillance Areas (California, Georgia, Tennessee, and Maryland), 1993 through 1998.
The Healthy People 2010 objectives, released by the U.S. Department of Health and Human Services, constitute a national prevention strategy for substantially improving the health of people in the United States.16 Live births for 1998 were approximated on the basis of 1997 data.
The overall rate of late-onset disease, in contrast, changedlittle between 1990 and 1998 (Figure 1). Between 1993 and 1998,there was a downward trend in the incidence of late-onset diseasethat was marginally significant by Poisson regression (slope=–0.05,2=3.3, P=0.07). In Georgia the rate of late-onset disease increasedfrom 0.34 per 1000 live births in 1997 to 0.52 per 1000 livebirths in 1998, whereas in other sites there were declines inthe rate of late-onset disease between 1997 and 1998.
Childhood and Adult Disease
We identified 175 culture-confirmed cases among children 90days to 14 years old. Although childhood disease representeda much smaller percentage of the disease burden than did neonataldisease (Table 2), patients from 90 days to 14 years of agewere roughly twice as likely to die from group B streptococcaldisease as newborns with early-onset disease (relative risk,1.9; 95 percent confidence interval, 1.1 to 3.2; P= 0.02). Twothirds (116 of 175, or 66 percent) of the cases among children90 days to 14 years old occurred in those less than 1 year ofage, with 54 percent (94 of 175) in children less than 6 monthsof age.
Of the 5118 cases among nonpregnant adults, the majority (53percent) presented with bacteremia, although adults presentedwith a wider variety of syndromes than did neonates. Rare manifestations(fewer than 30 cases during the surveillance period) includedabscess (28 cases), necrotizing fasciitis (14 cases), pericarditis(9 cases), and epiglottitis (2 cases). Only 2 percent of adultswith disease presented with meningitis.
The incidence of invasive disease in pregnant girls and womendeclined significantly, from 0.29 per 1000 live births in 1993to 0.23 per 1000 live births in 1998 (slope=–0.08, 2=4.86,P<0.03). The data from these patients were not sufficientlydetailed to determine the proportion of cases occurring duringlabor or after delivery. Among pregnant girls and women (345cases), bacteremia was again the primary manifestation, accountingfor 64 percent of cases. Bacteremic chorioamnionitis and endometritiseach occurred in 10 percent of cases (35 of 345), and septicabortion accounted for 7 percent of cases (23 of 345). From1993 to 1998, group B streptococcal disease among pregnant girlsand women represented 6.3 percent of all adult cases of invasivedisease (345 of 5463). Among those for whom the outcome of pregnancywas known (281 of 345, or 81 percent of pregnant girls and womenwith disease), 54 percent had infants who did not have clinicalillness, 17 percent had infants who had clinical illness butsurvived, and 29 percent had spontaneous abortions, stillborninfants, or infants who died of the infection.
The case fatality rate associated with adult disease was significantlyhigher than that associated with neonatal disease (12 percentvs. 4 percent; relative risk, 2.5; 95 percent confidence interval,2.0 to 3.1; P< 0.001). Moreover, adults 65 years of age orolder were at higher risk of dying from group B streptococcaldisease than adolescents and adults 15 to 64 years of age (15percent vs. 8 percent; relative risk, 1.9; 95 percent confidenceinterval, 1.7 to 2.4; P<0.001) (Table 2). Adults with meningitiswere also more likely to die than adults with other clinicalsyndromes (28 percent vs. 12 percent; relative risk, 2.1; 95percent confidence interval, 1.4 to 3.2; P=0.003). During thesix-year study period, one pregnant woman died of invasive groupB streptococcal disease.
For the surveillance areas in which underlying conditions associatedwith invasive disease were recorded (California starting in1994 and Connecticut, New York, and Oregon starting in 1997),information on the presence of underlying conditions was availablefor 63 percent of adults with invasive disease (1164 of 1854).The majority (70 percent) of these adults had at least one ofthe following underlying conditions: diabetes mellitus (37 percent),cardiovascular disease (23 percent), nonhematologic cancer (19percent), congestive heart failure (15 percent), alcoholism(11 percent), and cirrhosis (8 percent).
The rates of adult disease fluctuated during the six-year periodbut showed no evidence of a decline. Moreover, in contrast toearly-onset disease, the rate of adult disease in blacks didnot decline from 1993 to 1998 (slope=–0.004, 2=0.06, P=0.80);in 1998 the risk of invasive disease among black adults at least15 years of age remained twice that among white adults (relativerisk, 2.0; 95 percent confidence interval, 1.7 to 2.3; P<0.001).
Projections to the U.S. Population in 1998
On the basis of data from all surveillance areas in 1998, theprojected number of cases of invasive group B streptococcaldisease in the United States according to the age at diseaseonset is shown in Table 3. For those 15 years of age or over,the gap in incidence between blacks and whites remains large(data not shown).
Table 3. Projected Cases of Invasive Group B Streptococcal Disease in the United States as a Whole, 1998.
Using surveillance data from 1993 to project incidence to theUnited States as a whole, we estimated a base-line number of6100 cases of early-onset disease annually before active preventionefforts began. We thus estimate that in 1998, 3900 early-onsetneonatal cases and 200 neonatal deaths were prevented in theUnited States by the intrapartum use of antibiotic prophylaxis.
Discussion
The incidence of early-onset neonatal group B streptococcaldisease declined by a striking 65 percent from 1993 to 1998within our surveillance areas. Evidence of a decline in somesurveillance areas was first apparent in 1994 and 19956 andcan be documented in all four areas of continuous surveillanceby 1997. This decline was due in part to a large decrease inthe incidence of early-onset disease in black neonates from1993 to 1998. The gap between black and white infants in theincidence of early-onset disease was reduced by 75 percent duringthis period. If one assumes that the rate of early-onset diseasein 1998 would have remained unchanged from 1993 in the absenceof active prevention measures, then nearly 4000 cases of early-onsetdisease were prevented in the United States in 1998.
Declining rates of early-onset neonatal disease coincide withthe active public health and clinical efforts to increase theadministration of prophylactic intrapartum antibiotics to mothersat risk of transmitting the disease to their newborns. Between1994 and 1997, the proportion of hospitals with a policy forthe prevention of neonatal group B streptococcal disease increasedfrom 39 percent to 58 percent.17
It remains unclear why the rates of invasive group B streptococcalinfection are higher among blacks than in other racial groups.However, implementation of prevention in this group at higherrisk has effectively reduced the rate of early-onset diseaseamong black newborns.
The potential effect of intrapartum antibiotic prophylaxis onlate-onset disease has not been evaluated. In some infants,late-onset infections develop after passage through a heavilycolonized birth canal, and reduction in the degree of colonizationmight result from the use of parenteral antibiotics during labor.However, late-onset disease has a maternal origin in only 50percent of cases.18 We did not find evidence of a significantdecline in the incidence of late-onset disease as a result ofperinatal preventive efforts (Figure 1), although there is evidenceto suggest a small downward trend. It is possible that the sizeof the population under study in our surveillance areas wasinsufficient for an adequate assessment of the effect of pre-ventiveefforts on the incidence of late-onset disease.
Because pregnant women who have been colonized by group B streptococciare at increased risk for amnionitis,19,20 perinatal disease-preventionstrategies may also reduce the incidence of disease among pregnantwomen. A recent study found that rates of chorioamnionitis andendometritis decreased significantly after the adoption of aggressivestrategies for the prevention of group B streptococcal disease.21In the areas with continuous surveillance from 1993 to 1998,the incidence of invasive disease in pregnant girls and womendeclined significantly.
In contrast to the decline in early-onset neonatal disease,the rate of adult disease did not decline from 1993 to 1998.The gap in the incidence of disease between black adults andwhite adults also remained unchanged.5
The epidemiologic features of adult disease during this periodare similar to those described before active efforts for theprevention of neonatal disease. As observed in 1990, adultsover the age of 65 remained at the highest risk of dying frominvasive group B streptococcal disease.5 Similarly, the casefatality rate for adults with meningitis was higher than thatfor adults with other clinical presentations. Adults also hadunderlying conditions that have been previously identified asindependent risk factors for invasive disease in adults.7
The surveillance data that we analyzed have certain limitations.Foremost is the low representation of Hispanics and membersof races other than blacks and whites in our surveillance population,factors that may bias our projections of the incidence of diseasein the United States as a whole. Furthermore, clinicians insurveillance areas were exposed to preventive education andsurveys and thus may have had a heightened awareness of groupB streptococcal disease, as compared with practitioners in otherregions. In addition, the areas participating in the active-surveillanceprogram changed during the period from 1993 to 1998, thus limitingour analyses of trends over time to four areas with continuoussurveillance.
Despite these limitations, our surveillance system was ableto capture laboratory-confirmed cases of invasive disease froma large, multistate population base; the resulting data providedthe opportunity to characterize key clinical and epidemiologiccharacteristics of group B streptococcal disease in the eraof perinatal disease prevention. The trends we observed suggestthat preventive strategies have led to substantial declinesin the incidence of early-onset disease. However, we estimatethat there were still over 2000 cases of early-onset group Bstreptococcal disease in neonates in the United States in 1998.Assessing how many of these cases represent failures of preventionwill be important in setting objectives for prevention in thefuture. Moreover, as the use of intrapartum antibiotic prophylaxisincreases, closer surveillance for antibiotic resistance amongall bacteria causing neonatal sepsis is important.22 To date,penicillin remains the first-line antibiotic for intrapartumprophylaxis, and penicillin-resistant group B streptococci havenot yet been detected. However, erythromycin resistance hasbeen found in 7.4 to 15 percent of isolates, and clindamycinresistance in 3.4 to 13 percent of isolates.23,24
Development of vaccines against group B streptococci may decreasethe need for antibiotic prophylaxis in the future.25,26 Suchvaccines may also offer protection for pregnant women and forthe elderly,25 for whom the incidence of disease and case fatalityrates remain high.27
Supported by the CDC National Center for Infectious DiseasesEmerging Infection Program Network and the National VaccineProgram.
We are indebted to the Active Bacterial Core Surveillance teamand to the infection-control practitioners and clinical microbiologylaboratory personnel who participated in collection of the data.
Source Information
From the Centers for Disease Control and Prevention, Atlanta (S.J.S., S.Z., A.S.); the Emory University School of Medicine and Veterans Affairs Medical Services, Atlanta (M.M.F.); the School of Public Health, University of California, Berkeley (A.L.R.); the Johns Hopkins School of Hygiene and Public Health, Baltimore (L.H.H.); Vanderbilt Medical Center, Nashville (L.B.L.); the Connecticut Department of Public Health, Hartford (J.L.H.); the Minnesota Department of Health, Minneapolis (R.D.); and the Department of Human Resources, Portland, Oreg. (P.R.C.). The members of the surveillance team are listed in the Appendix.
Address reprint requests to Dr. Schrag at the Respiratory Diseases Branch, MS-C23, Division of Bacterial and Mycotic Disease, Centers for Disease Control and Prevention, 1600 Clifton Rd., Atlanta, GA 30333, or at zha6{at}cdc.gov.
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Appendix
The members of the surveillance team were P. Adams, M. Bardsley,B. Barnes, N. Barrett, W. Baughman, L. Billmann, M. Cassidy,P. Daily, J. Donegan, D. Dwyer, L. Gelling, S. Ladd-Wilson,C. Morin, P. Mshar, N. Mukerjee, M. Pass, Q. Phan, J. Rainbow,K.A. Robinson, N. Rosenstein, G. Rothrock, M. Sattah, K. Stefonek,L. Triden, K. White, S. Whitfield, C. Whitney, C. Wright, andE. Zell.
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