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Group B streptococcal infection in pregnant individuals

Group B streptococcal infection in pregnant individuals
Authors:
Karen M Puopolo, MD, PhD
Lawrence C Madoff, MD
Section Editor:
Daniel J Sexton, MD
Deputy Editor:
Milana Bogorodskaya, MD
Literature review current through: Mar 2022. | This topic last updated: Dec 01, 2021.

INTRODUCTION — Group B streptococcus (GBS; Streptococcus agalactiae) is a gram-positive coccus that frequently colonizes the human genital and gastrointestinal tracts, and less frequently, the upper respiratory tract of children and adults [1,2]. It is an important cause of illness in neonates, young infants, pregnant women, and adults with underlying medical conditions [3].

In pregnant and postpartum women, GBS is a frequent cause of asymptomatic bacteriuria, urinary tract infection, upper genital tract infection (ie, intra-amniotic infection or chorioamnionitis), post-caesarean wound infection, postpartum endometritis, pneumonia, puerperal sepsis, and bacteremia without a focus. GBS accounts for 1 to 5 percent of UTIs during pregnancy and 5 to 10 percent of peripartum bacteremia [4,5]. It also can cause focal infection such as meningitis and endocarditis, albeit rarely [6,7]. The serotype distribution of invasive GBS infection in pregnant women is similar to that of early-onset neonatal disease [8].

GBS infection in pregnant women will be reviewed here. The microbiology of GBS; GBS infection in neonates, young infants, and nonpregnant adults; and prevention strategies through chemoprophylaxis and vaccination are discussed separately. (See "Group B Streptococcus: Virulence factors and pathogenic mechanisms" and "Group B streptococcal infection in neonates and young infants" and "Group B streptococcal infections in nonpregnant adults" and "Prevention of early-onset group B streptococcal disease in neonates" and "Management of neonates at risk for early-onset group B streptococcal infection" and "Vaccines for the prevention of group B streptococcal disease".)

EPIDEMIOLOGY — GBS infections in pregnant women include urinary tract infection, intra-amniotic infection, endometritis, post-caesarean wound infection, and bacteremia [6,9,10]. Invasive maternal infection with GBS is associated with pregnancy loss, preterm delivery, and stillbirth [8,11,12]. Prior to the widespread use of maternal intrapartum chemoprophylaxis in the United States, maternal colonization with GBS conferred an increased risk of chorioamnionitis, and early postpartum infection [13,14]. There is no causal relationship between maternal GBS colonization during pregnancy and preterm delivery [15], but there is a strong association in most studies, and GBS does cause third trimester stillbirths [7,12].

In the Centers for Disease Control and Prevention (CDC) surveillance study including data collected from 1999 to 2005, the rate of invasive infection (defined as isolation of GBS from a blood or other usually sterile body site, excluding urine) in pregnant women was 0.12 per 1000 live births (range 0.11 to 0.14 per 1000 births) [8]. Upper genital tract infection accounted for approximately one-half of cases, isolated bacteremia occurred in one-third of cases, and GBS was isolated from maternal blood in approximately one-half of cases. Among women for whom pregnancy outcome data were available, approximately one-half of the maternal GBS infections led to fetal death, neonatal infections, neonatal death, or pregnancy loss.

A recent surveillance study from the United Kingdom (UK), where routine antenatal GBS screening and intrapartum chemoprophylaxis are not done, identified 185 invasive GBS infections (with GBS isolated from blood cultures) in pregnant or postpartum women during 2014, an incidence of 0.29 per 1000 pregnancies [7]. The vast majority of these infections (96 percent) occurred in the third trimester, and nearly half were associated with emergency caesarean delivery. Stillbirth and extreme prematurity (<28 weeks) occurred in 3.4 and 3.7 percent, respectively, which were higher than the UK baseline rate for each of 0.5 percent. There were no maternal deaths.

COLONIZATION — Colonization of pregnant women by GBS is a major risk factor for early- and late-onset infant GBS infection. Issues related to management of colonization and antibiotic prophylaxis for prevention of neonatal infection are discussed separately. (See "Prevention of early-onset group B streptococcal disease in neonates".)

INFECTIONS

Urinary tract — GBS is a frequent cause of asymptomatic bacteriuria, cystitis, and pyelonephritis during pregnancy. Meta-analyses of the impact of asymptomatic bacteriuria in pregnancy demonstrate an association between untreated, asymptomatic bacteriuria (independent of the bacterial species) with progression to pyelonephritis, and with low birth weight or preterm delivery [16,17]. The risk of adverse outcome is decreased with antibiotic treatment of asymptomatic bacteriuria in pregnancy [16,17].

Asymptomatic GBS bacteriuria in pregnancy is a marker for heavy genital colonization with GBS and, as such, is associated with increased risk of upper genital tract infection and postpartum endometritis [10,18]. Although Escherichia coli is the most frequently isolated organism in bacteriuria, cystitis, and pyelonephritis in pregnancy, GBS is isolated in 7 to 30 percent of pregnancy-associated cases of asymptomatic bacteriuria [19,20]. (See "Asymptomatic bacteriuria in adults", section on 'Pregnancy'.)

Asymptomatic bacteriuria — Asymptomatic bacteriuria is identified by screening urine cultures that are obtained during prenatal visits. At least one screening culture should be obtained during early pregnancy [21]. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Asymptomatic bacteriuria'.)

Intrapartum chemoprophylaxis at the time of delivery is recommended for women with any GBS bacteriuria (ie, at any colony count) to prevent neonatal infection. (See "Prevention of early-onset group B streptococcal disease in neonates".)

However, whether asymptomatic GBS bacteriuria during pregnancy warrants treatment at the time of identification depends on the quantification of bacteria (in colony-forming units [CFU] per mL) in the urine:

Bacteriuria ≥105 CFU per mL – We use a threshold of ≥105 CFU per mL for significant bacteriuria that warrants antimicrobial treatment in addition to later intrapartum chemoprophylaxis. This is based on the cutoff for reporting bacteriuria that is recommended by the Infectious Diseases Society of America (IDSA) [22] and American College of Obstetricians and Gynecologists (ACOG) guidelines [22,23]. Treatment of asymptomatic bacteriuria is associated with decreased rates of adverse pregnancy outcomes, as discussed below.

Antibiotic therapy is typically with amoxicillin, penicillin, or cephalexin. These drugs have not been associated with an increased risk of adverse pregnancy outcome or teratogenic effects. For patients with a history of penicillin allergy, ACOG recommends formal allergy testing to determine if they have true penicillin allergy [24]. For those determined to have severe IgE-mediated hypersensitivity that precludes penicillin and cephalosporin use, we suggest either nitrofurantoin or fosfomycin; these antibiotics are among the first-line options for cystitis in nonpregnant women [25]. Clindamycin should not be used for bacteriuria because it is poorly concentrated in the urine. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Antimicrobial treatment' and "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Antibiotic safety in pregnancy'.)

The optimal duration of therapy for asymptomatic bacteriuria in pregnancy is uncertain [22,24]; we generally give beta-lactam antibiotics for five to seven days. A repeat urine culture is typically performed following treatment to document clearance of bacteriuria. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Follow-up'.)

Bacteriuria <105 CFU per mL – We do not treat asymptomatic bacteriuria at these counts; it remains a reflection of anogenital colonization and an indication for intrapartum chemoprophylaxis. (See "Prevention of early-onset group B streptococcal disease in neonates".)

The utility of treating GBS bacteriuria at colony counts <105 prior to 35 weeks of gestation is controversial. Some studies have suggested that treating GBS bacteriuria at any colony count is associated with better pregnancy outcomes, as detailed below. Thus, some practitioners favor treatment as an attempt to prevent the subsequent development of pyelonephritis and to prevent preterm delivery [26]. However, low colony counts are more likely to reflect contamination from vaginal colonization rather than true bacteriuria, and colonization is not eradicated by antibiotic treatment [19,27]. We believe the risk of selecting for antimicrobial resistance outweighs the uncertain benefit of treatment of low colony counts.

Data evaluating the treatment of GBS asymptomatic bacteriuria during pregnancy are limited. In a trial of 69 women with GBS bacteriuria at 27 to 31 weeks of gestation, penicillin treatment at all colony counts reduced rates of preterm labor (5 versus 38 percent) and preterm rupture of the membranes (11 versus 53 percent) compared with placebo [28]. In a retrospective study of 305 women in early pregnancy (122 with bacteriuria of any colony count and 183 without bacteriuria), an association was observed between untreated GBS bacteriuria and chorioamnionitis at delivery (adjusted odds ratio 7.2; 95% CI 2.4-21.2) [18]. The study size was too small to stratify the association by colony count.

Cystitis — Cystitis is diagnosed by a positive urine culture in the clinical setting of urinary frequency, urgency, and dysuria without fever. It is treated with the same oral antibiotic regimens as asymptomatic GBS bacteriuria (see 'Asymptomatic bacteriuria' above). A repeat urine culture is typically performed following treatment to document clearance of bacteriuria. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Follow-up'.)

Women with GBS cystitis should receive intrapartum chemoprophylaxis at the time of delivery to prevent neonatal infection. Since GBS bacteriuria is a marker for "heavy" anogenital GBS colonization, which persists regardless of therapy for bacteriuria, women with documented GBS bacteriuria should not be screened again for GBS rectal/vaginal colonization later in pregnancy. (See "Prevention of early-onset group B streptococcal disease in neonates".)

Pyelonephritis — Pyelonephritis during pregnancy is diagnosed by a positive urine culture in the clinical setting of fever, urinary symptoms, nausea/vomiting, flank pain, and/or costovertebral angle tenderness. Treatment includes intravenous hydration and empiric intravenous antibiotics pending urine culture and susceptibility results (see "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Acute pyelonephritis'). In a series of 440 cases of pyelonephritis in pregnancy, GBS accounted for 10 percent of cases [29].

Treatment – If GBS is identified as the cause of pyelonephritis, we suggest directed treatment with penicillin G or ceftriaxone. In uncomplicated cases, the parenteral agent can be switched to an oral agent (eg, penicillin or cephalexin) after resolution of fever and other severe symptoms. The total duration of treatment is typically 10 to 14 days.

Severe beta-lactam allergy – In the setting of a confirmed, serious IgE-mediated allergy that precludes penicillin or cephalosporin use, we suggest vancomycin for initial parenteral therapy for pyelonephritis due to GBS. Once there is a clinical and microbiological response (ie, negative urine culture), transition to an oral regimen to complete a 10- to 14-day course may be appropriate, although options are limited. If the organism is susceptible, and the patient is in the second or early third trimester, trimethoprim sulfamethoxazole is a reasonable choice. Oral clindamycin can be used in any trimester if the GBS isolate is susceptible, although it is not typically used in pyelonephritis, and renal penetration is uncertain; nevertheless, it is reasonable to use in this limited situation if necessary [24]. If neither of these are options because of resistance and there is concern about other agents active against GBS (eg, fluoroquinolones or linezolid) because of uncertain safety in pregnancy, intravenous vancomycin can be used for the complete course. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy" and "Acute simple cystitis in women".)

Subsequent intrapartum chemoprophylaxis – Women with GBS pyelonephritis should receive intrapartum chemoprophylaxis at the time of delivery to prevent neonatal infection. Since GBS bacteriuria is a marker for "heavy" anogenital GBS colonization, which persists regardless of therapy for bacteriuria, women with documented GBS bacteriuria should not be screened again for GBS rectal/vaginal colonization later in pregnancy. (See "Prevention of early-onset group B streptococcal disease in neonates".)

Intra-amniotic infection — Intra-amniotic infection (IAI, also called chorioamnionitis) refers to infection of the amniotic fluid, membranes, placenta, and/or umbilical cord [30]. Clinical manifestations include fever, uterine tenderness, maternal and fetal tachycardia, purulent amniotic fluid, and maternal leukocytosis.

Microbiologic and pathologic criteria for GBS intra-amniotic infection include isolation of GBS from culture of placenta, amniotic fluid or amniotic membranes, or from fetal parts in case of pregnancy loss. However, these tissues are frequently contaminated during delivery. An uncontaminated amniotic fluid culture can be obtained by amniocentesis prior to rupture of the fetal membranes. After delivery, the best procedure for placental culture is to peel the amnion off the chorion for a significant amount of fetal surface, and then swab the exposed (and untouched) surface with a sterile swab several times before using the swab for culture inoculation. Fetal cultures can be performed on blood from the umbilical vessels or tissues/body fluids collected at autopsy.

Treatment is discussed separately. (See "Intraamniotic infection (clinical chorioamnionitis)", section on 'Maternal management'.)

Endometritis — Colonization with GBS significantly increases the risk of developing postpartum endometritis [11]. In studies of endometritis, GBS has been identified as a single pathogen in 2 to 14 percent of cases but is more commonly a component of polymicrobial infections [31]. Endometritis is treated with broad-spectrum antibiotics including anaerobic coverage. Treatment of endometritis is discussed in detail elsewhere. (See "Postpartum endometritis", section on 'Treatment'.)

Bacteremia — In a study of obstetric patients in the 1970s, GBS was the second most common cause of bacteremia [32]. In a Finnish review of women with peripartum sepsis in the 1990s, GBS was the single most common organism isolated [33]. Both studies demonstrated a variety of aerobic and anaerobic gram-positive and gram-negative pathogens other than GBS, suggesting that empiric therapy for suspected bacteremia must consist of broad-spectrum therapy that includes anaerobic coverage. Since implementation of maternal intrapartum GBS chemoprophylaxis, data on the distribution of organisms causing peripartum bacteremia have been lacking. A study of 195 peripartum bacteremia bacterial isolates in the era of screening-based GBS prophylaxis (2000-2008) demonstrated that only 4 percent of blood culture isolates were due to GBS [34]; in a subsequent study of 120 bacteremic peripartum individuals between 2009 and 2016, GBS was isolated in 11 percent of cases [4].

GBS bacteremia is discussed further separately. (See "Group B streptococcal infections in nonpregnant adults".)

Other infections — GBS rarely has been associated with a variety of unusual peripartum infections such as maternal meningitis (both antepartum and postpartum), endocarditis, abdominal abscess, and necrotizing fasciitis [31,35,36], following both live births and elective pregnancy termination [37,38]. These are discussed further separately. (See "Group B streptococcal infections in nonpregnant adults".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Group B streptococcal infection in pregnant women and neonates".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Group B streptococcal disease and pregnancy (The Basics)")

Beyond the Basics topic (see "Patient education: Group B streptococcus and pregnancy (Beyond the Basics)")

SUMMARY

Group B streptococcus (GBS; Streptococcus agalactiae) is a gram-positive coccus that frequently colonizes the human genital and gastrointestinal tracts and, less commonly, the upper respiratory tract. It is an important cause of illness in neonates, young infants, pregnant women, and adults with underlying medical conditions. (See 'Introduction' above.)

Invasive maternal infection with GBS is associated with pregnancy loss and preterm delivery. Prior to the widespread use of maternal intrapartum chemoprophylaxis, maternal colonization with GBS conferred an increased risk of intra-amniotic infection, and early postpartum infection. It is not clear whether there is an association between maternal GBS colonization during pregnancy and preterm delivery, but GBS does cause third trimester stillbirths. Issues related to management of colonization and antibiotic prophylaxis for prevention of neonatal infection are discussed separately. (See 'Epidemiology' above and "Prevention of early-onset group B streptococcal disease in neonates".)

GBS is a frequent cause of asymptomatic bacteriuria, cystitis, and pyelonephritis during pregnancy. There is an association between untreated, asymptomatic bacteriuria (independent of the bacterial species) with progression to pyelonephritis, and with low birth weight or preterm delivery. The risk of adverse outcome is decreased with antibiotic treatment of asymptomatic bacteriuria in pregnancy. (See 'Urinary tract' above.)

Asymptomatic GBS bacteriuria in pregnancy is a marker for heavy genital colonization with GBS and, as such, is associated with increased risk of upper genital tract infection and postpartum endometritis. Asymptomatic bacteriuria is identified by screening urine cultures that are obtained during prenatal visit. At least one screening urine culture should be obtained during early pregnancy. (See 'Urinary tract' above and 'Asymptomatic bacteriuria' above.)

The threshold for treatment of asymptomatic bacteriuria with GBS is a colony count ≥105, as in the general approach to asymptomatic bacteriuria in pregnant women. We suggest antibiotic therapy with penicillin, amoxicillin, or cephalexin for five to seven days (Grade 2C). A repeat urine culture is typically performed following treatment to document clearance of bacteriuria. (See 'Asymptomatic bacteriuria' above.)

Genital colonization with GBS persists despite adequate therapy for GBS bacteriuria. Documented GBS bacteriuria during pregnancy is an indication for intrapartum chemoprophylaxis at the time of delivery. (See "Prevention of early-onset group B streptococcal disease in neonates".)

Cystitis is diagnosed by a positive urine culture in the clinical setting of urinary frequency, urgency, and dysuria without fever. It is treated with the same oral antibiotic regimens as asymptomatic GBS bacteriuria in pregnancy. A repeat urine culture is typically performed following treatment to document clearance of bacteriuria. (See 'Cystitis' above.)

Pyelonephritis during pregnancy is diagnosed by a positive urine culture in the clinical setting of fever, urinary symptoms, nausea/vomiting, flank pain, and/or costovertebral angle tenderness. Treatment includes intravenous hydration and intravenous antibiotics. If GBS is identified as the cause of pyelonephritis, we suggest initial treatment with penicillin G or ceftriaxone (Grade 2C). In uncomplicated infection following clinical improvement, the regimen can be transitioned to an oral antibiotic for a total 10- to 14-day course. (See 'Pyelonephritis' above.)

Other infections associated with GBS include intra-amniotic infection (chorioamnionitis), endometritis, and bacteremia. Rare peripartum infections include maternal meningitis (both antepartum and postpartum), endocarditis, abdominal abscess, and necrotizing fasciitis. (See 'Intra-amniotic infection' above and 'Endometritis' above and 'Bacteremia' above and 'Other infections' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Carol J Baker, MD, who contributed to an earlier version of this topic review.

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