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Based on these prospective studies, nearly two-thirdsof infants born to colonized mothers will be infected withGBS.

Table 1. Epidemiology of GBS perinatal infection.

Despite high prevalence rates for vertical transmission,the incidence of GBS infection during the rst seven daysof life ranges from 1.3 to 3 per 1,000 livebirths; after 7days, the range is 1.0 to 1.7 per 1,000 livebirths (thesedata are before the use of prophylaxis) (3, 8). Only 1%to 2% of infants of colonized women develop early-onsetGBS infection. In addition to maternal-infant transmission,nosocomial acquisition of GBS occurs (15). From 16% to47% of nursery personnel are carriers of GBS and maybe sources for neonatal transmission (2). Risk factorsthat predispose the neonate to clinical infection have alsobeen identied (Table 2).

Table 2. Risk Factors for early-onset neonatal infection withGBS.

There is a signicant increase (10 to 15 fold) in the risk

for GBS early-onset infection in preterm infants (8, 12-14,16). Eighty percent of infants with GBS disease weighedless than 2,500 grams (Table 3) (8). Numerous studiesreported that the duration of rupture of the membranes(ROM) and intrapartum fever, to be an importantcorrelate of neonatal GBS infection (8, 13) (Table 3).

In a CDC review of 278 cases of infant GBS disease,224 (80.7%) were early-onset cases and 54 (19.3%)were late-onset cases. The case fatality rate was5.8% (16/278), with no difference in rates for early

Although group B Streptococcus agalactiae (GBS) wasrecognized in veterinary medicine for many years as a

cause of bovine mastitis, it wasvirtually ignored as a humanpathogen until 1964, whenEickhoff and associates notedits role in perinatal infections(1). In the following years, GBSbecame the leading bacterialpathogen in perinatal infections,replacing Escherichia colias the

most frequent microorganisms associated with bacteremiaor meningitis among infants during the rst 2 months oflife (2). In 1990, there were an estimated 7,600 cases ofneonatal GBS disease, accounting for an incidence rate of1.8 per 1,000 liveborn infants. These cases resulted in anestimated 310 deaths from GBS disease among infantsyounger than 90 days of age in the United States (3,4).GBS has been recognized as one of the most importantpathogens in obstetric patients and can cause urinary tractinfections, amnionitis, post-partum endometritis, woundinfection, and intrapartum and/or postpartum bacteremia(5, 6). GBS infection may also lead to premature ruptureof membranes and preterm delivery (3, 4, 7).

EPIDEMIOLOGY

Asymptomatic vaginal colonization with GBS occurs inapproximately 20% (range 4.6% to 40.6%) of pregnantwomen (Table 1) (1, 8-11). The reported prevalenceof vaginal colonization with GBS in pregnant womenvaries according to geographic locale, age at pregnancy,duration of gestation, and the location and number of sitescultured.

The presence of GBS in the maternal tract is themajor determinant of both infection in the neonate andcolonization of the newborn (8, 10, 12-14). Verticaltransmission from mother to fetus occurs either via anascending route in utero, most commonly with rupturedmembranes, or by acquisition during passage throughthe birth canal intrapartum. The risk of transmission hasbeen shown to range from 42% to 72% among neonatesborn to colonized mothers; approximately 8% of infantsborn to noncolonized mothers become colonized (8-11).

Feature Rate

Maternal carriage 20% (range 10%-30%)

Early-onset neonatal GBS sepsis 1.5/1,000 l ive births (0.15%)

Overall neonatal colonization 5%-20%

Neonatal early onset GBS sepsis, if

mother positiveApproximately 1%

Prematurity (100.4C)

Rupture of membranes for longer than 12-18 hours

Previously delivered infant with invasive GBS disease

Vaginal Group B Streptococcus

Streptococcus agalactiae

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versus late-onset disease. Thirteen (81.3%) of thedeaths occurred in infants of less than 34 weeksgestation and eight of the infants were black (17).

Table 3. Colonization rates of neonatal GBS early-onset diseaseaccording to perinatal characteristics.a

PATHOGENESIS

GBS are facultative, Gram positive diplococci that grow

on a variety of bacteriologic media. Isolated colonies onsheep blood agar are 3 to 4 mm in diameter and coloredgrayish-white. Obtaining specimens for culture fromboth the anorectum and the distal vagina increases thelikelihood of obtaining GBS by a considerable percentage(5% to 25%) over vaginal culture alone (3). Within thegenital tract, the highest isolation rates are reported fromthe introitus and the lowest from the cervix. Pregnancydoes not inuence the colonization rate.

CLINICAL SIGNIFICANCE

As the incidence of neonatal GBS infections rose duringthe 1970s, a bimodal distribution of cases by age at theonset of symptoms became apparent. Two distinctiveclinical syndromes related to age were described byFranciosi and coworkers (18) (acute and delayed) andby Baker, et. al. (19) (early and late-onset). Early-onset infection, dened as the development of systemicinfection during the rst 6 days of life, has a mean age of12 hours at its onset. Maternal obstetric complications

are frequent (50% to 60%), and infants born at lessthan 37 weeks of gestation have signicantly higherattack rates than infants born at full-term. The threemajor clinical expressions of infection are bacteremia,pneumonia, and meningitis, which occur at frequenciesof approximately 60%, 30%, and 10%, respectively.The presenting signs of early-onset GBS infection arelethargy, poor feeding, jaundice, abnormal temperature,

grunting respirations, and hypotension. Thesesymptoms are indistinguishable from those of neonateswith bacterial infections of other causes (19). Increasedawareness of the disease and improvements insupportive therapy have resulted in decreased mortalityamong infants with early-onset GBS infection, andpresent rates range from 5% to 10% (21, 22). Mortalityrates are inversely proportional to birthweight (Table 3).

This syndrome has an onset from 7 days to 3 months ofage, with a mean of about 24 days. Maternal obstetriccomplications are uncommon and the case fatality

rate is low (21, 22). Occult bacteremia or meningitisare common clinical manifestations of late-onsetinfection, but a variety of focal infections, usually withaccompanying bacteremia, also are described. Thenonspecic initial signs of late-onset disease, suchas lethargy, poor-feeding, and irritability, generallyoccur in association with fever (temperature 38C).These infants may present with fulminating infectionscharacterized by rapid progression to a moribund statewith septic shock, seizures and cerebrospinal uid Gramstains with sheets of organisms. An increased risk

of death or permanent neurologic sequelae occurs inpatients with this serious presentation (23). Twenty-veto 50% of survivors of GBS meningitis, whether earlyor late-onset, have permanent neurologic sequelae (20,23, 24).

Bone and joint infections are other clinical forms of late-onset GBS disease that occur relatively frequently (25).GBS osteomyelitis is characterized by an indolent onsetin which diminished movement of the involved extremityis the most common symptom. Bone and joint infectionsare associated with minimal inammatory changes, and

fever is reported in only 20% of patients.

Infants older than 3 months constitute 10% to 15%of the total cases of late-onset disease (22, 26). Theterm beyond early infancy is appropriate for patientswith GBS disease who are older than 3 months andyounger than 18 years (27). Many of these infectionsoccur among very low birth weight infants who may stillbe hospitalized for complications of prematurity; others

occur in healthy infants with occult bacteremia (26).

Characteristic No. of livebirthsColonization Rates(Per 1000 livebirths)

Fatality

(%)

Birthweight501-1,000

1,001-1,500

1,501-2,000

2,001-2,500

>2,500

382

499

798

2,102

28,603

26.2

8.0

8.8

4.3

1.1

90

25

29

33

3

ROMb (hrs)

48

19,665

5,391

3,277

1,943

1,276

832

0.8

1.9

1.5

5.7

8.6

10.8

33

10

40

27

18

33

Intrapartum Temp

>37.5C 30,530 1.5 29

Risk factors

Present

Absent

5,942

26,442

7.6

0.6

33

6

a Data presented are for all women, regardless of GBS carriagestatus.

b ROM, rupture of the membranes.


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Congenital heart disease and immune deciency,including human immunodeciency virus infection, shouldbe considered when GBS disease is diagnosed beyondearly infancy(27, 28).

GBS can cause symptomatic infection of the urinary tractor cervix and myometrial infection during or immediatelyafter parturition. These symptomatic infections, due to

GBS, are clinically indistinguishable from infection ofthe same anatomic sites by other bacteria. The GBSmay act as the sole or predominant bacteria causingsymptomatic maternal infection, or the GBS may act incombination with other aerobes and anaerobes (29). TheGBS-colonized woman who remains afebrile during laboris unlikely to develop endometritis if there has been anatraumatic vaginal delivery. However, the GBS positivewoman, who delivers by cesarean section, has a highprobability of developing endomyometritis once there isamniotic uid infection, even if antibiotics are given asprophylaxis or early treatment (30). Other scenarios ofsymptomatology that may require treatment of the motherfor GBS include:

Urinary tract infections: These should be treatedas often as symptoms recur and when a GBS test ispositive.

Cervicitis: A copious yellow, purulent discharge due toGBS may be present more often in the presence of acerclage suture.

Preterm amenorrhea or labor: There is some evidencethat GBS colonization is a minor risk factor for theseconditions (31,32).

DIAGNOSIS

Since current culture-based strategies for prevention ofearly-onset neonatal GBS disease depends on screeningpregnant women who are carriers, it is important forclinicians and laboratories to use the methods that willmaximize carrier detection (3, 12, 33). Recovery of GBSfrom clinical specimens depends on both the site ofcollection and the culture media. Obtaining specimensfrom the anorectum and vaginal introitus increases

the likelihood of isolation of GBS by 5% to 37% overobtaining specimens from the vagina alone (3, 34, 35).Appreciation of this point is critically important for thedevelopment and effective implementation of clinicalscreening protocols. While many obstetricians havebeen trained to carefully sample the endocervix whenattempting to diagnose gonorrhea or chlamydia, this isnot the best way to screen for GBS. In the case of aGBS infection, a positive endocervical sample may haveup to a 50% positive predictive value for the mother

or the baby for developing a symptomatic perinatalinfection; however, the incidence of positive endocervicalcultures is very low (


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Specicity was determined by attemptingamplication of DNA extracted from 40 knownhuman pathogens and other organisms purchasedfrom the ATCC and mixed in various cocktails. Noneof the organisms listed were amplied (Table 4).

RECOMMENDATIONS

1. Firmly, yet gently, sample the vagina and/or theanorectum with the sterile Dacron swab, rotating 360for 10 to 30 seconds to ensure adequate sampling.

2. Remove the swab and place into the vial. Snap off theshaft to t completely in the vial. To prevent leakage, besure the swab ts into the vial prior to capping. Tightlycap the vial.

3. If diagnostic testing for other STDs are required, anadditional cervical swab can be collected and insertedinto the same transport vial.

The following updated recommendations for theprevention of GBS disease are based on critical multistatepopulation-based observational data and several studiesfrom individual institutions that have been completedsince the publication of previous, ACOG (47), AAP (48)and CDC (49) recommendations. These guidelinesreplace previous recommendations from the CDC (3).

Obstetric-care practitioners, in conjunction with supportinglaboratories, and labor and delivery facilities, shouldadopt the following strategy for the prevention of perinatal

GBS disease based on prenatal screening for GBScolonization. The risk-based approach is no longer anacceptable alternative except for circumstances in whichscreening results are not available before delivery.

All pregnant women should be screened at 35 37weeks gestation for vaginal and rectal GBS colonization(Figure 3). Colonization during a previous pregnancyis not an indication for intrapartum prophylaxis insubsequent deliveries.

Women with GBS isolated from the urine in anyconcentration during their current pregnancy shouldreceive intrapartum chemoprophylaxis because suchwomen are usually heavily colonized with GBS and areat risk of delivering an infant with an early-onset GBSdisease. Women with symptomatic or asymptomaticGBS urinary tract infection detected during pregnancyshould be treated according to current standard of carefor urinary tract infection during pregnancy.

Adenovirus EBV

Anaplasma phagocytophilum Gardnerella vaginalis

Aspergillus fumigatus Helicobacter pylori

Babesia microti HHV-6

Bacteroides fragilis HHV-8

Bartonella bacilliformis HPV-16

Bartonella henselae HSV-1

Bartonella quintana HSV-2

Borrelia burgdorferi HTLV-1Brucella abortis Mobiluncus curtisii

Candida albicans Mobiluncus mulieris

Candida glabrata Mycoplasma fermentans

Candida parapsilosis Mycoplasma genitalium

Candida tropicalis Mycoplasma hominus

Chlamydia pneumoniae Mycoplasma pneumoniae

Chlamydia psittaci Mycoplasma salivarium

Chlamydia trachomatis Neiserria gonorrhoeae

CMV Trichomonas vaginalis

Coxsackie Virus Trichosporon

Cryptococcus neoformans Ureaplasma urealyticum

Figure 2. pBstrepMF plasmid dilutions: Red lines representplasmid alone. Blue lines represent plasmid with DNA. From leftto right: 5x106, 5x105, 5x104, 5x103, and 5x102 copies/reaction.

Table 4. Validated organisms purchased from the ATCC fortesting specicity for GBS.

Sensitivity was determined using serial dilutions of DNAextracted from known validated organisms purchasedfrom ATCC and/or plasmid standards. A range of 5x108to 500 copies can be detected with an r2 value of 0.97645(Figure 1).

A lack of interference from other substances inherent tothe specimen type was determined by adding 500 ng of

DNA extracted from a clinical sample that had testednegative for the pathogens in question to a dilutionof plasmid standards. The addition of the extractedsample DNA did not signicantly alter the detection ofthe target DNA. A range of 5x106 to 5x102 copies can

be detected with an r2 value of 0.90270 (Figure 2).


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Culture techniques that maximize the likelihood ofGBS recovery are required for prenatal screening.Specimen collection is of paramount importance fora successful laboratory test. This procedure involvesswabbing the lower vagina and rectum (i.e. through theanal sphincter). Because lower vaginal, as opposedto cervical cultures, are recommended, cultures shouldnot be collected by speculum examination.

Health-care providers should inform women of theirGBS screening test result and the recommendedinterventions. In the absence of GBS urinary tractinfection, antimicrobial agents should not be used beforethe intrapartum period to treat GBS colonization.

GBS-colonized women, who have a planned cesareandelivery performed before rupture of membranes and

onset of labor, are at low risk for having an infant withearly-onset GBS disease. These women should notroutinely receive intrapartum chemoprophylaxis forperinatal GBS disease prevention.

For intrapartum chemoprophylaxis, the followingregimen is recommended for women without penicillinallergies (Figure 4); Penicillin G, 5 million unitsintravenously initial dose, followed by 2.5 million unitsintravenously every 4 hours until delivery. Because ofits narrow spectrum of activity, penicillin is the preferred

agent of treatment. An alternative regimen is ampicillin,2g intravenously initial dose, then 1g intravenouslyevery 4 hours until delivery.

Intrapartum chemoprophylaxis for penicillinallergicwomen takes into account increasing resistance toclindamycin and erythromycin among GBS isolates(Figure 4). During prenatal care, a history of penicillinallergy should be assessed to determine whether apatient is at high-risk for anaphylaxis, i.e., has a historyof immediate hyper-sensitivity reactions to penicillin, ora history of asthma or other conditions that would makeanaphylaxis more dangerous.

Local and state public health agencies, in conjunctionwith appropriate hospitals groups, are encouraged toestablish surveillance for early-onset GBS diseasein their states. Efforts to monitor the emergence ofperinatal infections caused by other organisms arealso encouraged.

Intrapartum Prophylaxis

Not Indicated

Previous pregnancy with a positiveGBS screening culture (unless a

culture was also positive during

the current pregnancy.)

Planned cesarean delivery

performed in the absence of labor

or membrane rupture, regardless

of maternal GBS culture status.

Negative vaginal and rectal GBS

screening culture in late gestation

during the current pregnancy,

regardless of intrapartum risk

factors.

Intrapartum Prophylaxis

Indicated

Previous infant with invasive GBS

GBS bacteriuria during current

pregnancy

Positive GBS screening laboratory

test during current pregnancy

Unknown GBS status because

culture not attempted, or results

unknown, or any of the following:

Delivery at 18 hrs

Intrapartum temperature

>100.4F (>38.0C)

Vaginal and rectal GBS screening culture at 35-37 weeks gestation for

ALL pregnant women

Figure 3. Indications for intrapartum antibiotic prophylaxisto prevent perinatal GBS disease under a universal prenatalscreening strategy based on combined vaginal and rectal culturescollected at 35 37 weeks gestation from all pregnant women.

Recommended Penicillin G, 5 million units IV initial dose,

then 2.5 million unit IV every 4 hours until

delivery.

Alternative Ampicillin, 2g IV initial dose, then 1g IV

every 4 hours until delivery.

If Pencillin-allergic

Patients not at highrisk for anaphylaxis Cefazolin, 2g IV initial dose, then 1g IVevery 8 hours until delivery.

Patients at high risk

for anaphylaxis

GBS susceptible

to clindamycin and

erythromycin

Clindamycin, 900mg IV every 8 hours until

delivery.

OR

Erythromycin, 500mg IV every 6 hours until

delivery.

GBS resistant to

clindamycin or

erythromycin or

susceptibility unknown

Vancomycin, 1g IV every 12 hours until

delivery.

Figure 4. Recommended regimens for intrapartum antimicrobialprophylaxis for perinatal GBS disease prevention.

If the result of GBS culture is not known at the onsetof labor, intrapartum chemoprophylaxis should beadministered to women with any of the following riskfactors: gestation


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