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Prevention of Perinatal Group B Streptococcus Infections

Fan, Shang-Rong1,2; Tasneem, Umber3; Liu, Xiao-Ping4,∗; Yan, Shao-Mei5

Editor(s): Pan, Yang; Shi, Dan-Dan

Author Information
doi: 10.1097/FM9.0000000000000041
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Group B streptococcus (GBS), or Streptococcus agalactiae, is a gram-positive bacterium that can colonize the human gastrointestinal and genitourinary tracts asymptomatically and is a leading cause of morbidity and mortality in newborn infants. Neonatal infection results from vertical transmission of maternal colonization of the anal, perineal, and/or vaginal regions. A strong correlation has been observed between maternal GBS colonization and GBS early-onset disease (EOD) which is defined as the condition that occurs within 7 days of birth. GBS may also cause maternal urinary tract infections, intraamniotic infections, or endometritis and is associated with preterm labor and stillbirth.1–3 In 2010, the Centers for Disease Control and Prevention, in collaboration with several professional groups, including the American College of Obstetricians and Gynecologists (ACOG), issued its third set of GBS prevention guidelines.4 In 2018, the work of implementing up-to-date GBS EOD prophylaxis guidelines was transferred from Centers for Disease Control and Prevention to ACOG and the American Academy of Pediatrics. The guidelines were published in 2019.1 This article aims to review the current GBS EOD burden in newborn infants, prevalence of maternal GBS colonization, antenatal screening for GBS, intrapartum antibiotic prophylaxis (IAP) and the up-to-date knowledge.

GBS disease burden in newborn infants and the prevalence of maternal GBS colonization

GBS EOD, which presents within 7 days after birth and occurs secondary to vertical transmission, to fetal or neonatal aspiration during labor and birth, or to both is characterized primarily by sepsis, pneumonia or, less frequently, meningitis and is most likely to manifest within the first 12–48 hours after birth; however, GBS late-onset disease, which presents between 7 days after birth and 2 to 3 months of age, and is characterized by bacteremia, meningitis or, less commonly, organ or soft tissue infection.1,4 The most common organisms associated with early-onset neonatal sepsis are GBS and Escherichia coli. In an academic-based neonatal centers study, 389 newborn infants had early-onset sepsis (0.98 cases per 1 000 live births), with 43% due to GBS (0.41 per 1 000 live births) and 29% due to Escherichia coli (0.28 per 1 000 live births).5

In the absence of IAP, approximately 50% of newborn infants born to mothers who are positive for GBS become colonized with GBS, and of these infants, 1%–2% develop GBS EOD.1,6,7 The mortality rates for GBS EOD are markedly higher for preterm newborns than term newborns (19.2% vs. 2.1%).8

In the USA, the implementation of national guidelines for IAP has resulted in a reduction in the incidence of GBS EOD by over 80%, from 1.8 per 1 000 live births in the 1990s to 0.23 newborns per 1 000 live births in 2015.8 In Germany, Wicker et al. reported a 32% reduction in the GBS incidence in infants, from 0.47 per 1 000 live births in 2001–2003 to 0.34 per 1 000 live births in 2009–2010, after the implementation of the guidelines for universal GBS screening for all pregnant women.9 In England, when a risk-factor approach was introduced in November 2003, a slight increase of infant GBS infections was detected (0.35 per 1 000 live births in 2003 to 0.41 in 2010).10 In the Netherlands, where a risk-factor approach was also applied, a 60% increase in the incidence of infant GBS infections resulted (0.20 per 1 000 live births in 1987 and 0.32 per 1 000 live births in 2011).11 In the UK and Republic of Ireland, the incidence is estimated to be 0.57 per 1 000 live births. Affected neonates present with sepsis in 63% of cases, pneumonia in 24% of cases, meningitis in 13% of cases, and approximately 5%–10% die as a result. Neurological impairment is reported in up to 16% of cases that survive the infection.12 In New Zealand, by contrast, the incidence of GBS EOD was reduced by more than half after the implementation of a single, risk-based approach (0.5 per 1 000 live births in 1998–1999 to 0.23 in 2009–2011).13 Russell et al. reviewed 30 articles including 20 328 GBS-colonized pregnant women. The risk of GBS EOD in settings without an IAP policy was 1.1%. As IAP increased, the risk of GBS EOD decreased, with a linear relationship. Based on linear regression, the risk of GBS EOD in settings with 80% IAP coverage was estimated to be 0.3%.14 Madrid et al. reviewed 135 studies with data on the incidents (n = 90), case fatality risk (n = 64), or serotype (n = 45). The pooled incidence of invasive GBS disease in infants was 0.49 per 1 000 live births and was highest in Africa (1.12) and lowest in Asia (0.30). The EOD incidence was 0.41, and the late-onset disease incidence was 0.26. The case fatality risk was 8.4%. Serotype III (61.5%) dominated, with 97% of cases caused by serotypes Ia, Ib, II, III, and V.15 GBS was estimated to cause more than 319 000 infant infections, 90 000 infant deaths, and 57 000 stillbirths annually worldwide.3

Risk factors for GBS EOD

Maternal vaginal-rectal colonization with GBS during the intrapartum period is a prerequisite for GBS EOD. The risk factors for GBS EOD are as follows: increased duration of rupture of membranes (ROM) promotes the process of ascending colonization and infection of the uterine compartment and fetus. The risk factors for neonatal infection include: (1) preterm birth; (2) very low birth weight; (3) prolonged ROM (>18 hours); (4) intra-amniotic infection; (5) socioeconomic disadvantage; (6) low maternal levels of anti-capsular antigen; (7) young maternal age (<20 year); (8) maternal African American race; (9) previous delivery of a GBS EOD-affected baby; (10) intrapartum pyrexia; (11) maternal GBS bacteriuria; (12) other twin with current GBS EOD.1,7,13Figure 1 shows the ascending perinatal GBS infection course.

Figure 1
Figure 1:
Ascending perinatal GBS infection. GBS go from the vagina, ultimately lead bacterial invasion of placental membranes, the amniotic cavity, and the fetus. A Vagina. B Cervix. C Placenta. D Amniotic fluid. E Fetus. GBS: Group B streptococcus.

Prevalence of maternal GBS colonization

The prevalence of maternal colonization by GBS varies by the region and detection method. Globally, 10%–30% of women carry GBS in their vaginal and/or rectal flora. Russell et al. reviewed datasets regarding colonization and included 390 articles, 85 countries, and a total of 299 924 pregnant women in their review. The estimated maternal GBS colonization worldwide was 18%, with regional variation (11%–35%) and a lower prevalence in southern Asia (12.5%) and eastern Asia (11%). Bacterial serotypes I–V accounted for 98% of identified colonizing GBS isolates worldwide. Serotype III, associated with invasive disease, accounted for 25% but it was less frequent in some South American and Asian countries. The serotypes VI–IX were more common in Asia.14

The risk factors for GBS colonization during pregnancy

The risk factors for GBS colonization during pregnancy include: (1) obesity; (2) African-American or Caucasian race; (3) older age and older age at first pregnancy; (4) history of GBS during a previous pregnancy; (5) being multigravida; (6) meconium-stained amniotic fluid; (7) longer duration of premature ROM; (8) smoking.16–19

Antenatal screening for GBS

The purpose of screening for GBS in late pregnancy is to identify a group of women who are eligible for intravenous IAP as a means of preventing GBS EOD. The universal culture-based screening strategy for identifying candidates for GBS IAP was demonstrated to be superior to risk-based screening protocols for the prevention of GBS EOD.1,4 In 1998 and 1999, a large USA multistate study of 626 912 live births demonstrated that in a group of 5 144 births, the risk of EOD was significantly lower for infants of universally screened mothers than those born to mothers managed with the risk-based approach. The finding led to the recommendation of universal screening for GBS in pregnant women in the USA.1,4,20,21

Timing of screening

The recommended time for universal culture-based screening for GBS is ranges from 36 0/7 to 37 6/7 weeks of gestation.1 The GBS cultures have a high degree of accuracy in predicting GBS colonization status at birth if cultures are collected within 5 weeks of birth. The predictive ability of prenatal cultures for GBS decreases significantly when the culture-to-birth interval is longer than 5 weeks.1 Virranniemi et al. studied the effect of the screening-to-labor interval on the sensitivity of late-pregnancy culture in the prediction of GBS colonization at labor. The sensitivity of late-pregnancy culture was 94.1% and 87.0% when the screening-to-labor interval was 1 week and 6 weeks, respectively.22

Specimen collection and processing for GBS

Culture-based testing remains the standard for maternal antenatal GBS screening. Swab the lower vagina, then the rectum using the same swab or two separate swabs. The speculum should not be used for vaginal collection. Cervical, perianal or perineal specimens are not acceptable.1,4 Place the swab(s) into a nonnutritive transport medium. Appropriate transport systems are commercially available. GBS isolates remain viable in transport media for several days at room temperature; however, the recovery period of isolates declines from 1 to 4 days, especially at elevated temperatures, which can lead to false-negative results. When feasible, specimens should be refrigerated before processing. Specimen requisitions should clearly indicate that specimens are for GBS testing.

Other laboratory methods include direct latex agglutination tests or nucleic acid amplification testing (NAAT) on the enriched selective broth as an additional or alternative method for processing antepartum cultures. NAAT methods for GBS detection can also be used for intrapartum management as a rapid test performed at the time of presentation in labor or for women at term who have unknown or unavailable antepartum GBS screening test results. Miller et al. compared the AmpliVue, BD Max System, and illumigene Molecular Assays for detection of GBS in Antenatal Screening Specimens and found that all three NAATs were more sensitive (sensitivity, 90.9%–100.0%) than culture (sensitivity, 53.6%).23 Feuerschuette et al. assessed the sensitivity and specificity of real-time polymerase chain reaction compared to the reference standard culture in selective broth media, that are collected from the rectovaginal tracts of laboring women, in fifteen studies including 6 368 women. The sensitivity and specificity of real-time polymerase chain reaction were 93.7% and 97.6%, respectively.24 Guerrero et al. examined the direct latex agglutination test for the detection of group B streptococci and found that latex agglutination testing could detect 98.0% (99/101) of selective broth medium positive specimens.25 Fay et al. examined antenatal and the intrapartum nucleic acid amplification test for GBS screening in the USA and found that 18.7% of laboratories used GBS NAATs in 2016.26 Seto et al. assessed the accuracy of self-screening of GBS in pregnant women and found that the sensitivities of self-screening and the screening by health care workers were 61.4% (51/83) and 97.6% (81/83), respectively. The sensitivity of self-screening for GBS reported from Hong Kong (China) was lower than the sensitivity of screening by health care workers for GBS.27Table 1 shows the sensitivity and specificity of different diagnosis methods for GBS.23,24,28–41

Table 1
Table 1:
Sensitivity and specificity of different diagnosis methods for GBS.

Patients who state that they are allergic to penicillin should be evaluated for risk for anaphylaxis. If a woman is determined to be at high risk for anaphylaxis, susceptibility testing for clindamycin and erythromycin should be ordered.1,4Figure 2 shows the laboratory culture and identification for GBS during pregnancy.

Figure 2
Figure 2:
The laboratory culture and identification for GBS during pregnancy. A Colonies of GBS is a small, 3–4 mm, circular, semi-transparent, grey-white, non-pigmented, smooth, catalase negative, and convex with entire margin with a complete or clear zone of hemolysis on 5% sheep blood agar after 24 hours of incubation at 37°C. Growth is in aerobic atmosphere. B Smear made from colony of organism isolated from vagina of patients on 5% sheep blood agar and stained with gram staining. GBS shown as gram-positive, β-hemolytic, non-motile, non-spore forming cocci, spherical or ovoid, 0.6–1.2 μm in diameter that divides to form chains and some in pairs (diplococci). Presence of short chains are due to the smear that is made from solid media. Chains become larger in liquid media so length of the chain varies with cultural conditions. (Gram stain, 1 000×) C Electrophoresis picture of 1% agarose gel stained with ethidium bromide showing polymerase chain reaction (PCR) amplification generated by GBS with species specific primer Sag 59 and Sag 190. Results of amplification fragments shows length of about 156 bps according to the length of the marker used. D Mass spectrum discriminating peaks of GBS taken by ClinToff (time of flight mass spectrometry system) from 24-hour culture on 96 test box plates with positive control of GBS. The intensities and masses (in Da) of the ions are shown on Y-axis and X-axis. Mass to charge ratio represent the “m/z” value. For each spectrum, 500 laser shots were collected and analyzed. In a typical analysis of GBS, 70 prominent ion peaks were noted in the spectra in the region between 2 000 and 12 000 Da, with the highest-intensity peaks being consistently in the range of 3 000 to 10 000 Da. GBS: Group B streptococcus; Da: Dalton.

Intrapartum antibiotic prophylaxis

Sixty of ninety-five (63%) countries have a national IAP policy. Twenty-five of sixty (42%) use a risk factor-based approach, and thirty-five of sixty (58%) use both microbiological screening and risk factor approaches.28 The estimated coverage of microbiological-based screening or risk-based screening or microbiological and risk-based screening is shown on Figure 3.42 IAP is hypothesized to prevent GBS EOD in three ways: (1) by temporarily decreasing the maternal vaginal GBS colonization burden; (2) by preventing surface and mucus membrane colonization of the fetus or newborn; (3) by reaching levels above the minimum inhibitory concentration of the antibiotic for killing GBS in the newborn bloodstream.

Figure 3
Figure 3:
Estimated coverage rate based on microbiological-based or risk-based or microbiological and risk-based screening for the prevention of GBS disease worldwide. The data are from reference 42. The map was generated by Adobe PhotoShop CS6 (version 13.0, USA). The copyright holder grants anyone the right to use this work for any purpose, without any conditions, unless such conditions are required by law. GBS: Group B streptococcus.

Penicillin remains the main agent of choice for IAP, and ampicillin is an acceptable alternative. The definition of adequate IAP has been clarified to be at least 4 hours of penicillin, ampicillin, or cefazolin. Ampicillin IAP decreases maternal vaginal colonization and prevents neonatal surface colonization in 97% of cases if IAP is administered at least 2 hours before delivery.7 Viel-Theriault et al. reviewed the transplacental passage of commonly used intrapartum antibiotics and found that newborns exposed to intrapartum penicillin, ampicillin, cefazolin and/or gentamicin, especially within 30 minutes to 2 hours before delivery, are expected to have a high serum antibiotic concentration that far exceeds the minimum inhibitory concentration against GBS. The neonatal blood cultures drawn at birth before starting empirical antibiotic therapy may have decreased sensitivity in diagnosis EOS, and clinical factors should also be considered to guide the postnatal antibiotic duration. These antibiotics also have better effects for intrauterine infant therapy.43 The regimens and algorithms for antenatal GBS screening and IAP are shown in Figure 4.

Figure 4
Figure 4:
Regimens and algorithms for antenatal GBS screening and intrapartum antibiotic prophylaxis. GBS: Group B streptococcus; h: Hour; GBS EOD: Group B streptococcus early-onset disease; IV: Intravenous.

Antibiotic resistance of GBS

The proportions of GBS isolates with in vitro resistance to clindamycin or erythromycin have increased over the past 20 years. In a meta-analysis, the resistance rates of GBS for clindamycin and erythromycin were 25% and 27%, respectively.44 Vancomycin is recommended for use as GBS IAP for women with a penicillin allergy who are at high risk for anaphylaxis if colonized with clindamycin-resistant GBS isolates.1Table 2 shows the selected reports of antibiotic resistance of GBS worldwide.45–59

Table 2
Table 2:
GBS susceptibility rate in selected reports.

Penicillin-allergic patients

When a woman reports a penicillin allergy, the recommended antibiotic for intrapartum antibiotic prophylaxis, if she is colonized with GBS, is based on her risk of anaphylaxis and the susceptibility of the GBS isolate to clindamycin. Penicillin-allergic women who do not have a history of anaphylaxis, angioedema, respiratory distress, or urticaria after the administration of penicillin or a cephalosporin should receive cefazolin. Penicillin-allergic women at high risk of anaphylaxis should receive clindamycin if their GBS isolate is susceptible or vancomycin if their GBS isolate is intrinsically resistant to clindamycin.1 In the UK, clindamycin is no longer recommended as intra-partum prophylaxis to prevent GBS EOD in women with a history of penicillin allergy.60 Desravines et al. identified 190 GBS-colonized pregnant women who self-reported a penicillin/cephalosporin allergy, including 5% reported cases of anaphylaxis, 44% reported cases of high-risk symptoms, and 51% reported cases of low-risk symptoms. Two-thirds (63%) had alternative antibiotic prophylaxis.61 Shenoy et al. suggested that many patients report that they are allergic to penicillin but few have clinically significant reactions. One should carefully evaluate the presence of a penicillin allergy before deciding not to use penicillin or other β-lactam antibiotics.62Table 3 shows regimens for IAP for prevention of GBS EOD.

Table 3
Table 3:
Regimens for intrapartum antibiotic prophylaxis for prevention of GBS EOD.

Other obstetric issues


Asymptomatic bacteriuria is diagnosed by quantitative culture using two consecutive voided urine specimens with isolation of the same bacterial strain in quantitative counts ≥105 colony forming unit (CFU)/mL or a single catheterized urine specimen with one bacterial species isolated in a quantitative count ≥100 CFU/mL. ACOG recommends that if GBS is present in the urine at concentrations ≥105 CFU/mL at any time during pregnancy GBS, antibiotics for asymptomatic bacteriuria or a symptomatic urinary tract infection should be administered as they would be for any other organism detected at significant concentrations. Asymptomatic women with urinary GBS colony counts <105 CFU/mL during pregnancy should not be treated with antibiotics for the prevention of adverse maternal and perinatal outcomes such as pyelonephritis, chorioamnionitis, or preterm birth. Women with documented GBS bacteriuria should not be re-screened by genital tract culture or urinary culture in the third trimester, as they are presumed to be GBS colonized.63

Cesarean delivery performed before labor onset in women with intact amniotic membranes and GBS positivity

Intrapartum prophylaxis that is specific for GBS is not recommended for women undergoing a planned cesarean birth in the absence of labor and ROM, regardless of the gestational age, even among women who are GBS positive.1

Obstetric procedure

(1) Limited evidence suggests that membrane sweeping does not appear to be associated with adverse outcomes in women colonized with GBS. (2) Currently, no recommendation can be made either for or against the timing of antibiotic prophylaxis in women colonized with GBS undergoing mechanical cervical ripening. (3) In women receiving intrapartum antibiotic prophylaxis, vaginal examinations should be performed when clinically indicated. (4) There are no data to suggest that artificial ROM increases the risk of neonatal disease when appropriate IAP is given; therefore, amniotomy is reasonable to perform if clinically indicated. (5) There are no data to suggest that intrauterine monitoring increases the risk of neonatal disease when appropriate IAP is given, and GBS colonization should not be considered a contraindication to obstetrically indicated intrauterine monitoring, either of the fetal heart rate or of contractions.1

Management of newborn infants

Currently, available GBS prevention strategies do not prevent all cases of GBS EOD. Rapid detection of neonatal infections and initiation of appropriate treatment is needed to minimize morbidity and mortality. The causes of GBS EOD sepsis include: (1) a negative screening culture (61%–82%); (2) adequate prophylaxis (2%–5%); (3) inadequate prophylaxis, unavoidable (14%–31%); (4) inadequate prophylaxis, avoidable (4%–8%).64

GBS EOD is diagnosed by blood or cerebrospinal fluid CSF culture. Common laboratory tests, such as the complete blood cell count and C-reactive protein, do not perform well in predicting GBS EOD, particularly among well-appearing infants at the lowest baseline risk of infection.

The recommended management strategy for newborn infants of mothers with vaginal and/or rectal GBS is as follows: (1) all newborn infants with signs of sepsis should undergo a full diagnostic evaluation and receive empirical antimicrobial therapy; (2) all well-appearing newborn infants born to women who are diagnosed with chorioamnionitis by their obstetrical providers should undergo a limited diagnostic evaluation and receive empirical antimicrobial therapy; (3) for all women who receive adequate IAP defined as penicillin, ampicillin, or cefazolin for 4 or more hours before delivery, their newborn infants require only routine care and observation in the hospital for 48 hours. If these infants meet other discharge criteria, including term birth and ready access to medical care, discharge can occur as early as 24 hours after birth with follow-up care by a care provider within 48–72 hours; (4) the well-appearing term newborn infants whose mothers receive no or inadequate IAP and had ROM for less than 18 hours require only observation for 48 hours; (5) well-appearing term infants born to women with no or inadequate IAP and ROM for 18 hour or more before delivery should undergo a limited evaluation and observation for at least 48 hours; (6) all preterm infants born to women with no or inadequate IAP should undergo a limited evaluation and observation for at least 48 hours.7,65 Penicillin G is the preferred antibiotic for the definitive treatment of GBS disease in infants; ampicillin is an acceptable alternative. Table 3 and Table 4 present the recommended intravenous antibiotic treatment regimens for confirmed early-onset GBS bacteremia and meningitis.7

Table 4
Table 4:
Recommended antibiotic regimens for confirmed GBS early onset bacteremia and meningitis7

The debate and research direction

Maternal anaphylaxis associated with GBS IAP may occur though it is rare. The morbidity associated with anaphylaxis is balanced by the reduction in adverse outcomes associated with GBS colonization. Universal prenatal screening or risk-based prenatal screening still has debates. GBS screening guidelines in the USA, Canada, and Australia were universal culture-based screening of all pregnant women at 35–37 weeks of gestation is recommended. In the UK, routine antepartum GBS screening for GBS is not recommended.60 Despite the implementation of a risk-based screening approach since 2003, the incidence of GBS EOD disease appeared to have increased slightly (0.57/1 000 in 2015 vs. 0.48/1 000 live births in 2000), which suggests that the current approach in the UK does not reduce the risk of GBS EOD disease.66,67 Gopal Rao et al. compared the GBS EOD rates in the risk-based IAP with screening-based IAP and found an over fivefold increase in GBS EOD rates in risk-based IAP.68 Seedat et al. have indicated that universal GBS screening is a complex field and that the current evidence about screening is unclear in terms of whether it would do more good than harm.12 The harms of universal screening and IAP include maternal antibiotic reactions, the development of antibiotic-resistant bacteria, the impact on the infant microbiome, and healthcare expenditures.69 Future research directions should focus on cost-effectiveness studies regarding universal screening GBS and IAP. The development of vaccines for maternal immunization against GBS disease should be prioritized.70


Figure 1 was drawn by Shengmenart with modification.


This research was supported by the Shenzhen Science and Technology Plan (JCYJ20180228162311024).

Conflicts of Interest



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Streptococcal infections; Pregnancy; Screening; Intrapartum antibiotic prophylaxis

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