What antibiotics treat group B streptococcus?

Onset of group B streptococcal infection in babies

The two types of GBS disease that affect babies include:

• early-onset – the newborn shows signs of illness shortly after birth or within one to two days of birth. Early-onset GBS disease is the most common type
• late-onset – infants show signs of illness one week to several months after birth. This form of GBS disease is comparatively rare. Only around half of all babies with late-onset GBS disease contract the illness from their infected mothers. For the remainder of cases, the source of infection is unknown.

Diagnosis and treatment for group B streptococcal infection

GBS infection is diagnosed from specimens collected from blood, urine or spinal fluid. Vaginal swabs may be collected from pregnant women to determine if they are asymptomatic carriers of these bacteria.

The principal form of treatment for GBS is intravenous antibiotics, usually given in hospital. If the bacteria are found in a pregnant woman, intravenous antibiotics are given during the labour.

Screening methods for group B streptococcal infection

There is no standard screening procedure for GBS in Australia and the protocols vary from hospital to hospital. Some facilities screen only ‘at-risk’ pregnant women for GBS infection, while others screen all pregnant women at 35 to 37 weeks. A recent Australian review of the published evidence reported lower rates of GBS disease among infants in hospitals where all pregnant women were screened for GBS. However, it acknowledged that there are advantages and disadvantages to each approach to screening. A recent statement from the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) listed both of the above approaches to GBS screening as being acceptable.

The main screening test is a swab of the vagina. A swab of the rectum (back passage) may also be taken. Research indicates that screening tests taken late in pregnancy are more reliable. For example, around 10 to 20 per cent of pregnant woman who have GBS-negative swabs at 28 weeks gestation are carrying the bacteria at the time of delivery.

Risk factors for group B streptococcal infection

If a pregnant woman is found to be a GBS carrier, the infection can easily be treated with intravenous antibiotics. Risk factors that may prompt your obstetrician to screen for GBS infection include:

• a GBS-positive swab in a previous pregnancy
• a previous baby with GBS infection
• pre-term labour
• rupturing of the membranes well before the onset of labour (18 hours or more)
• signs of infection around the time of labour or delivery (such as fever in the mother)
• prolonged labour.

For non-pregnant women and others, chronic diseases such as diabetes or cancer make you more vulnerable to getting GBS infection.

Where to get help

• Your doctor
• NURSE-ON-CALL. Tel. 1300 60 60 24 – for expert health information and advice (24 hours, 7 days)
• Your obstetrician or midwife
• Your maternity hospital.

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Group B Streptococcus (GBS) is a gram-positive bacteria that colonizes the gastrointestinal and genitourinary tract. It is known to cause both early onset and late onset infections in neonates. This activity describes the evaluation and management of group B Streptococcus and explains the role of the interprofessional team in improving care for patients with this condition.

Objectives:

• Describe the epidemiology of group B Streptococcus infection.

• Review the use of rectovaginal culture for the evaluation of group B Streptococcus infection in pregnant females.

• Outline the use of intravenous penicillin G in the treatment of group B Streptococcus infection.

• Summarize the importance of improving care coordination among the interprofessional team members to enhance the delivery of care for patients affected by group B Streptococcus infection.

Group B Streptococcus (GBS) or Streptococcus agalactiae is a gram-positive bacteria which colonizes the gastrointestinal and genitourinary tract[1]. In the United States of America, GBS is known to be the most common infectious cause of morbidity and mortality in neonates[2][3][2]. GBS is known to cause both early onset and late onset infections in neonates, but current interventions are only effective in the prevention of early-onset disease[1][4][1]. Early onset GBS infections occur within the first week of life, whereas late-onset disease occurs beyond the first week of life[1][4][1]. The following chapter will focus on the current guidelines regarding screening of pregnant patients for GBS during prenatal care and intrapartum prophylaxis aimed at the prevention of early-onset GBS infection.

The main risk factor for early-onset GBS infection is colonization of the maternal genital tract with Group B Streptococcus during labor[2][5][2]. GBS is a normal flora of the gastrointestinal (GI) tract, which is thought to be the main source for maternal colonization[2][6][2]. GBS cultures should be obtained with each pregnancy because colonization may be temporary[2]. Positive GBS urinary tract infection at any time during the pregnancy is a marker of heavy colonization, and these patients should receive prophylaxis even if GBS culture is negative between 35 to 37 weeks[2]. Additional risk factors for early onset GBS disease include young maternal age and black race[2]. Preterm labor (less than 37 weeks), maternal fever during labor (greater than 100.4 F or 36 C), and prolonged rupture of membranes (greater than 18 hours) are also labor characteristics which are risk factors for early-onset GBS disease. GBS colonization has an incidence of 10-30% in pregnancy[2]. Without preventative measures, early onset GBS infection occurs in 1% to 2% of neonates born to mothers with GBS colonization[2].

As stated above, GBS colonization has an incidence of 10-30% in pregnancy[2]. Over the last 20 years, developments in screening for GBS colonization, intrapartum prophylaxis, and secondary prevention of early-onset GBS disease have resulted in a significant decrease in the incidence of early-onset GBS infection[2]. In the early 1990s, there were approximately 1.7 cases of early-onset GBS infection per 1000 live births. This has decreased to 0.34 to 0.37 per 1000 live births in recent years[2]. Seventy percent of cases of early-onset GBS infection are in term infants (greater than 37 weeks)[2]. Interestingly, 60% of early-onset infections occur in patients with a negative rectovaginal GBS culture between 35 to 37 weeks[2]. Group B streptococcus colonization in the rectovaginal area is discontinuous. Up to 33% of patients whom have a positive GBS culture at 35-37 weeks, are not colonized at delivery. On the contrary approximately 10% of women who are colonized at delivery will have a negative culture at 35-37 weeks. [7]

The principal route of neonatal early onset GBS infection is vertical transmission from colonized mothers during passage through the vagina during labor and delivery[8]. The majority of infants exposed to GBS during delivery become colonized with GBS and do not develop signs or symptoms of GBS infection[2]. The fetus is also susceptible to ascending infection into the amniotic fluid, with or without rupture of membranes[2]. 

The principal defense against early-onset GBS infection is the administration of antibiotic prophylaxis to mothers during labor and delivery. Identification of patients who will benefit from intrapartum prophylaxis is an important aspect of routine prenatal care[9][10]. The Center for Disease Control and Prevention (CDC) recommends a universal culture-based screening[2]. Obstetrics providers should perform a rectovaginal culture for GBS in all patients between 35 and 37 weeks of gestation[1]. Cultures are performed at this point in gestation because the negative predictive value of the GBS culture is highest (95% to 99%) in the first 5 weeks after collection[2]. Patients who have an indication for preterm or early term induction of labor will benefit from GBS culture at or before 35 weeks, whereas nulliparous patients with unfavorable cervix may benefit from GBS culture collection at 37 weeks[2]. Antibiotic susceptibility testing must be performed on all GBS cultures to guide antibiotic prophylaxis in penicillin-allergic patients[2].

GBS bacteriuria is another marker of genital tract colonization[2]. All pregnant patients should be screened for asymptomatic bacteriuria during pregnancy, and all women with GBS bacteriuria at any point during the pregnancy should receive intrapartum prophylaxis[2]. 

If GBS status is unknown, antibiotic prophylaxis should be initiated in patients with preterm labor (less than 37 weeks gestation), maternal fever during labor (greater than 100.4 F or 38 C), membranes ruptured greater than 18 hours, and/or in patients with a history of a previous child with invasive early-onset GBS infection[1].

Intravenous penicillin G is the treatment of choice for intrapartum antibiotic prophylaxis against Group B Streptococcus[1][11][1]. Penicillin G 5 million units intravenous is administered as a loading dose, followed by 2.5 to 3 million units every 4 hours during labor until delivery[1]. Ampicillin is a reasonable alternative to penicillin G if penicillin G is unavailable[1]. Ampicillin is administered as a 2 gm intravenous loading dose followed by 1 gm intravenous every 4 hours during labor until delivery[1].

Penicillin G and ampicillin should not be used in patients with penicillin allergy. Antibiotic prophylaxis in patients with a history of anaphylaxis, angioedema, respiratory distress, or urticaria following penicillin or cephalosporin is guided by antibiotic susceptibility testing[1]. If GBS is sensitive to both clindamycin and erythromycin, then clindamycin 900 mg intravenous every 8 hours is recommended for GBS prophylaxis during labor until delivery[1]. Occasionally GBS susceptibility testing will return susceptible to clindamycin but resistant to erythromycin. Resistance to erythromycin can induce resistance to clindamycin even in the presence of a culture that appears sensitive to clindamycin. For this reason, if the culture returns resistant to erythromycin, vancomycin 1 gm intravenously every 12 hours is recommended for GBS prophylaxis[1].

In patients without GBS susceptibility testing with penicillin allergy, vancomycin is recommended for GBS prophylaxis with dosing as described above[1]. However, resistance to fluoroquinolones, macrolides and vancomycin has been reported[12][13][14].

Cefazolin 2 gram intravenous loading dose followed by 1 gm every 8 hours may be used in patients without a history of anaphylaxis, angioedema, respiratory distress, or urticaria following penicillin or cephalosporin administration[1].

Initiating antibiotic prophylaxis greater than 4 hours before delivery is considered to be adequate antibiotic prophylaxis and is effective in the prevention of transmission of GBS to the fetus. However, antibiotic prophylaxis administered at a shorter interval will provide some protection. If a patient presents in active labor and delivery is expected in less than 4 hours, antibiotic prophylaxis should still be initiated[2].

GBS vaccines show promise to combat early-onset GBS infection, but there are currently no approved GBS vaccines on the market[2][15][2].

Differential Diagnosis

• Urinary tract infection in females

• Dermatologic manifestations of necrotizing fasciitis

• Osteomyelitis in emergency medicine

• Urinary tract infection in pregnancy

Since the initiation of universal screening for GBS colonization and intrapartum antibiotic prophylaxis, the incidence of early-onset GBS infection has decreased approximately 80%[2][16][2][17][2]. Efficacy of intrapartum antibiotic prophylaxis is estimated between 86% to 89%[2]. GBS culture screening during prenatal care will not identify all women with GBS colonization during labor because genital tract colonization can be temporary. Approximately 60% of cases of early-onset GBS infection occur in neonates born to patients with negative GBS culture at 35 to 37 weeks[2].

Early-onset GBS infection typically presents in the first 24 to 48 hours of life. Symptoms include respiratory distress, apnea, with signs of sepsis[2]. Sepsis and pneumonia commonly result from early-onset GBS infection, but rarely meningitis can occur[2]. Mortality from early-onset GBS infection is much higher in preterm infants than term infants. Preterm infants with early-onset GBS infection have a case fatality rate between 20% to 30% compared to 2% to 3% in term infants[2].

Infection and colonization of maternal group B streptococcus (GBS) can result in various adverse outcomes, which include increased rates of febrile morbidity and chorioamnionitis that can lead to maternal sepsis[18][19][20]. In addition, maternal GBS is also responsible for causing endometritis, cesarean delivery, postoperative wound infections, pyelonephritis, and other ascending infections resulting in maternal sepsis and subsequently preterm births[21][22][23][24]. Furthermore, maternal mastitis and breast abscess can also be caused by maternal group B streptococcus[25][26]. Lastly, meningitis, endocarditis, and osteomyelitis have also been described as complications in rare instances[27][28][29].

Pearls and Other Issues

• In the United States of America, GBS is known to be the most common infectious cause of morbidity and mortality in neonates[2].

• Intrapartum antibiotic prophylaxis is only effective in the prevention of early-onset GBS infection[2].

• The CDC recommends universal screening with GBS rectovaginal culture between 35 to 37 weeks in each pregnancy[2]. 

• Intrapartum antibiotic prophylaxis is recommended with positive GBS rectovaginal culture, GBS bacteriuria at any time during the pregnancy, or a history of delivery of infant affected by early onset GBS infection[2].

• If GBS status is unknown, antibiotic prophylaxis is recommended during preterm labor and delivery (less than 37 weeks), in the presence of maternal fever during labor, or with prolonged rupture of membranes (greater than 18 hours)[2].

• Intravenous Penicillin G is the antibiotic of choice for intrapartum prophylaxis[1].

• Additional options for antibiotic prophylaxis are ampicillin, cefazolin, clindamycin, or vancomycin[1].

Prevention of GBS infection during pregnancy requires an interprofessional team effort. All healthcare workers who look after pregnant women should screen these patients for GBS. This may include physicians, physician's assistants, nurse practioners, midwives and/or nurses.

Since the initiation of universal screening for GBS colonization and intrapartum antibiotic prophylaxis, the incidence of early-onset GBS infection has decreased approximately 80%[2]. Efficacy of intrapartum antibiotic prophylaxis is estimated between 86% to 89%[2]. GBS culture screening during prenatal care will not identify all women with GBS colonization during labor because genital tract colonization can be temporary. Approximately 60% of cases of early-onset GBS infection occur in neonates born to patients with negative GBS culture at 35 to 37 weeks[2].

Review Questions

1.

ACOG Committee Opinion No. 485: Prevention of early-onset group B streptococcal disease in newborns. Obstet Gynecol. 2011 Apr;117(4):1019-1027. [PubMed: 21422882]

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 Nov 19;59(RR-10):1-36. [PubMed: 21088663]

Ahmadzia HK, Heine RP. Diagnosis and management of group B streptococcus in pregnancy. Obstet Gynecol Clin North Am. 2014 Dec;41(4):629-47. [PubMed: 25454995]

Borghesi A, Stronati M, Fellay J. Neonatal Group B Streptococcal Disease in Otherwise Healthy Infants: Failure of Specific Neonatal Immune Responses. Front Immunol. 2017;8:215. [PMC free article: PMC5339282] [PubMed: 28326082]

Shane AL, Stoll BJ. Neonatal sepsis: progress towards improved outcomes. J Infect. 2014 Jan;68 Suppl 1:S24-32. [PubMed: 24140138]

Alshengeti A, Alharbi A, Alraddadi S, Alawfi A, Aljohani B. Knowledge, attitude and current practices of pregnant women towards group B streptococcus screening: cross-sectional study, Al-Madinah, Saudi Arabia. BMJ Open. 2020 Feb 12;10(2):e032487. [PMC free article: PMC7045259] [PubMed: 32054626]

Regan JA, Klebanoff MA, Nugent RP, Eschenbach DA, Blackwelder WC, Lou Y, Gibbs RS, Rettig PJ, Martin DH, Edelman R. Colonization with group B streptococci in pregnancy and adverse outcome. VIP Study Group. Am J Obstet Gynecol. 1996 Apr;174(4):1354-60. [PubMed: 8623869]

Schrag SJ, Verani JR. Intrapartum antibiotic prophylaxis for the prevention of perinatal group B streptococcal disease: experience in the United States and implications for a potential group B streptococcal vaccine. Vaccine. 2013 Aug 28;31 Suppl 4:D20-6. [PubMed: 23219695]

Darlow B, Campbell N, Austin N, Chin A, Grigg C, Skidmore C, Voss L, Walls T, Wise M, Werno A. The prevention of early-onset neonatal group B streptococcus infection: New Zealand Consensus Guidelines 2014. N Z Med J. 2015 Nov 20;128(1425):69-76. [PubMed: 26905989]

Santhanam S, Arun S, Rebekah G, Ponmudi NJ, Chandran J, Jose R, Jana AK. Perinatal Risk Factors for Neonatal Early-onset Group B Streptococcal Sepsis after Initiation of Risk-based Maternal Intrapartum Antibiotic Prophylaxis-A Case Control Study. J Trop Pediatr. 2018 Aug 01;64(4):312-316. [PubMed: 29036682]

Raabe VN, Shane AL. Group B Streptococcus (Streptococcus agalactiae). Microbiol Spectr. 2019 Mar;7(2) [PMC free article: PMC6432937] [PubMed: 30900541]

Park SY, Park Y, Chung JW, Huh HJ, Chae SL, Kim YA, Lee SS. Group B streptococcal bacteremia in non-pregnant adults: results from two Korean centers. Eur J Clin Microbiol Infect Dis. 2014 Oct;33(10):1785-90. [PubMed: 24825185]

Seki T, Kimura K, Reid ME, Miyazaki A, Banno H, Jin W, Wachino J, Yamada K, Arakawa Y. High isolation rate of MDR group B streptococci with reduced penicillin susceptibility in Japan. J Antimicrob Chemother. 2015 Oct;70(10):2725-8. [PubMed: 26169560]

Piccinelli G, Gargiulo F, Corbellini S, Ravizzola G, Bonfanti C, Caruso A, De Francesco MA. Emergence of the first levofloxacin-resistant strains of Streptococcus agalactiae isolated in Italy. Antimicrob Agents Chemother. 2015 Apr;59(4):2466-9. [PMC free article: PMC4356756] [PubMed: 25666148]

Donders GG, Halperin SA, Devlieger R, Baker S, Forte P, Wittke F, Slobod KS, Dull PM. Maternal Immunization With an Investigational Trivalent Group B Streptococcal Vaccine: A Randomized Controlled Trial. Obstet Gynecol. 2016 Feb;127(2):213-21. [PubMed: 26942345]

Madhi SA, Dangor Z, Heath PT, Schrag S, Izu A, Sobanjo-Ter Meulen A, Dull PM. Considerations for a phase-III trial to evaluate a group B Streptococcus polysaccharide-protein conjugate vaccine in pregnant women for the prevention of early- and late-onset invasive disease in young-infants. Vaccine. 2013 Aug 28;31 Suppl 4:D52-7. [PubMed: 23973347]

Nanduri SA, Petit S, Smelser C, Apostol M, Alden NB, Harrison LH, Lynfield R, Vagnone PS, Burzlaff K, Spina NL, Dufort EM, Schaffner W, Thomas AR, Farley MM, Jain JH, Pondo T, McGee L, Beall BW, Schrag SJ. Epidemiology of Invasive Early-Onset and Late-Onset Group B Streptococcal Disease in the United States, 2006 to 2015: Multistate Laboratory and Population-Based Surveillance. JAMA Pediatr. 2019 Mar 01;173(3):224-233. [PMC free article: PMC6439883] [PubMed: 30640366]

Minkoff HL, Sierra MF, Pringle GF, Schwarz RH. Vaginal colonization with Group B beta-hemolytic streptococcus as a risk factor for post-cesarean section febrile morbidity. Am J Obstet Gynecol. 1982 Apr 15;142(8):992-5. [PubMed: 7041653]

Krohn MA, Hillier SL, Baker CJ. Maternal peripartum complications associated with vaginal group B streptococci colonization. J Infect Dis. 1999 Jun;179(6):1410-5. [PubMed: 10228062]

Yancey MK, Duff P, Clark P, Kurtzer T, Frentzen BH, Kubilis P. Peripartum infection associated with vaginal group B streptococcal colonization. Obstet Gynecol. 1994 Nov;84(5):816-9. [PubMed: 7936518]

Tita AT, Andrews WW. Diagnosis and management of clinical chorioamnionitis. Clin Perinatol. 2010 Jun;37(2):339-54. [PMC free article: PMC3008318] [PubMed: 20569811]

Rouse DJ, Landon M, Leveno KJ, Leindecker S, Varner MW, Caritis SN, O'Sullivan MJ, Wapner RJ, Meis PJ, Miodovnik M, Sorokin Y, Moawad AH, Mabie W, Conway D, Gabbe SG, Spong CY., National Institute of Child Health And Human Development, Maternal-Fetal Medicine Units Network. The Maternal-Fetal Medicine Units cesarean registry: chorioamnionitis at term and its duration-relationship to outcomes. Am J Obstet Gynecol. 2004 Jul;191(1):211-6. [PubMed: 15295368]

Cape A, Tuomala RE, Taylor C, Puopolo KM. Peripartum bacteremia in the era of group B streptococcus prophylaxis. Obstet Gynecol. 2013 Apr;121(4):812-818. [PubMed: 23635682]

Romero R, Mazor M, Oyarzun E, Sirtori M, Wu YK, Hobbins JC. Is there an association between colonization with group B Streptococcus and prematurity? J Reprod Med. 1989 Oct;34(10):797-801. [PubMed: 2677355]

Arias-Camison JM. Late onset group B streptococcal infection from maternal expressed breast milk in a very low birth weight infant. J Perinatol. 2003 Dec;23(8):691-2. [PubMed: 14647171]

Le Doare K, Kampmann B. Breast milk and Group B streptococcal infection: vector of transmission or vehicle for protection? Vaccine. 2014 May 30;32(26):3128-32. [PMC free article: PMC4037808] [PubMed: 24736004]

Lischke JH, McCreight PH. Maternal group B streptococcal vertebral osteomyelitis: an unusual complication of vaginal delivery. Obstet Gynecol. 1990 Sep;76(3 Pt 2):489-91. [PubMed: 2199869]

Sexton DJ, Rockson SG, Hempling RE, Cathey CW. Pregnancy-associated group B streptococcal endocarditis: a report of two fatal cases. Obstet Gynecol. 1985 Sep;66(3 Suppl):44S-47S. [PubMed: 3895083]

Aharoni A, Potasman I, Levitan Z, Golan D, Sharf M. Postpartum maternal group B streptococcal meningitis. Rev Infect Dis. 1990 Mar-Apr;12(2):273-6. [PubMed: 2184496]