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Group B streptococcal infection in pregnant women

Group B streptococcal infection in pregnant women
Authors:
Karen M Puopolo, MD, PhD
Lawrence C Madoff, MD
Carol J Baker, MD
Section Editor:
Daniel J Sexton, MD
Deputy Editor:
Milana Bogorodskaya, MD
Literature review current through: Aug 2021. | This topic last updated: Sep 24, 2019.

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), postpartum endometritis (8 percent), pneumonia (2 percent), puerperal sepsis (2 percent), and bacteremia without a focus (31 percent). It also can cause focal infection such as meningitis and endocarditis, albeit rarely. The serotype distribution of invasive GBS infection in pregnant women is similar to that of early-onset neonatal disease [4].

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 "Early-onset neonatal group B streptococcal disease: Prevention" 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, and bacteremia [5,6]. Invasive maternal infection with GBS is associated with pregnancy loss and preterm delivery [4,7]. Prior to the widespread use of maternal intrapartum chemoprophylaxis, maternal colonization with GBS conferred an increased risk of chorioamnionitis, and early postpartum infection [8,9]. There is no clear association between maternal GBS colonization during pregnancy and preterm delivery [10], but GBS does cause third trimester stillbirths [11].

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) [4]. 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.

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 "Early-onset neonatal group B streptococcal disease: Prevention".)

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 [12,13]. The risk of adverse outcome is decreased with antibiotic treatment of asymptomatic bacteriuria in pregnancy [12,13].

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 [6,14]. 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 [15,16]. (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 [17]. (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 "Early-onset neonatal group B streptococcal disease: Prevention".)

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 American College of Obstetricians and Gynecologists (ACOG) guidelines [18,19] and is consistent with obstetric expert opinion. 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 [19]; some patients are still able to take beta-lactams. For those determined to have severe IgE-mediated hypersensitivity to penicillins and cephalosporins, clindamycin is the only oral alternative, if the GBS isolate is susceptible. For cases in which the isolate is resistant to clindamycin, investigation and confirmation of the nature of the allergy is critical, and ultimately desensitization may be warranted. (See "Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam antibiotics", section on 'Allergy evaluation and penicillin skin testing'.)

The optimal duration of therapy for asymptomatic bacteriuria in pregnancy is uncertain [18,19]; 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 "Early-onset neonatal group B streptococcal disease: Prevention".)

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 [20]. 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 [15,21]. 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 [22]. 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) [14]. 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 "Early-onset neonatal group B streptococcal disease: Prevention".)

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. In a series of 440 cases of pyelonephritis in pregnancy, GBS accounted for 10 percent of cases [23]. Empiric treatment includes intravenous hydration and intravenous antibiotics (table 1). If GBS is identified as the cause of pyelonephritis, treatment with penicillin G may be administered for a total duration of 10 days, tailored to evidence of clinical improvement [24]. In otherwise uncomplicated cases, treatment can be continued with an oral agent (eg, penicillin or cephalexin) after resolution of fever and other severe symptoms.

In the setting of a serious IgE mediated allergy to penicillin and cephalosporins, vancomycin should be employed until there is a clinical and microbiological response (ie, negative urine culture). Oral clindamycin can be used, if the GBS isolate is susceptible, to complete the course of therapy (eg, 10 to 14 days depending on clinical response). Even though clindamycin is not a typical agent for pyelonephritis, it is a reasonable option in this limited situation. In the setting of known or suspected clindamycin resistance, oral cephalexin is an alternative if the patient is able to tolerate a test dose before hospital discharge. Otherwise, intravenous vancomycin can be used for the complete course. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy" and "Acute simple cystitis in women".)

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 "Early-onset neonatal group B streptococcal disease: Prevention".)

Intra-amniotic infection — Intra-amniotic infection (IAI, also called chorioamnionitis) refers to infection of the amniotic fluid, membranes, placenta, and/or umbilical cord [25]. 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 or triple I)", section on 'Maternal management'.)

Endometritis — Colonization with GBS significantly increases the risk of developing postpartum endometritis [7]. 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 [26]. 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 [27]. In a Finnish review of women with peripartum sepsis in the 1990s, GBS was the single most common organism isolated [28]. 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. E. coli and enterococci accounted for over half of all isolates, and 13 percent of isolates were anaerobic species [29].

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 [26,30,31], following both live births and elective pregnancy termination [32,33]. 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 (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 "Early-onset neonatal group B streptococcal disease: Prevention".)

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. Antibiotic therapy is typically with penicillin, amoxicillin, or cephalexin for five to seven days. 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 "Early-onset neonatal group B streptococcal disease: Prevention".)

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. 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, treatment with penicillin G may be administered for a total duration of 10 days, tailored to evidence of clinical improvement. (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.)

REFERENCES

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  2. Eichenwald EC. Perinatally transmitted neonatal bacterial infections. Infect Dis Clin North Am 1997; 11:223.
  3. Verani JR, McGee L, Schrag SJ, Division of Bacterial Diseases, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention (CDC). Prevention of perinatal group B streptococcal disease--revised guidelines from CDC, 2010. MMWR Recomm Rep 2010; 59:1.
  4. Phares CR, Lynfield R, Farley MM, et al. Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005. JAMA 2008; 299:2056.
  5. Regan JA, Klebanoff MA, Nugent RP, et al. Colonization with group B streptococci in pregnancy and adverse outcome. VIP Study Group. Am J Obstet Gynecol 1996; 174:1354.
  6. Krohn MA, Hillier SL, Baker CJ. Maternal peripartum complications associated with vaginal group B streptococci colonization. J Infect Dis 1999; 179:1410.
  7. Zaleznik DF, Rench MA, Hillier S, et al. Invasive disease due to group B Streptococcus in pregnant women and neonates from diverse population groups. Clin Infect Dis 2000; 30:276.
  8. Schrag SJ, Zywicki S, Farley MM, et al. Group B streptococcal disease in the era of intrapartum antibiotic prophylaxis. N Engl J Med 2000; 342:15.
  9. Prevention of perinatal group B streptococcal disease: a public health perspective. Centers for Disease Control and Prevention. MMWR Recomm Rep 1996; 45:1.
  10. Valkenburg-van den Berg AW, Sprij AJ, Dekker FW, et al. Association between colonization with Group B Streptococcus and preterm delivery: a systematic review. Acta Obstet Gynecol Scand 2009; 88:958.
  11. Seale AC, Bianchi-Jassir F, Russell NJ, et al. Estimates of the Burden of Group B Streptococcal Disease Worldwide for Pregnant Women, Stillbirths, and Children. Clin Infect Dis 2017; 65:S200.
  12. Romero R, Oyarzun E, Mazor M, et al. Meta-analysis of the relationship between asymptomatic bacteriuria and preterm delivery/low birth weight. Obstet Gynecol 1989; 73:576.
  13. Mittendorf R, Williams MA, Kass EH. Prevention of preterm delivery and low birth weight associated with asymptomatic bacteriuria. Clin Infect Dis 1992; 14:927.
  14. Anderson BL, Simhan HN, Simons KM, Wiesenfeld HC. Untreated asymptomatic group B streptococcal bacteriuria early in pregnancy and chorioamnionitis at delivery. Am J Obstet Gynecol 2007; 196:524.e1.
  15. Wood EG, Dillon HC Jr. A prospective study of group B streptococcal bacteriuria in pregnancy. Am J Obstet Gynecol 1981; 140:515.
  16. Persson K, Bjerre B, Elfström L, et al. Group B streptococci at delivery: high count in urine increases risk for neonatal colonization. Scand J Infect Dis 1986; 18:525.
  17. Nicolle LE, Bradley S, Colgan R, et al. Infectious Diseases Society of America guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults. Clin Infect Dis 2005; 40:643.
  18. Nicolle LE, Gupta K, Bradley SF, et al. Clinical Practice Guideline for the Management of Asymptomatic Bacteriuria: 2019 Update by the Infectious Diseases Society of America. Clin Infect Dis 2019; 68:e83.
  19. Prevention of Group B Streptococcal Early-Onset Disease in Newborns: ACOG Committee Opinion, Number 782. Obstet Gynecol 2019; 134:1.
  20. Aungst M, King J, Steele A, Gordon M. Low colony counts of asymptomatic group B streptococcus bacteriuria: a survey of practice patterns. Am J Perinatol 2004; 21:403.
  21. Persson K, Christensen KK, Christensen P, et al. Asymptomatic bacteriuria during pregnancy with special reference to group B streptococci. Scand J Infect Dis 1985; 17:195.
  22. Thomsen AC, Mørup L, Hansen KB. Antibiotic elimination of group-B streptococci in urine in prevention of preterm labour. Lancet 1987; 1:591.
  23. Hill JB, Sheffield JS, McIntire DD, Wendel GD Jr. Acute pyelonephritis in pregnancy. Obstet Gynecol 2005; 105:18.
  24. ACOG educational bulletin. Antimicrobial therapy for obstetric patients. Number 245, March 1998 (replaces no. 117, June 1988). American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet 1998; 61:299.
  25. Hitti J, Tarczy-Hornoch P, Murphy J, et al. Amniotic fluid infection, cytokines, and adverse outcome among infants at 34 weeks' gestation or less. Obstet Gynecol 2001; 98:1080.
  26. Isada NB, Grossman JH. Perinatal Infections. In: Obstetrics: Normal and Problem Pregnancies, Gabbe SG, Niebyl JR, Simpson JL (Eds), Churchill Livingstone, New York 1991. p.1276.
  27. Blanco JD, Gibbs RS, Castaneda YS. Bacteremia in obstetrics: clinical course. Obstet Gynecol 1981; 58:621.
  28. Kankuri E, Kurki T, Carlson P, Hiilesmaa V. Incidence, treatment and outcome of peripartum sepsis. Acta Obstet Gynecol Scand 2003; 82:730.
  29. Cape A, Tuomala RE, Taylor C, Puopolo KM. Peripartum bacteremia in the era of group B streptococcus prophylaxis. Obstet Gynecol 2013; 121:812.
  30. Guerin JM, Leibinger F, Mofredj A, Ekherian JM. Streptococcus B meningitis in post-partum. J Infect 1997; 34:151.
  31. Braun TI, Pinover W, Sih P. Group B streptococcal meningitis in a pregnant woman before the onset of labor. Clin Infect Dis 1995; 21:1042.
  32. Deziel PJ, McGuire N, Brown PD. Group B streptococcal meningitis complicating elective abortion: report of 2 cases. Clin Infect Dis 2000; 31:E23.
  33. Palys EE, Li J, Gaut PL, Hardy WD. Tricuspid valve endocarditis with Group B Streptococcus after an elective abortion: the need for new data. Infect Dis Obstet Gynecol 2006; 2006:43253.
Topic 3170 Version 31.0

References

1 : Edwards MS, Nizet V, Baker CJ. Group B Streptococcal Infections. In: Infectious Diseases of the Fetus and Newborn Infant, 8th ed, Remington JS, Klein JO, Wilson CB, et al (Eds), Elsevier Saunders, Philadelphia 2016. p.411.

2 : Perinatally transmitted neonatal bacterial infections.

3 : Prevention of perinatal group B streptococcal disease--revised guidelines from CDC, 2010.

4 : Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005.

5 : Colonization with group B streptococci in pregnancy and adverse outcome. VIP Study Group.

6 : Maternal peripartum complications associated with vaginal group B streptococci colonization.

7 : Invasive disease due to group B Streptococcus in pregnant women and neonates from diverse population groups.

8 : Group B streptococcal disease in the era of intrapartum antibiotic prophylaxis.

9 : Prevention of perinatal group B streptococcal disease: a public health perspective. Centers for Disease Control and Prevention.

10 : Association between colonization with Group B Streptococcus and preterm delivery: a systematic review.

11 : Estimates of the Burden of Group B Streptococcal Disease Worldwide for Pregnant Women, Stillbirths, and Children.

12 : Meta-analysis of the relationship between asymptomatic bacteriuria and preterm delivery/low birth weight.

13 : Prevention of preterm delivery and low birth weight associated with asymptomatic bacteriuria.

14 : Untreated asymptomatic group B streptococcal bacteriuria early in pregnancy and chorioamnionitis at delivery.

15 : A prospective study of group B streptococcal bacteriuria in pregnancy.

16 : Group B streptococci at delivery: high count in urine increases risk for neonatal colonization.

17 : Infectious Diseases Society of America guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults.

18 : Clinical Practice Guideline for the Management of Asymptomatic Bacteriuria: 2019 Update by the Infectious Diseases Society of America.

19 : Prevention of Group B Streptococcal Early-Onset Disease in Newborns: ACOG Committee Opinion, Number 782.

20 : Low colony counts of asymptomatic group B streptococcus bacteriuria: a survey of practice patterns.

21 : Asymptomatic bacteriuria during pregnancy with special reference to group B streptococci.

22 : Antibiotic elimination of group-B streptococci in urine in prevention of preterm labour.

23 : Acute pyelonephritis in pregnancy.

24 : ACOG educational bulletin. Antimicrobial therapy for obstetric patients. Number 245, March 1998 (replaces no. 117, June 1988). American College of Obstetricians and Gynecologists.

25 : Amniotic fluid infection, cytokines, and adverse outcome among infants at 34 weeks' gestation or less.

26 : Amniotic fluid infection, cytokines, and adverse outcome among infants at 34 weeks' gestation or less.

27 : Bacteremia in obstetrics: clinical course.

28 : Incidence, treatment and outcome of peripartum sepsis.

29 : Peripartum bacteremia in the era of group B streptococcus prophylaxis.

30 : Streptococcus B meningitis in post-partum.

31 : Group B streptococcal meningitis in a pregnant woman before the onset of labor.

32 : Group B streptococcal meningitis complicating elective abortion: report of 2 cases.

33 : Tricuspid valve endocarditis with Group B Streptococcus after an elective abortion: the need for new data.