Epidemiology of Invasive Group B Streptococcal Disease in the United States, 1999-2005

ORIGINAL CONTRIBUTION

Epidemiology of Invasive Group BStreptococcal Disease in the United States,1999-2005Christina R. Phares, PhDRuth Lynfield, MDMonica M. Farley, MDJanet Mohle-Boetani, MDLee H. Harrison, MDSusan Petit, MPHAllen S. Craig, MDWilliam Schaffner, MDShelley M. Zansky, PhDKen Gershman, MDKaren R. Stefonek, MPHBernadette A. Albanese, MDElizabeth R. Zell, MStatAnne Schuchat, MDStephanie J. Schrag, DPhil

IN THE 1970S, GROUP B STREPTOCOC-cus emerged as the leading causeof sepsis and meningitis in the firstweek of life.1 By 1996, a perinatal

disease prevention strategy based on in-trapartum chemoprophylaxis was is-sued by the Centers for Disease Con-trol and Prevention (CDC), theAmerican College of Obstetricians andGynecologists, and the American Acad-emy of Pediatrics.2-4 Two recom-mended approaches for identifying che-moprophylaxis candidates were widelyadopted in the United States and re-sulted in substantial declines in dis-ease in infants younger than 7 days (alsoknown as early onset disease).5,6

In 2002, revised guidelines recom-mended antenatal culture-based screen-ing as the optimal method for identi-fying chemoprophylaxis candidates.7

Disease trends following the release ofthese guidelines have not yet been wellstudied. In addition to illness in the firstweek of life, group B streptococcus alsocauses invasive disease in older in-fants, pregnant women, children andyoung adults with underlying medicalconditions, and older adults. Cases out-side the perinatal risk period account

for nearly 90% of the national burdenof disease,8 and the proportion of pa-tients who die in these age groups, par-ticularly the elderly, are higher than for

Author Affiliations are listed at the end of this ar-ticle.Corresponding Author: Christina R. Phares, PhD, Cen-ters for Disease Control and Prevention, 1600 CliftonRd NE, Mailstop E-03, Atlanta, GA 30333 ([email protected]).

Context Group B streptococcus is a leading infectious cause of morbidity in new-borns and causes substantial disease in elderly individuals. Guidelines for preventionof perinatal disease through intrapartum chemoprophylaxis were revised in 2002. Can-didate vaccines are under development.

Objective To describe disease trends among populations that might benefit fromvaccination and among newborns during a period of evolving prevention strategies.

Design and Setting Analysis of active, population-based surveillance in 10 statesparticipating in the Active Bacterial Core surveillance/Emerging Infections Program Net-work.

Main Outcome Measures Age- and race-specific incidence of invasive group Bstreptococcal disease.

Results There were 14 573 cases of invasive group B streptococcal disease during1999-2005, including 1348 deaths. The incidence of invasive group B streptococcaldisease among infants from birth through 6 days decreased from 0.47 per 1000 livebirths in 1999-2001 to 0.34 per 1000 live births in 2003-2005 (P� .001), a relativereduction of 27% (95% confidence interval [CI], 16%-37%). Incidence remained stableamong infants aged 7 through 89 days (mean, 0.34 per 1000 live births) and preg-nant women (mean, 0.12 per 1000 live births). Among persons aged 15 through 64years, disease incidence increased from 3.4 per 100 000 population in 1999 to 5.0 per100 000 in 2005 (�2

1 for trend, 57; P� .001), a relative increase of 48% (95% CI, 32%-65%). Among adults 65 years or older, incidence increased from 21.5 per 100 000 to26.0 per 100 000 (�2

1 for trend, 15; P� .001), a relative increase of 20% (95% CI, 8%-35%). All 4882 isolates tested were susceptible to penicillin, ampicillin, and vanco-mycin, but 32% and 15% were resistant to erythromycin and clindamycin, respec-tively. Serotypes Ia, Ib, II, III, and V accounted for 96% of neonatal cases and 88% ofadult cases.

Conclusions Among infants from birth through 6 days, the incidence of group Bstreptococcal disease was lower in 2003-2005 relative to 1999-2001. This reductioncoincided with the release of revised disease prevention guidelines in 2002. However,the disease burden in adults is substantial and increased significantly during the studyperiod.JAMA. 2008;299(17):2056-2065 www.jama.com

2056 JAMA, May 7, 2008—Vol 299, No. 17 (Reprinted) ©2008 American Medical Association. All rights reserved.

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newborns.5 Moreover, black race is as-sociated with an increased incidence ofinvasive group B streptococcal diseaseacross the age spectrum.

Current prevention strategies may beinadequate to address racial dispari-ties in incidence of early onset dis-ease.9 Furthermore, strategies to pre-vent disease after the first week of lifehave yet to emerge. New preventionstrategies are therefore critical, andpolysaccharide-protein conjugate vac-cines have been developed for each ofthe major disease-causing group Bstreptococcus capsular types (Ia, Ib, II,III, and V), and their safety and immu-nogenicity have been evaluated inhealthy nonpregnant adults and preg-nant women.10-18

The epidemiology of group B strep-tococcal disease is dynamic, and con-tinued surveillance to monitor trendsacross age groups is necessary. For ex-ample, an increase in disease inci-dence among nonpregnant adults hasbeen documented in past decades,19 butwhether that trend has continued is un-known. In addition, the long-term im-pact of widespread intrapartum che-moprophylaxis against perinatal diseaseon incidence trends and antimicrobialsusceptibilities is still unfolding. Fi-nally, current information on disease-causing serotypes is critical to opti-mize conjugate vaccine formulations forgroup B streptococcus. To address theseissues, we evaluated trends and char-acteristics among nearly 15 000 casesof laboratory-confirmed invasive groupB streptococcal disease identified bypopulation-based, multistate surveil-lance over a recent 7-year period (1999-2005).

METHODSSurveillance

Data were collected through the Ac-tive Bacterial Core surveillance (ABCs)/Emerging Infections Program Net-work, a collaboration between the CDC,state health departments, and univer-sities. The ABCs methods have beendescribed elsewhere.20 Briefly, partici-pating states conduct active, popula-tion-based, laboratory surveillance for

invasive disease due to group B strep-tococcus and other pathogens. A groupB streptococcus case is defined as iso-lation of the organism from a nor-mally sterile site (for example, blood orcerebrospinal fluid [CSF]) in a surveil-lance area resident. Cases with groupB streptococcus isolated from a sterilesite in a stillborn infant—or from theplacenta, amniotic fluid, or conceptusin the context of a fetal death—wereclassified as maternal, since the infantwas not live born. For the case of live-born infants, placental and amniotic iso-lates were not considered sterile sites.Cases were actively ascertained by rou-tine contact with all laboratories pro-cessing sterile-site specimens for sur-veillance area residents. Periodiclaboratory audits were performed to en-sure completeness of reporting. Epide-miologic and clinical data, including pa-tient deaths, were captured by medicalrecord review using a standardizedform. However, cause of death (as de-termined, for example, at autopsy) wasnot captured.

For case individuals younger than 1year, areas under continuous surveil-lance for group B streptococcus from1999-2005 included all of Connecti-cut, Maryland, and Minnesota, andparts of California (3 Bay Area coun-ties), Georgia (20-county Atlanta area),New York (15-county Rochester and Al-bany areas), Oregon (Clackamas, Mult-nomah, and Washington counties), andTennessee (5 urban counties). After thestart of the study period, surveillancewas expanded to cover 6 additional ur-ban counties in Tennessee (since Au-gust 1, 1999), the 5-county Denver areain Colorado (since July 1, 2000), andall of Georgia and New Mexico (sinceJanuary 1, 2004). For individuals 1 yearor older, the same surveillance areas ap-plied with the following exceptions: inConnecticut and Colorado (5-countyDenver area), data were collected foronly 1999-2003; in Georgia, surveil-lance was limited to the 20-county At-lanta area throughout 1999-2005. Over-all, in 2005, surveillance covered apopulation of 27 350 255 persons and454 476 live births.

DefinitionsNeonatal cases were categorized asearly onset if group B streptococcuswas isolated from infants youngerthan 1 week or as late-onset if infantswere 7 through 89 days old. Neonatalcases were classified as fatal when aliveborn infant with invasive diseasedied; stillbirths and spontaneousabortions were not counted as neona-tal fatalities. Preterm birth wasdefined as birth at less than 37 weeks’gestation and was captured for casesyounger than 90 days. After earlyinfancy, cases were classified as pedi-atric (90 days-14 years and not preg-nant), pregnancy-associated, or adult(�15 years and not pregnant).

Clinical syndromes were assignedbased on physician diagnoses re-corded in the medical record; for men-ingitis, all cases of group B streptococ-cus isolated from CSF were alsoincluded. Cases could be categorizedinto multiple syndromes with the ex-ception of bacteremia without focus,which was defined as a positive bloodculture result in the absence of an-other clinical syndrome. Race was de-termined by medical record review (andthus may represent self-identificationor clinician identification) and catego-rized by ABCs personnel.

Group B Streptococcus Isolates

Two reference laboratories (CDC andMinnesota Department of Health) per-formed group B streptococcus serotyp-ing and susceptibility testing on a sub-set of isolates. Isolates were serotypedwith rabbit antisera to group B strep-tococcus capsular polysaccharide typesIa, Ib, and II through VIII by latex ag-glutination.21 When latex tests were in-determinate, the Lancefield methodwas used.22 When both tests were in-determinate, the isolate was classifiedas nontypeable. Isolate susceptibility topenicillin, ampicillin, erythromycin,clindamycin, and vancomycin was de-termined by broth dilution using in-terpretive standards established by theClinical and Laboratory Standards In-stitute.23 Inducible clindamycin resis-tance was not evaluated.

INVASIVE GROUP B STREPTOCOCCAL DISEASE IN THE UNITED STATES, 1999-2005

©2008 American Medical Association. All rights reserved. (Reprinted) JAMA, May 7, 2008—Vol 299, No. 17 2057


Statistical AnalysisIncidence calculations for case indi-viduals 90 days or older used NationalCenter for Health Statistics bridged-race postcensal population estimatesas denominators for the years 2000-2005 and US Bureau of Census esti-mates for 1999. Incidence data forthose younger than 90 days and forpregnancy-associated cases used thenumber of live births to surveillancearea residents as determined byState Vital Records or National VitalStatistics Reports from 1999-2004;2004 data were used for the 2005denominator.

To ensure comparability over time,annual incidence calculations ex-cluded New Mexico, since data fromthis state were only available during2004-2005; for cases 1 year or older,Connecticut, Colorado, and areas ofGeorgia outside the 20-county At-lanta area were excluded, since data forthese areas were not collected in 2004-2005. Other analyses comparing casecharacteristics over time were simi-larly restricted. Analyses of isolate char-acteristics were limited to areas forwhich at least 50% of case isolates wereserotyped annually, which includedGeorgia, New York, and Oregon (1999-2005); Colorado and Minnesota (2001-2005); Maryland (2003-2005); and NewMexico (2005). All other analyses usedall available data.

Risk ratios (RRs) and confidenceintervals (CIs) are presented for cat-egorical data. To evaluate annualtrends over time, �2 for trend was cal-culated after confirming no departuresfrom linearity. Percentage change wasused to compare incidence from abaseline period to a later period (eg,before vs after the release of earlyonset disease guidelines or first vslast year of study period). Percentagechange was calculated as [(laterr a t e − b a s e l i n e r a t e ) / b a s e l i n erate]�100. To assess seasonal vari-ability, a 3-month moving average wasused to calculate monthly incidenceover time. For all incidence calcula-tions, cases with unknown race weredistributed according to those withknown race for each surveillance sitewithin 8 age categories (�1 year, 1year, 2-4 years, 5-17 years, 18-34years, 35-49 years, 50-64 years, and�65 years). For all other statistics (forexample, the proportion of individualswho died, by race), race as recordedwas used. For national estimates ofcases, age- and race-specific incidenceof disease were applied from theaggregate surveillance area to the ageand racial distribution of the US popu-lation or live births as appropriate.Data were analyzed using SAS version9 (SAS Institute Inc, Cary, NorthCarolina); P� .05 was considered sta-tistically significant.

ApprovalsThe CDC determined that our surveil-lance activities, including isolate col-lection, were exempt from CDC insti-tutional review and did not requireinformed consent. Each of the 10 par-ticipating surveillance sites alsoreviewed the protocol and eitherobtained appropriate institutionalreview board approval or determinedthat the activity was exempt fromreview.

RESULTS

From 1999 through 2005, surveil-lance identified 14 573 cases of inva-sive group B streptococcal disease.TABLE 1 shows the standardized inci-dence and estimated national burdenof disease and death associated withgroup B streptococcus by age group forthe United States in 2005, when an es-timated 21 500 cases occurred, includ-ing 1700 fatalities. The observed inci-dence among surveillance area residentsin 2005 was 7.5 per 100 000 popula-tion; among individuals with knownoutcome (2027/2056 [98.6%]), 160(7.9%) died.

Among all 2056 case individualsidentified in 2005, 1119 (54%) werewhite, 566 (28%) were black, 51 (2%)were Asian or Pacific Islander, 33(�2%) were American Indian orAlaska Native, and 287 (14%) were ofunknown race. Incidence of invasive

Table 1. Number of Cases of Invasive Group B Streptococcal Disease, Number of Deaths, and Incidence by Age in Surveillance Areas(1999-2005) and the United States as a Whole (2005)

Age Group

Birth-6 d 7-89 d 1-14 y 15-64 ya �65 y Total

Observed counts for surveillance areas,1999-2005

No. of cases 1232 1036 90 6496 5576 14 573b

No. of deathsc 83 48 11 472 730 1348d

Estimated incidence and projected countsfor United States, 2005e

Incidence 0.35/1000live births

0.33/1000live births

0.22/100 000population




No. of cases 1425 1375 124 9207 9308 21 439

No. of deathsc 63 46 8 557 1067 1741a Includes 409 pregnant women.bTotal number of cases includes 143 individuals aged 90 days to 12 months.cOutcome was known for 99% of surveillance individuals younger than 1 year and 95% of those 1 year or older; thus, the observed and projected number of deaths is a minimum

and should not be used to generate direct estimates of case-fatality rates.dTotal number of deaths includes 4 deaths among individuals aged 90 days to 12 months.eAge- and race-specific incidence of disease was applied from the aggregate surveillance area to the age and racial distribution of the US population or US live births as appro-

priate.




group B streptococcal disease was 12.8per 100 000 among blacks, 6.5 per100 000 among whites, and 5.1 per100 000 among all other races com-bined. Overall incidence among blackswas 2 times higher than among whites(RR, 2.0; 95% CI, 1.8-2.2) and at least1.5 times higher in every age category(FIGURE 1A). The magnitude of theassociation was greatest for neonates(RR for early onset disease, 4.0; 95%CI, 2.9-5.5; RR for late-onset disease,5.1; 95% CI, 3.7-7.0) and pregnantwomen (RR, 5.0; 95% CI, 2.9-8.7)and least for adults 15 years or older(RR, 2.0; 95% CI, 1.5-2.6). Finally,the proportion who died was signifi-cantly higher for blacks than whitesamong individuals younger than 7days and those 45 years or older(Figure 1B).

Early Onset Disease

Surveillance identified 1232 cases ofearly onset disease. Disease incidencedecreased 27% (95% CI, 16%-37%)after the 2002 release of revised earlyonset disease prevention guidelines,from 0.47 per 1000 live births in

1999-2001 to 0.34 per 1000 live birthsin 2003-2005 (FIGURE 2). However,successive small increases in inci-dence occurred in 2004 and 2005(Figure 2). These increases weredriven primarily by black infants, in

whom there was a s ign i f i can tincrease in incidence from 0.52 per1000 in 2003 to 0.89 per 1000 in2005 (�2

1 for trend, 7.9; P = .005).From 2003-2005, white infants bornat term were the only group in whom

Figure 2. Incidence of Invasive Group B Streptococcal Disease Among Infants (�90 Days)and Pregnant Women in Select US Areas, 1999-2005

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Early onset disease (age <7 d)Late-onset disease (age 7-89 d)

Rates correspond to areas under continuous surveillance since 1999 (California [3-county Bay Area], Con-necticut [state; children aged �1 year only], Georgia [20-county Atlanta area], Maryland [state], Minnesota[state], New York [15 Rochester and Albany counties], Oregon [Clackamas, Multnomah, and Washington coun-ties], and Tennessee [5 urban counties]), with the addition of 6 further urban counties in Tennessee in 2000and the 5-county Denver area in Colorado in 2001 (children aged �1 year only).

Figure 1. Incidence of Invasive Group B Streptococcal Disease and Proportion of Individuals Who Died, by Race and Age in Select US Areas,2005

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Incidence of invasive group B streptococcal disease by raceand age in select US areas, 2005

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Birth-6 7-89 1-24 25-34 35-44 45-54 55-64 65-74 75-84 >84

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Days Years

Individuals with unknown race (287/2056 [14%]) were distributed according to those with known race within site and age strata. Those with unknown race other thanblack or white are excluded here. A, Incidence was significantly higher among blacks than among whites for every age category (ie, the lower 95% confidence limit foreach age-specific black-to-white rate ratio was �1). For individuals 90 days or older, denominator corresponds to population estimates for 2005; for those youngerthan 90 days, denominator corresponds to estimates of live births for 2004. Incidence rates correspond to the following surveillance areas: California (3-county BayArea), Colorado (5-county Denver area; children aged �1 year only), Connecticut (state; children aged �1 year only), Georgia (20-county Atlanta area), Maryland(state), Minnesota (state), New York (15 Rochester and Albany counties), Oregon (Clackamas, Multnomah, and Washington counties), and Tennessee (11 urbancounties). B, Proportion based on all available data from 1999-2005. P� .05 for �2

1 test comparing proportion who died, by race, for individuals from birth through6 days, 45-54 years, 55-64 years, and �84 years. P� .01 for �2

1 test comparing proportion who died, by race, for adults aged 65-74 years and 75-84 years.




incidence trended toward a decline,from 0.23 per 1000 to 0.16 per 1000(�2

1 for trend, 3.1; P=.08).Among infants with early onset

disease, 72% had positive sterile-siteculture results within the first 24 hoursof life, and 95% had positive resultswithin the first 48 hours. Most iso-lates were from blood (96%) or CSF(4%). The most commonly identifiedsyndromes were bacteremia without fo-cus (83%), pneumonia (9%), and men-ingitis (7%). Overall, among 1224 in-fants for whom outcome was known,83 (6.8%) died. The proportion whodied varied by year (range, 5%-9%), al-though no trend over time was ob-served. It also varied by syndrome, from9% (10/114) for pneumonia to 4% (3/81) for meningitis. Among infants withearly onset disease, 23% were born pre-term. From 1999-2005, the percent-age of infants with early onset diseasewho were born preterm increased from18% to 33% (�2

1 for trend, 16; P� .001);however, the incidence of early onsetdisease among preterm infants did notincrease significantly. The median ges-tational age of infants born preterm was31 weeks (first and third quartiles, 26and 35 weeks), and the risk of deathamong preterm cases was nearly 8 timesthat of term cases (preterm: 19.9% died;term: 2.6% died [RR, 7.7; 95% CI, 4.9-12.3]).

Late-Onset Disease

Surveillance identified 1036 cases oflate-onset disease. Incidence re-mained generally stable, averaging 0.34per 1000 live births. Similar to early on-set disease, incidence of late-onset dis-ease increased slightly during 2003-2005 (Figure 2).

The median age at first positive cul-ture result for infants with late-onsetdisease was 37 days (first and thirdquartiles, 23 and 53 days). Isolateswere predominantly obtained fromblood (79%) or CSF (19%). Whencompared with early onset cases, ahigher proportion of late-onset casesmanifested as meningitis (27% vs 7%;�2

1 test, P� .001). Other disease mani-festations included bacteremia without

focus (65%), bacteremic cellulitis(3%), and pneumonia (3%). Overall,the proportion of infants with knownoutcome who died was 4.7% (48/1027). By syndrome, the proportionwho died was 3% (23/669) for bacter-emia without focus, 18% (5/28) forpneumonia, and 7% (19/279) for men-ingitis. Among the 69% (718/1036) oflate-onset cases for whom gestationalage was known, 52% (373/718) wereborn preterm, and that proportion wasstable over time. Among infants withlate-onset disease that occurred in2003-2005 (for whom information ongestational age was �90% complete),the median gestational age of infantsborn preterm was 30 weeks (first andthird quartiles, 27 and 34 weeks), andthe risk of death for preterm infantswas more than 3 times that of terminfants (preterm: 5.3% died; term:1.4% died [RR, 3.7; 95% CI, 1.1-13.0]).

Pregnancy-Associated Disease

A total of 409 invasive group B strep-tococcal infections occurred in preg-nant teenagers and women (0.12 per1000 live births; yearly range: 0.11-0.14 per 1000 live births) (Figure 2).The median age at onset was 28 years(first and third quartiles, 22 and 33years). Half (203/409) of these caseswere associated with infection of theupper genital tract, placenta, or amni-otic sac, resulting in fetal death. Othermanifestations included bacteremiawithout focus (31%), endometritiswithout fetal death (8%), chorioamni-onitis without fetal death (4%), pneu-monia (2%), and puerperal sepsis(2%). Endocarditis was observed in 1case.

A total of 211 (52%) isolates frompregnancy-associated cases were ob-tained from blood; 187 (46%) from theplacenta, amniotic fluid, or concep-tus; 8 (2%) from peritoneal fluid; andthe remainder from other sterile sites.One individual with pregnancy-associated disease died. Among thosefor whom pregnancy outcome wasknown (368/409 [90%]), 61% had aspontaneous abortion or stillborn in-

fant, 30% had infants without appar-ent illness, 5% had live-born infantswho developed clinical infections, and4% had induced abortions. Most preg-nancy-related cases (330/409 [81%])occurred in the absence of additionalunderlying conditions; 79 occurredwith at least 1 additional underlyingcondition or risk factor including, in or-der of decreasing frequency, smoking,asthma, diabetes, obesity, and alcoholor drug abuse.

Childhood Disease

Surveillance identified 233 cases ofinvasive group B streptococcal diseasein children aged 90 days through 14years. Incidence of pediatric diseasewas 0.56 per 100 000 (yearly range,0.37-0.73 per 100 000), and no sus-tained change over time was observed.Sixty-one percent (143/233) of thesecases occurred in children aged 90days through 12 months, and theremaining third (90/233) were evenlydistributed among children aged 1through 14 years. Among all 233 chil-dren, bacteremia without focus wasthe most common syndrome, account-ing for 58% of the cases, followed bymeningitis (19%), pneumonia (7%),septic arthritis (5%), and peritonitis(4%). The proportion with knownoutcome who died was lower amongchildren aged 90 days through 12months (4/142 [3%]) than amongthose aged 1 through 14 years (11/85[13%]). Only 11% (16/143) of chil-dren aged 90 days through 12 monthshad an underlying condition (exclud-ing preterm birth), but 44% (40/90) ofchildren aged 1 through 14 years hadat least 1 condition. Among these 40older children, the most commonunderlying factors were neurologicdisorders (25%), immunosuppressiveconditions (23%), asthma (23%),malignancy (15%), and renal disease(13%).

Adult Disease

Surveillance identified 6087 casesamong persons aged 15 through 64years (and not pregnant) and 5576among those 65 years or older (me-




dian age overall, 63 years; first andthird quartiles, 50 and 77 years). Dis-ease incidence increased significantlyduring the study period (FIGURE 3).Among persons aged 15 through 64years, incidence increased from 3.4per 100 000 population in 1999 to5.0 per 100 000 in 2005 (�2

1 for trend,57; P � .001), a relative increase of48% (95% CI, 32%-65%); amongthose 65 years or older, incidenceincreased from 21.5 per 100 000 to26.0 per 100 000 (�2

1 for trend, 15;P� .001), a relative increase of 20%(95% CI, 8%-35%).These valuestranslate to a 32% (95% CI, 22%-43%) increase in the overall inci-dence of adul t d i sease , whichincreased from 6.0 per 100 000 in1999 to 7.9 per 100 000 in 2005 (�2

1

for trend, 63; P� .001). The propor-tion with known outcome who diedwas highest in the oldest age groups(Figure 1B). Seasonal variability wasevident, with distinct peaks occur-ring each year during the later sum-mer months (FIGURE 4). The sameseasonal periodicity was observed forboth age groups (data not shown).

Among all 11 663 adults, 81%were diagnosed by blood culturesalone and the remainder from syno-vial fluid (7%), bone (6%), peritonealfluid (3%), pleural fluid (1%), CSF(1%), and other sites (�1%). Themost common clinical syndromeswere bacteremia without focus(48%), bacteremic cellulitis (22%),pneumonia (11%), osteomyelitis(9%), arthritis (9%), peritonitis (3%),and abscess (3%). Less commonmanifestations included endocarditis/pericarditis, meningitis, necrotizingfasciitis, and toxic shock–like syn-drome. In 2005, underlying condi-tions and factors included diabetesmellitus (41%), heart disease (36%),and malignancy (17%). Other com-mon factors associated with casesamong adults included smoking,obesity, neurologic disorders, renaldisease, immunosuppressive condi-tions, liver disease, and lung disease.Altogether, nearly 88% of adult caseshad at least 1 underlying condition.

Serotypes and AntimicrobialSusceptibilityIn the 7 surveillance areas that col-lected isolates during all or part of thestudy period, 8153 cases occurred; se-rotyping was performed on 6156 (76%)of these and susceptibility testing on4882 (60%). Individuals for whom iso-

lates were and were not serotyped didnot differ with respect to age, sex, orfatalities. Isolates collected from bloodor CSF were more likely to be sero-typed than isolates collected from othersterile sites (�2

1 test, P� .001).Among 528 early onset cases with

serotype testing, the most frequent

Figure 3. Incidence of Invasive Group B Streptococcal Disease Among Adults (�15 Years) inSelect US Areas, 1999-2005

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Rates correspond to areas under continuous surveillance since 1999 (California [3-county Bay Area], Georgia[20-county Atlanta area], Maryland [state], Minnesota [state], New York [15 Rochester and Albany counties],Oregon [Clackamas, Multnomah, and Washington counties], and Tennessee [5 urban counties]), with the ad-dition of 6 further urban counties in Tennessee in 2000.

Figure 4. Monthly Incidence of Invasive Group B Streptococcal Disease Among Adults (�15Years) in Select US Areas, 1999-2005

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Three-month moving average of rates corresponds to areas under continuous surveillance since 1999 (Cali-fornia [3-county Bay Area], Georgia [20-county Atlanta area], Maryland [state], Minnesota [state], New York[15 Rochester and Albany counties], Oregon [Clackamas, Multnomah, and Washington counties], and Ten-nessee [5 urban counties]), with the addition of 6 further urban counties in Tennessee in 2000.




serotypes were Ia (30%), III (28%), V(18%), and II (13%). The distributionof serotypes for 172 pregnancy-associated cases was similar. In con-trast, among 469 late-onset cases withtesting, serotype III accounted for half(239/469 [51%]) of all cases; theremainder were predominately sero-types Ia (24%) and V (14%). In 4987nonpregnant pediatric and adult cases,serotype V predominated, accountingfor 31% of cases, followed by sero-types Ia (24%), II (12%), and III(12%). Serotype distribution in 2005was similar to the overall distributiondescribed above.

TABLE 2 shows the proportion ofcases associated with death or menin-gitis by serotype and age at onset. Inseparate regression models thatadjusted for age at onset, cases causedby serotype Ia had a significantlyhigher risk of death than did thosecaused by any other serotype (RR, 1.3;95% CI, 1.1-1.6), while those causedby serotype III were associated with anincreased risk of meningitis as com-pared with those caused by other sero-types (RR, 1.6; 95% CI, 1.3-2.1).

All 4882 isolates submitted for sus-ceptibility testing were susceptible topenicillin and ampicillin; 12 isolates,however, had minimum inhibitoryconcentrations approaching the up-per level of susceptibility for 1 or more

�-lactam agents. All isolates were sus-ceptible to vancomycin; 1566 (32%)were resistant to erythromycin; and 757(15%) were resistant to clindamycin.Virtually all (751/757 [99%]) isolatesthat were resistant to clindamycin werealso resistant to erythromycin. Eryth-romycin resistance was highest amongserotype V isolates as compared withother serotypes (50% vs 26%; �2

1 test,P� .001).

COMMENT

The ABCs system, now covering acatchment of approximately 26 mil-lion residents, has provided the UnitedStates with a powerful tool for guidingand evaluating group B streptococcusprevention strategies. Following theissuance of the first consensus group Bstreptococcal disease preventionguidelines, this network documenteda 68% decline in incidence of earlyonset group B streptococcal disease,from 1.7 per 1000 live births in 1993to 0.6 per 1000 live births in 1998.5,7

Guidelines issued in 2002 that recom-mended universal antenatal screeningfor group B streptococcus were pre-dicted to further reduce incidence to0.32 per 1000 live births.24 Our analy-sis indicates that incidence of earlyonset disease in the years followingthe guidelines decreased to 0.34 per1000 live births, very close to the pre-

dicted impact. Although robust fordetecting changes in disease trendsover time, our data underestimate thetrue burden of perinatal diseasebecause the ABCs system focuses onculture-proven disease—thus missingcases of clinical sepsis—and excludesstillbirths and spontaneous abortions,which may be caused by group Bstreptococcal infection.

Although the overall incidence ofearly onset disease in 2003-2005 waslower than in preceding years, smallsuccessive increases were observed in2004 and 2005. Whether this trend con-tinues remains to be seen. The signifi-cant increase in incidence among blackinfants in this period is particularly con-cerning and requires investigation. Ad-ditional studies including cases andnoncases for comparison are needed toclarify the driving factors.25

Analyses of late-onset disease inci-dence trends in the 1990s suggested thatintrapartum chemoprophylaxis doesnot prevent late-onset disease.5,26 Ouranalysis of late-onset disease trendsfrom 1999-2005 further supports thisconclusion. Future years of surveil-lance will be important to assesswhether the upturn in incidence in2003-2005 is sustained.

Prior analyses suggested that intra-partum chemoprophylaxis against earlyonset disease also protected against ma-

Table 2. Proportion of Cases Associated With Death or Meningitis by Serotype and Age at Onset, 1999-2005

Cases

Serotype, No. (%)

Ia Ib II III V Othera Total

Early Onset Disease (Birth Through 6 d)

Cases, No. (% of total)b 157 (29.7) 37 (7.0) 69 (13.1) 146 (27.7) 93 (17.6) 26 (4.9) 528 (100)

Fatal cases (% of serotype)c 10 (6.4) 2 (5.4) 3 (4.3) 6 (4.2) 8 (8.6) 1 (3.8) 30 (5.7)

Meningitis cases (% of serotype) 12 (7.6) 2 (5.4) 1 (1.4) 17 (11.6) 3 (3.2) 0 35 (6.6)

Late-Onset Disease (7-89 d)

Cases, No. (% of total) 111 (23.7) 31 (6.6) 9 (1.9) 239 (51.0) 65 (13.9) 14 (3.0) 469 (100)

Fatal cases (% of serotype)c 8 (7.2) 1 (3.2) 0 5 (2.1) 5 (7.7) 0 19 (4.1)

Meningitis cases (% of serotype) 29 (26.1) 7 (22.6) 2 (22.2) 68 (28.5) 10 (15.4) 5 (35.7) 121 (25.8)

Pediatric and Adult Disease (�90 d and Not Pregnant)

Cases, No. (% of total) 1203 (24.1) 434 (8.7) 605 (12.1) 611 (12.3) 1563 (31.3) 571 (11.4) 4987 (100)

Fatal cases (% of serotype)c 136 (11.8) 30 (7.1) 66 (11.3) 52 (8.8) 150 (9.9) 52 (9.3) 486 (9.7)

Meningitis cases (% of serotype) 22 (1.8) 16 (3.7) 6 (1.0) 11 (1.8) 17 (1.1) 6 (1.1) 78 (1.6)a Includes IV, VI, VII, VIII, and nontypeable serotypes.bDenominator = number of cases per age stratum.cWith known outcome.




ternal pregnancy-associated dis-ease.5,27 Pregnancy-associated diseaseincidence did not show further de-clines during the present study pe-riod; however, current incidence (0.11-0.14 per 1000 live births) remains wellbelow that of the preprevention era(0.29 per 1000 live births).5

In contrast to neonatal and preg-nancy-associated disease trends, the in-cidence of group B streptococcal dis-ease among nonpregnant adultsincreased 32% during 1999-2005,reaching 7.9 per 100 000 in 2005. Thisvalue represents an increase over ratesreported in a series of population-based studies in metropolitan Atlanta,which documented an incidence of 2.4per 100 000 in 1982-1983, 4.4 per100 000 in 1989-1990, and 5.9 per100 000 in 1992-1993.28-30 The highprevalence of underlying medical con-ditions among infected adults, docu-mented in previous studies,31,32 wasagain seen here. Some investigatorshave speculated that the increasing in-cidence of invasive disease in nonpreg-nant adults may be related to in-creases in the prevalence of underlyingmedical conditions such as diabetes orto an aging population. Although wewere unable to evaluate the former, wenote that the age distribution of non-pregnant adults remained constantthroughout. Factors such as the in-creasing burden of chronic conditionsare likely important over the long termbut may not fully explain the rela-tively rapid increase observed duringour short 7-year study period. The sea-sonality in adult disease with peaks inthe late summer months has not beenestablished previously and further sug-gests that factors in addition to age orchronic conditions affect the inci-dence of disease. Possibilities includeseasonal environmental factors affect-ing the occurrence of skin and soft tis-sue infections, since those were promi-nent among adults with diabetes, or apossible enteric source of disease ex-posure.33,34

Previous studies identified blackrace as an independent risk factor forboth early onset24,35 and late-onset dis-

ease.35,36 Collectively, these studiessuggest that the effects of race cannotbe fully explained by prematurity,birth weight, maternal age, adequacyof prenatal care, or socioeconomic sta-tus, although the latter has not beenwell measured. Others have observedthat black women are more frequentlyheavily colonized with group B strep-tococcus than nonblack women37 andthat the risk of neonatal group B strep-tococcal disease is greater in infantsborn to heavily colonized mothers.38

This association may explain thehigher disease incidence among blackinfants,1 but direct evidence is lacking.Among adults (�15 years) in our sur-veillance system, disease incidencewas 2 times higher in black than inwhite populations—a value that issimilar to adult black-to-white rateratios of 1.5 reported in 1982-198328

and 2.0 reported in 1989-199029 and1998.5 Thus, although the overall inci-dence of adult disease has increasedsubstantially since the 1980s, relativeincidence for black vs white adults hasremained constant.

In general, our data confirm that theburden of group B streptococcal dis-ease remains disproportionately highamong black populations for all agegroups and pregnant women. Similardisparities are observed for other strep-tococcal pathogens.39,40 Reasons forthese disparities are not yet under-stood, and our surveillance system islimited in its ability to evaluate pos-sible explanations in that only case dataare captured, and potentially impor-tant cofactors such as socioeconomicstatus and access to health care aremissed. Furthermore, race data are col-lected by medical record review, whichincludes clinician-identified race de-terminations of unknown accuracy.

In the United States in 2005, groupB streptococcus caused an estimated21 500 cases of invasive disease and1700 deaths. Serotype data indicate thata pentavalent conjugate vaccine that in-cluded types Ia, Ib, II, III, and V couldpotentially prevent up to 96% of neo-natal disease and 88% of pediatric,adult, and pregnancy-associated dis-

ease, which translates to approxi-mately 19 000 cases in 2005. These find-ings are consistent with other recentstudies in North America, which re-port that the same 5 types caused 95%to 100% of early onset cases, 91% to98% of late-onset cases, 8% to 97% ofadult cases, and 91% to 100% of preg-nancy-associated cases.19,41-44 In addi-tion to serotype prevalence, virulenceis another important consideration forvaccine formulation. We found mod-est positive associations between sero-type Ia and fatality and between sero-type III and meningitis after controllingfor age at onset. Otherwise, we foundthat age, rather than the infecting se-rotype, was the dominant predictor ofoutcome.

Despite increasing antibiotic use, allisolates tested were susceptible to peni-cillin and ampicillin (the first-lineagents for intrapartum prophylaxisagainst early onset disease) and vanco-mycin. However, 32% of isolates wereresistant to erythromycin, clindamy-cin, or both. This observation under-scores the importance of performingsusceptibility testing among pregnantwomen colonized with group B strep-tococcus who are at high risk for peni-cillin anaphylaxis before administer-ing erythromycin or clindamycin forintrapartum prophylaxis to ensure ac-tivity against the isolate.

Although further reductions in in-cidence of early onset disease were seenfollowing the release of revised guide-lines for intrapartum chemoprophy-laxis, this strategy is unlikely to elimi-nate the remain ing burden ofpregnancy-associated and early onsetdisease—especially in preterm in-fants, who bear the highest risk ofdeath—and cannot prevent fetal infec-tions and losses occurring before the in-trapartum period. Moreover, wide-spread use of prophylactic antibioticsintroduces selection pressure for resis-tance not only among group B strep-tococcus but also among other sepsispathogens. Finally, this strategy doesnot address late-onset disease or thesubstantial and growing burden of dis-ease among adults. For these reasons,




maternal group B streptococcus vacci-nation trials should be a public healthpriority, followed by expanded vac-cine development to target diseaseamong elderly and younger adults withchronic underlying conditions.

Author Affiliations: Epidemic Intelligence Service Pro-gram, Office of Workforce and Career Development(Dr Phares) and Respiratory Diseases Branch (DrsPhares, Schuchat, and Schrag) and Biostatistics andInformation Management Branch (Ms Zell), Divisionof Bacterial Diseases, National Center for Immuniza-tion and Respiratory Diseases, Centers for Disease Con-trol and Prevention, Atlanta, Georgia; Minnesota De-partment of Health, St Paul (Dr Lynfield); EmoryUniversity School of Medicine and Atlanta VA Medi-cal Center, Georgia Emerging Infections Program, At-lanta, Georgia (Dr Farley); Infectious Diseases Branch,California Department of Health Services, Richmond(Dr Mohle-Boetani); Department of InternationalHealth, Johns Hopkins Bloomberg School of PublicHealth, Baltimore, Maryland (Dr Harrison); EmergingInfections Program, Connecticut Department of Pub-lic Health, Hartford (Ms Petit); Tennessee Depart-ment of Health, Nashville (Dr Craig); Department ofPreventive Medicine, Vanderbilt University School ofMedicine, Nashville, Tennessee (Dr Schaffner); NewYork State Department of Health, Albany (Dr Zan-sky); Colorado Department of Public Health and En-vironment, Denver (Dr Gershman); Oregon PublicHealth Services, Portland (Ms Stefonek); and NewMexico Department of Health Emerging Infections Pro-gram, Santa Fe (Dr Albanese).Author Contributions: Dr Phares had full access to allof the data in the study and takes responsibility forthe integrity of the data and the accuracy of the dataanalysis.Study concept and design: Phares, Lynfield,Mohle-Boetani, Schaffner, Stefonek, Schuchat, Schrag.Acquisition of data: Lynfield, Farley, Harrison, Petit,Craig, Schaffner, Zansky, Gershman, Stefonek,Albanese.Analysis and interpretation of data: Phares, Lynfield,Farley, Mohle-Boetani, Harrison, Schaffner, Zansky,Albanese, Zell, Schuchat,Drafting of the manuscript: Phares, Schrag.Critical revision of the manuscript for important in-tellectual content: Lynfield, Farley, Mohle-Boetani,Harrison, Petit, Craig, Schaffner, Zansky, Gershman,Stefonek, Albanese, Zell, Schuchat, Schrag.Statistical analysis: Phares, Zansky, Zell.Obtained funding: Farley, Zansky, Stefonek, Schuchat.Administrative, technical, or material support: Lynfield,Farley, Harrison, Craig, Schaffner, Stefonek, Albanese,Schuchat, Schrag.Study supervision: Farley, Craig, Schaffner, Gershman,Albanese, Schuchat, Schrag.Financial Disclosures: None reported.Funding/Support: This study was supported by theCenters for Disease Control and Prevention’s Emerg-ing Infections Program, the Antimicrobial ResistanceWorking Group of the National Center for InfectiousDiseases, and the National Vaccine Program Office.Role of the Sponsors: Neither the study sponsors norany commercial entity had any role in the design andconduct of the study; the collection, management,analysis, or interpretation of the data; or the prepa-ration, review, or approval of the manuscript.Active Bacterial Core surveillance/Emerging Infec-tions Program Network Personnel: Pamala Daily, MPH(California Emerging Infections Program, Oakland);Steve Burnite, Allison Daniels, MSPH, Nicole Haub-ert, MSPH (Colorado Department of Public Health andEnvironment); Nancy Barrett, MS, MPH, Zack Fraser,James L. Hadler, MD, MPH (Connecticut Depart-

ment of Public Health, Emerging Infections Program,Hartford); Kathryn E. Arnold, MD (Division of PublicHealth, Georgia Department of Human Resources);Pat Martell-Cleary, MSW (Georgia Emerging Infec-tions Program); Laurie Thomson Sanza, RN (Depart-ment of International Health, Johns Hopkins BloombergSchool of Public Health, Baltimore, Maryland); Patri-cia Ferrieri, MD, Aurea Flores, PhD (University of Min-nesota); John Besser, MS, Richard Danila, PhD, AnitaGlennen, Brenda Jewell, Susan Johnson, Billie Juni, MS,Craig Morin, MPH, Jean Rainbow, RN, MPH, LoriTriden (Minnesota Department of Health); Joseph Ba-reta, MS, Kathy Angeles, MPH, Karen Johnson, MS,Joanne Keefe, MPH, Lisa Butler, BUS (New MexicoDepartment of Health Emerging Infections Program,Santa Fe); Nancy Spina, Glenda Smith (New York StateEmerging Infections Program); Margaret Dragoon, RN,MPH, Dana Farland, RN, Anna Zeigler, RN (Mult-nomah County Health Department, Portland, Or-egon); Brenda G. Barnes, RN (Department of Preven-tive Medicine, Vanderbilt University School ofMedicine, Nashville, Tennessee); Timothy Bailiff, SheilaBashirian, Gloria Carvalho, John Elliott, PhD, RichardFacklam, PhD, Joy Findley, Alma Franklin, Genny Gal-lagher, PhD, Delois Jackson, Patricia Shewmaker, PhD,Tami Skoff, MS, Chris Van Beneden, MD, MPH, Shan-tia Warren, Emily Weston, MPH, Cynthia Whitney,MD, MPH, Carolyn Wright (Centers for Disease Con-trol and Prevention). None of these individuals re-ceived compensation for their contributions.

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Everyone is aware of the vast difference between anumber of men as a chance collection of individualsand the same number as an organized group or com-munity. A community has purpose and plan, and thereis in us an almost instinctive recognition of the con-nection between unity and strength.

—J. Glenn Gray (1913-1977)




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Epidemiology of Invasive Group B Streptococcal Disease in the United States, 1999-2005