Group B streptococcal infection

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [5]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [6]

Despite substantial progress in prevention of perinatal Group B Streptococal (GBS) disease since the 1990s, GBS remains the leading cause of early-onset neonatal sepsis in the United States. Universal screening at 35–37 weeks’ gestation for maternal GBS colonization and use of intrapartum antibiotic prophylaxis has resulted in substantial reductions in the burden of early-onset GBS disease among newborns. Although early-onset GBS disease has become relatively uncommon in recent years, the rates of maternal GBS colonization (and therefore the risk for early-onset GBS disease in the absence of intrapartum antibiotic prophylaxis) remain unchanged since the 1970s. Continued efforts are needed to sustain and improve on the progress achieved in the prevention of GBS disease. There also is a need to monitor for potential adverse consequences of intrapartum antibiotic prophylaxis (e.g., emergence of bacterial antimicrobial resistance or increased incidence or severity of non-GBS neonatal pathogens). In the absence of a licensed GBS vaccine, universal screening and intrapartum antibiotic prophylaxis continue to be the cornerstones of early-onset GBS disease prevention.

In the 1970s, the bacterium GBS emerged as the leading infectious cause of early neonatal morbidity and mortality in the United States.^[1][2][3][4] Beginning in the mid 1980s, clinical trials and well-designed observational studies demonstrated that administering intravenous antibiotics during labor to women at risk for transmitting GBS to their newborns could prevent invasive disease in the first week of life (i.e., early-onset disease).^{[5][6][7][8][9]} As a result of the collaborative efforts of clinicians, researchers, professional organizations, parent advocacy groups, and the public health community in the 1990s, recommendations for intrapartum prophylaxis to prevent perinatal GBS disease were issued in 1996 by the American College of Obstetricians and Gynecologists (ACOG)^[10] and CDC^[11] and in 1997 by the American Academy of Pediatrics (AAP).^[12] Revised guidelines for the prevention of early-onset GBS disease issued in 2002 recommended universal culture-based screening of all pregnant women at 35-37 weeks gestation to optimize the identification of women who should receive intrapartum antibiotic prophylaxis.^[13] The most recent CDC guidelines were published in 2010.^[14]

GBS infection can be classified into three main categories depending on the type of affected subjects. GBS infection can occur in pregnant women, neonates, or non-pregnant adults mainly the elderly.^[15] Neonatal GBS infection can be further classified into early-onset or late-onset depending on the timing of the onset of the symptoms. Infections in newborns occurring within the first week of life are designated as early-onset disease, whereas late-onset infections occur in infants aged >1 week, with most infections evident during the first 3 months of life. ^[14]

The gastrointestinal tract serves as the primary reservoir for GBS and is the likely source of vaginal colonization. Early-onset neonatal infections are acquired vertically through exposure to GBS from the vagina of a colonized woman. GBS is characterized by its ability to adhere to epithelial surfaces, such as the vagina, placental membranes, blood brain barrier, and respiratory tract. GBS can penetrate the host cell barriers and evade the host’s immune response. The polysaccharide antiphagocytic capsule is this bacterium’s main virulence factor.

GBS disease is caused by the infection with the bacterium GBS which is a beta hemolytic gram-positive streptococcus characterized by the presence of group B Lancefield antigen. GBS displays beta-hemolysis when cultured on a blood agar plate and produces zones of hemolysis that are only slightly larger than the colonies themselves. The species other name S. agalactiae, where “agalactiae” means “no milk”, alludes to this. GBS hydrolyzes sodium hippurate and gives a positive response in the CAMP test. GBS is also sensitive to bile and will lyse in its presence. GBS is a species of the normal flora of the gut and female urogenital tract. The polysaccharide antiphagocytic capsule is this bacterium’s main virulence factor.

GBS infection causes a wide variety of clinical presentations depending on the type of the affected subjects; therefore, the differential diagnosis of GBS infection varies based on the age of the patient and their health condition. Early-onset GBS infection in neonates might lead to pneumonia, meningitis, or sepsis and it must be differentiated from other types of infectious agents in this category of patients.

GBS causes invasive disease primarily in infants, pregnant or postpartum women, and older adults, with the highest incidence among young infants.^[16] Before active prevention was initiated, an estimated 7,500 cases of neonatal GBS disease occurred annually in the United States.^[17] Striking declines in disease incidence coincided with increased prevention activities in the 1990s,^[18] and a further reduction occurred following the issuance of the recommendation for universal screening in 2002.^[19] However, GBS disease remains the leading infectious cause of morbidity and mortality among newborns in the United States.^[16][20] The continued burden of disease and newly available data relevant to early-onset GBS disease prevention from the fields of epidemiology, obstetrics, neonatology, microbiology, molecular biology, and pharmacology prompted revision of the guidelines for early-onset GBS disease prevention.^[14]

Maternal intrapartum GBS colonization is the primary risk factor for early-onset disease in infants. Additional risk factors for early-onset disease in infants include gestational age < 37 completed weeks, longer duration of membrane rupture, intra-amniotic infection, young maternal age, and black race.^[14]

The Center of Disease Control and Prevention (CDC)’s screening guidelines for GBS infection recommend universal culture-based screening for all pregnant women for vaginal and rectal GBS colonization in order to determine which women should receive intrapartum GBS chemoprophylaxis. CDC recommended that women with unknown GBS colonization status at the time of delivery be managed according to the presence of intrapartum risk factors. CDC‘s guidelines recommend screening for vaginal and rectal GBS colonization at 35-37 weeks’ gestation. Swabbing both the lower vagina and rectum (through the anal sphincter) increases the culture yield substantially compared with sampling the cervix or the vagina without also swabbing the rectum.^[14] Routine screening for asymptomatic bacteriuria is recommended in pregnant women, and laboratories should screen urine culture specimens for the presence of GBS in concentrations of 104 colony-forming units (cfu)/ml or greater.^[14]

GBS is the leading infectious cause of morbidity and mortality among infants in the United States, particularly among preterm neonates.^[21][16][18] Most newborns with early-onset disease have symptoms on the day of birth. Babies who develop late-onset disease may appear healthy at birth and develop symptoms of GBS disease after the first week of life.

Symptoms of GBS infection in neonates include apnea, bluish color to skin, cold skin, difficulty breathing, difficulty feeding, and irritability.^[3] GBS infection in pregnancy is most commonly asymptomatic. If the adult patient is symptomatic, the constellation of symptoms depends on the type of infection GBS is causing.

The physical examination of neonates with GBS infection reveals lethargy, cyanosis, an unstable temperature that can be either high or low, tachycardia, and breathing difficulty. The breathing difficulty is manifested by flaring of the nostrils, grunting, and tachypnea with short periods of apnea. Hypotension might also be present. In case of early-onset GBS infection, the 5 minutes apgar score of the newborn may be low.^[22]

Any newborn with signs of sepsis should receive a full diagnostic evaluation and receive antibiotic therapy pending the results of the evaluation, regardless of the maternal GBS colonization status. Well-appearing newborns whose mothers had suspected chorioamnionitis should undergo a limited diagnostic evaluation and receive antibiotic therapy pending culture results. No routine diagnostic testing for GBS is recommended among well-looking infants unless either the gestational age is <37 weeks or the duration of membrane rupture before delivery was ≥18 hours.^[14] The diagnosis of GBS infection is confirmed by the isolation of the organism in either the blood or the cerebrospinal fluid (CSF).

GBS infection should be suspected as a causative agent for bacterial meningitis in infants less than two years of age, among whom empirical antibiotic therapy should be initiated immediately.^[23] Ampicillin or penicillin are recommended for the treatment of confirmed neonatal GBS meningitis.^[23] Intrapartum antibiotic treatment should be administered to asymptomatic pregnant women who are carriers of GBS because it provides prophylaxis against the transmission of the infection to the neonate. Penicillin remains the agent of choice for intrapartum antibiotic prophylaxis, with ampicillin as an acceptable alternative.^[14] Penicillin and ampicillin are generally effective for the treatment of GBS infection in non-pregnant adults.^[24]

Penicillin remains the agent of choice for intrapartum antibiotic prophylaxis for the primary prevention of early-onset GBS infection, with ampicillin as an acceptable alternative. Penicillin-allergic women who do not have a history of anaphylaxis, angioedema, respiratory distress, or urticaria following the administration of a penicillin or a cephalosporin should receive cefazolin. Antimicrobial susceptibility testing should be ordered for antenatal GBS cultures performed on penicillin-allergic women at high risk for anaphylaxis because of a history of anaphylaxis, angioedema, respiratory distress, or urticaria following the administration of a penicillin or a cephalosporin. Penicillin-allergic women at high risk for anaphylaxis should receive clindamycin if their GBS isolate is susceptible to clindamycin and erythromycin, as determined by antimicrobial susceptibility testing; if the isolate is sensitive to clindamycin but resistant to erythromycin, clindamycin may be used if testing for inducible clindamycin resistance is negative. Penicillin-allergic women at high risk for anaphylaxis should receive vancomycin if their isolate is intrinsically resistant to clindamycin as determined by antimicrobial susceptibility testing, if the isolate demonstrates inducible resistance to clindamycin, or if susceptibility to both agents is unknown. GBS vaccines have been investigated as a tool for reducing maternal colonization and preventing transmission to neonates; however, no licensed vaccine is available currently. The measures used to prevent early-onset GBS disease also might prevent some perinatal maternal infections;^[18][25] however, they do not prevent late-onset infant disease.^[26][14]

Currently available GBS infection prevention strategies will not prevent all cases of early-onset disease. Rapid detection of neonatal infections and initiation of appropriate treatment is needed to minimize morbidity and mortality among the cases that continue to occur. Any newborn with signs of sepsis should receive a full diagnostic evaluation and receive antibiotic therapy pending the results of the evaluation, regardless of the maternal colonization status. Well-appearing newborns whose mothers had suspected chorioamnionitis should undergo a limited evaluation and receive antibiotic therapy pending culture results. Well-appearing infants whose mothers had no chorioamnionitis and no indication for GBS prophylaxis should be managed according to routine clinical care. Well-appearing infants of any gestational age whose mother received adequate intrapartum GBS prophylaxis (≥4 hours of penicillin, ampicillin, or cefazolin before delivery) should be observed for ≥48 hours, and no routine diagnostic testing is recommended. For well-appearing infants born to mothers who had an indication for GBS prophylaxis but received no or inadequate prophylaxis, if the infant is well-appearing and ≥37 weeks and 0 days’ gestational age and the duration of membrane rupture before delivery was <18 hours, then the infant should be observed for ≥48 hours, and no routine diagnostic testing is recommended. If the infant is well-appearing and either <37 weeks and 0 days’ gestational age or the duration of membrane rupture before delivery was ≥18 hours, then the infant should undergo a limited evaluation and observation for ≥48 hours.^[14]

GBS vaccines have been investigated as a tool for reducing maternal colonization and preventing transmission to neonates;^[27] however, no licensed vaccine is available currently. Phase I and II clinical trials among healthy, non-pregnant adults of monovalent polysaccharide-protein conjugate vaccines of GBS disease-associated types have shown these vaccines to be well tolerated and immunogenic.^[28][29] A recent, double-blind randomized trial of a conjugate vaccine against GBS serotype III among non-pregnant women of reproductive age found a significant delay in acquisition of colonization with the vaccine-serotype among vaccine recipients.^[30][14]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [4]

In the 1970s, the bacterium group B Streptococcus (GBS) emerged as the leading infectious cause of early neonatal morbidity and mortality in the United States.^[1][2][3][4] Beginning in the mid 1980s, clinical trials and well-designed observational studies demonstrated that administering intravenous antibiotics during labor to women at risk for transmitting GBS to their newborns could prevent invasive disease in the first week of life (i.e., early-onset disease).^{[5][6][7][8][9]} As a result of the collaborative efforts of clinicians, researchers, professional organizations, parent advocacy groups, and the public health community in the 1990s, recommendations for intrapartum prophylaxis to prevent perinatal GBS disease were issued in 1996 by the American College of Obstetricians and Gynecologists (ACOG)^[10] and CDC^[11] and in 1997 by the American Academy of Pediatrics (AAP).^[12] Revised guidelines for the prevention of early-onset GBS disease issued in 2002 recommended universal culture-based screening of all pregnant women at 35-37 weeks gestation to optimize the identification of women who should receive intrapartum antibiotic prophylaxis.^[13] The most recent CDC guidelines were published in 2010.^[14]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Group B streptococcal (GBS) infection can be classified into three main categories depending on the type of affected subjects. GBS infection can occur in pregnant women, neonates, or non-pregnant adults mainly the elderly.^[1] Neonatal GBS infection can be further classified into early-onset or late-onset depending on the timing of the onset of the symptoms. Infections in newborns occurring within the first week of life are designated as early-onset disease, whereas late-onset infections occur in infants aged >1 week, with most infections evident during the first 3 months of life. ^[2]

GBS infection in pregnant women can lead to any of the following:

• No symptoms (asymptomatic carrier)
• Urinary tract infection
• Chorioamnionitis
• Endometritis
• Premature rupture of membrane

GBS infection in neonates can be classified as:^[2]

• Early onset infection (within 24-48 hours, up to one week after delivery), which can lead to any of the following:
  • Pneumonia
  • Sepsis
  • Meningitis
• Late onset infection (after the first week, up to 3 months of life), which can lead to any of the following:
  • Bacteremia without a focus of infection
  • Sepsis
  • Meningitis
  • Pneumonia
  • Focal infections (less commonly) such as adenitis, cellulitis, and arthritis^[3]

GBS infection in non pregnant adults occurs mainly in elderly and subjects with underlying disease, such as diabetes.^[1] GBS infection in elderly can manifest as any of the following:^[4]

• Pneumonia
• Skin and soft tissue infection
• Osteomyelitis
• Septic arthritis
• Urosepsis
• Peritonitis
• Meningitis
• Endocarditis
• IV catheter infection

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

The gastrointestinal tract serves as the primary reservoir for Group B Streptococcus (GBS) and is the likely source of vaginal colonization. Early-onset neonatal infections are acquired vertically through exposure to GBS from the vagina of a colonized woman. GBS is characterized by its ability to adhere to epithelial surfaces, such as the vagina, placental membranes, blood brain barrier, and respiratory tract. GBS can penetrate the host cell barriers and evade the host’s immune response. The polysaccharide antiphagocytic capsule is this bacterium’s main virulence factor.

GBS is characterized by its ability to adhere to epithelial surfaces, particularly the vaginal mucosa where the pH is low. The types of epithelium to which GBS adheres to are:

• Vagina
• Placental membranes
• Blood brain barrier
• Respiratory tract

The series of events that explain the pathogenesis of GBS infection can be summarized as follows:^[1]

• Extracellular matrix binding
• Direct cellular injury
• Invasion of epithelial cells and brain endothelium
• Resistance to intracellular killing
• Resistance to phagocytosis
• Activation of inflammatory cells
• Recruitment of neutrophils in the central nervous system

The polysaccharide antiphagocytic capsule is this bacterium’s main virulence factor.

Other key virulence factors include:^[1]

• Beta-hemolysin
• C protein
• C5a peptidase
• CAMP factor
• Fibrinogen receptor
• Hyaluronate lyase
• Lipotechoic acid
• Serine protease

The gastrointestinal tract serves as the primary reservoir for GBS and is the likely source of vaginal colonization.^[2]

Early-onset infections are acquired vertically through exposure to GBS from the vagina of a colonized woman. Neonatal infection occurs primarily when GBS ascends from the vagina to the amniotic fluid after onset of labor or rupture of membranes, although GBS also can invade through intact membranes. GBS can be aspirated into the fetal lungs, which in turn can lead to bacteremia. Infants also can become infected with GBS during passage through the birth canal; infants who are exposed to the organism through this route can become colonized at mucus membrane sites in the gastrointestinal or respiratory tracts, but these colonized infants most commonly remain healthy.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Group B Streptococcus (GBS) disease is caused by the infection with the bacterium GBS which is a beta hemolytic gram-positive streptococcus characterized by the presence of group B Lancefield antigen. GBS displays beta-hemolysis when cultured on a blood agar plate and produces zones of hemolysis that are only slightly larger than the colonies themselves. The species other name S. agalactiae, where “agalactiae” means “no milk”, alludes to this. GBS hydrolyzes sodium hippurate and gives a positive response in the CAMP test. GBS is also sensitive to bile and will lyse in its presence. GBS is a species of the normal flora of the gut and female urogenital tract. The polysaccharide antiphagocytic capsule is this bacterium’s main virulence factor.

Cellular organisms; Bacteria; Firmicutes; Bacilli; Lactobacillales; Streptococcaceae; Streptococcus

GBS is characterized by the following features:

• Gram-positive
• Cocci in pairs and short chains
• Group B Lancefield antigen
• Non-motile
• Catalase-negative
• Non-spore forming
• Polysaccharide antiphagocytic capsule (main virulence factor)
• Surface proteins
• Beta hemolysis

The CAMP test is an important test for identification. GBS are screened through this test. It is characterized by the presence of Lancefield antigen and by its ability to hydrolyze sodium hippurate.

GBS is also sensitive to bile, and will lyse in its presence.

Shown below is an image depicting an example of a positive CAMP test proving that GBS is present. The arrowhead formation on the Blood agarose gel, BAP (5% sheep blood) indicates that this bacteria is GBS.

Shown below is an image depicting colonies of GBS under microscope.

Shown below is an image depicting the growth of colonies of GBS on ChromID CPS chromogenic agar.

Shown below is an image depicting the growth of colonies of GBS on Columbia horse blood agar.

• 
  Right elbow of a patient with group B Streptococcus (GBS) bacteremia, with localized edema and erythema. From Public Health Image Library (PHIL). ^[1]
• 
  Group-B streptococci (GBS) identified by CAMP test, which takes advantage of the capacity of GBS to produce this CAMP factor that most other hemolytic streptococci do not produce. From Public Health Image Library (PHIL). ^[1]
• 
  Quantitative difference in hemolytic reactivity seen on BAP with group-D Streptococci (left wedge), group-B Streptococci (middle wedge), and group-A Streptococci (right wedge) bacteria. From Public Health Image Library (PHIL). ^[1]
• 
  Clindamycin-resistant Group-B Streptococcus (GBS), also known as S. agalactiae. From Public Health Image Library (PHIL). ^[1]

• Streptococcus agalactiae treatment (GBS-group B Streptococcus)

• 1. Early onset group B streptococcal infections^[2]

• 1.1 Bacteremia or sepsis or pneumonia

• 1.1.1 Empiric therapy

• Preferred regimen: Ampicillin 150 mg/kg IV q12h for 10 days AND Gentamicin 4 mg/kg IV q12h for 10 days-for infants born at ≥ 35 weeks gestation; Gentamicin 3 mg/kg IV q24h for 10 days-for infants born at < 35 weeks gestation

• 1.1.2 Definitive therapy

• Preferred regimen: Penicillin G 50,000-100,000 units/kg per day IV divided q12h for 10 days

• 1.2 Meningitis

• 1.2.1 Empiric therapy

• Preferred regimen: Ampicillin 100-150 mg/kg IV q8h for 14-21 days AND Gentamicin 4 mg/kg IV q24h for 14-21 days-for infants born at ≥ 35 weeks gestation; Gentamicin 3 mg/kg IV q24h for 14-21 days-for infants born at < 35 weeks gestation

• 1.2.2 Definitive therapy

• Preferred regimen: Penicillin G 250,000-450,000 units/kg per day IV divided q8h for 14-21 days

• Note: Cellulitis is the most frequent clinical manifestation of GBS-associated skin and soft tissue infections.

• 2. Late onset group b streptococcus infections in neonates and young infants (age > 1 week and body weight ≥ 1 kg with normal renal function)^[3]

• 2.1 Bacteremia without a focus

• 2.1.1 Empiric therapy

• Preferred regimen: Ampicillin IV for 10 days, Nafcillin IV for 10 days, (OR Vancomycin IV for 10 days) AND Gentamicin IV for 10 days (OR Cefotaxime IV for 10 days)

• 2.1.2 Definitive therapy

• Preferred regimen: Penicillin-G 75,000-150,000 units/kg per day IV divided q8h for 10 days

• 2.2 Meningitis

• 2.2.1 Empiric therapy

• Preferred regimen: Ampicillin IV for 14-21 days with or without Vancomycin IV for 14-21 day AND Gentamicin IV for 14-21 days OR Cefotaxime IV for 14-21 day

• 2.2.2 Definitive therapy

• Preferred regimen: Penicillin-G 450,000-500,000 units/kg per day IV divided q6h for 14-21 days

• 2.3 Cellulitis or adenitis

• 2.3.1 Empiric therapy

• Preferred regimen: Nafcillin IV for 10-14 days (OR [[Vancomycin IV for 10-14 days) AND Gentamicin IV for 10-14 days (OR Cefotaxime IV for 10-14 days)

• 2.3.2 Definitive therapy

• Preferred regimen: Penicillin-G 75,000-150,000 units/kg per day IV divided q8h for 10-14 days

• 2.4 Septic arthritis

• 2.4.1 Empiric therapy

• Preferred regimen: Nafcillin IV for 14-21 days OR Vancomycin IV for 14-21 days AND Cefotaxime IV for 14-21 days

• 2.4.2 Definitive therapy

• Preferred regimen: Penicillin-G 75,000-150,000 units/kg per day IV divided q8h for 14-21 days

• 2.5 Osteomyelitis

• 2.5.1 Empiric therapy

• Preferred regimen: Nafcillin IV for 21-28 days OR Vancomycin IV for 21-28 days AND Cefotaxime IV for 21-28 days

• 2.5.2 Definitive therapy

• Preferred regimen: Penicillin-G 75,000-150,000 units/kg per day IV divided q8h for 21-28 days

• 2.6 Urinary tract infection

• 2.6.1 Empiric therapy

• Preferred regimen: Ampicillin IV for 10 days, Nafcillin IV for 10 days, (OR Vancomycin IV for 10 days) AND Gentamicin IV for 10 days (OR Cefotaxime IV for 10 days)

• 2.6.2 Definitive therapy

• Preferred regimen: Penicillin-G 75,000-150,000 units/kg per day IV divided q8h for 10 days

• Neonatal prophylaxis^[4]

• Group B streptococcus infection (maternal dose for neonatal prophylaxis)

• Preferred regimen: Penicillin-G, Ampicillin 2 g IV initial dose, THEN 1 g q4h until delivery, Cefazolin ≥ 4h prior to delivery.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Group B Streptococcus (GBS) infection causes a wide variety of clinical presentations depending on the type of the affected subjects; therefore, the differential diagnosis of GBS infection varies based on the age of the patient and their health condition. Early-onset GBS infection in neonates might lead to pneumonia, meningitis, or sepsis and it must be differentiated from other types of infectious agents in this category of patients.

The differential diagnosis for early-onset GBS neonatal pneumonia or sepsis includes infection with any of the following:

• Escherichia coli (E.coli)
• Klebsiella
• Staphylococcus aureus
• Streptococcus pneumoniae
• Haemophilus influenza
• Herpes virus
• Candida
• Listeria (less commonly)
• Mycobacterium tuberculosis (less commonly)

The differential diagnosis for late-onset GBS neonatal pneumonia or sepsis includes infection with any of the following:

• Staphylococcus aureus
• Streptococcus pneumoniae
• Streptococcus pyogenes
• Viruses (adenovirus, enteroviruses, influenza, parainfluenza, rhinovirus, and respiratory syncytial virus)
• Candida (less commonly)
• Chlamydia trachomatis

Shown below is a table summarizing the different pathogens that can cause meningitis in infants.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [5]

Group B Streptococcus (GBS) causes invasive disease primarily in infants, pregnant or postpartum women, and older adults, with the highest incidence among young infants.^[1] Before active prevention was initiated, an estimated 7,500 cases of neonatal GBS disease occurred annually in the United States.^[2] Striking declines in disease incidence coincided with increased prevention activities in the 1990s,^[3] and a further reduction occurred following the issuance of the recommendation for universal screening in 2002.^[4] However, GBS disease remains the leading infectious cause of morbidity and mortality among newborns in the United States.^[1][5] The continued burden of disease and newly available data relevant to early-onset GBS disease prevention from the fields of epidemiology, obstetrics, neonatology, microbiology, molecular biology, and pharmacology prompted revision of the guidelines for early-onset GBS disease prevention.^[6]

Approximately 10%-30% of pregnant women are colonized with GBS in the vagina or rectum.^[7][8][9]

Before active prevention was initiated, an estimated 7,500 cases of neonatal GBS disease occurred annually in the United States.^[2]

As a result of prevention efforts, incidence of GBS has declined dramatically over the past 15 years, from 1.7 cases per 1,000 live births in the early 1990s to 0.34–0.37 cases per 1,000 live births in recent years. On the basis of data from CDC’s Active Bacterial Core surveillance (ABCs) system, a network of 10 sites across the United States that conduct active, population-based surveillance, CDC estimates that in recent years, GBS has caused approximately 1,200 cases of early-onset invasive disease per year;^[10] approximately 70% of cases are among babies born at term (≥37 weeks’ gestation).^[1]

Shown below is an image depicting the incidence of early- and late-onset invasive GBS disease between 1990 and 2008.

Abbreviations: ACOG = American College of Obstetricians and Gynecologists and AAP = American Academy of Pediatrics.

Source: CDC.gov Adapted from Jordan HT, Farley MM, Craig A, et al. Revisiting the need for vaccine prevention of late-onset neonatal group B streptococcal disease. Pediatr Infect Dis J 2008;27:1057–64.

The incidence of GBS infection is higher among black neonates compared to white. The disparity in early-onset GBS disease incidence between black and white infants has persisted after the 2002 CDC guidelines and is evident among both term and preterm infants.^[11][5] Preliminary surveillance data from 2008 suggest that the racial disparity was reduced somewhat in 2008.^[12] Incidence among all black infants declined to 0.49 cases per 1,000 live births, showing progress towards the Healthy People 2010 objective of 0.5 cases per 1,000 live births for all racial and ethnic groups.^[13]

Shown below is an image depicting the incidence per 1,000 live births of early-onset invasive group B streptococcal disease in the 10 Active Bacterial Core surveillance areas during 2000-2007. Data are displayed for four demographic subsets: term white infants, term black infants, preterm white infants, and preterm black infants.

Source: Adapted from CDC. Trends in perinatal group B streptococcal disease—United States, 2000–2006. MMWR 2009;58:109–12.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Maternal intrapartum Group B streptococcus (GBS) colonization is the primary risk factor for early-onset disease in infants. Additional risk factors for early-onset disease in infants include gestational age < 37 completed weeks, longer duration of membrane rupture, intra-amniotic infection, young maternal age, and black race.^[1]

Risk factors for GBS infection in neonates include:^[2][3][1]

• Maternal colonization
• Gestational age <37 completed weeks
• Longer duration of membrane rupture
• Intra-amniotic infection
• Young maternal age
• Black race
• Low maternal levels of GBS-specific anticapsular antibody
• Previous delivery of an infant with invasive GBS disease
• Obstetric procedures
  • Internal fetal monitoring devices
  • More than five or six digital vaginal examinations after onset of labor
  • Rupture of membranes

Maternal intrapartum GBS colonization is the primary risk factor for early-onset disease in infants. A classic prospective cohort study conducted during the 1980s revealed that pregnant women with GBS colonization were >25 times more likely than pregnant women with negative prenatal cultures to deliver infants with early-onset GBS disease.^[2][1]

Heavy colonization, defined as culture of GBS from direct plating rather than from selective broth only, is associated with higher risk for early-onset disease.^[4][5][1]

GBS identified in clean-catch urine specimens during any trimester is considered a surrogate for heavy maternal colonization and also is associated with a higher risk for early-onset GBS disease.^[6][7][1]

In a 1985 report of factors associated with early-onset disease, women with gestation <37 weeks, membrane rupture of >12 hours, or intrapartum temperature >99.5ºF (>37.5ºC) had 6.5 times the risk for having an infant with early-onset GBS disease compared with women who had none of these risk factors.^[2] Of note, women who had one of these risk factors but who had negative prenatal screening cultures were at relatively low risk for early-onset GBS disease (incidence: 0.9 cases per 1,000 births) compared with women who were colonized prenatally but had none of the risk factors (incidence: 5.1 cases per 1,000 births).^[2][1]

Some observational studies have reported an association between early-onset GBS disease and certain obstetric procedures, such as the use of internal fetal monitoring devices^[3][8] and more than five or six digital vaginal examinations after onset of labor or rupture of membranes.^[8] However, lack of randomization in observational studies can result in confounding, because certain procedures might be used more frequently in high-risk settings.^[9] Although concern has been raised about performing other obstetric procedures (e.g., membrane stripping and mechanical and/or pharmacologic cervical ripening) on GBS-colonized women, available data are not sufficient to determine whether these procedures are associated with an increased risk for early-onset disease.^[10][11][1]

Shown below is a list of conditions associated with a higher rate of GBS infection in non-pregnant adults:^[12]

• Advanced age
• Bedridden state
• Diabetes mellitus
• Cirrhosis
• Malignancy
• Seevre peripheral vascular disease
• Corticosteroid treatment
• Chronic renal failure
• Stroke
• Decubitus ulcer
• Neurogenic bladder
• Joint prosthesis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [3]

The Center of Disease Control and Prevention (CDC)’s screening guidelines for Group B streptococcal (GBS) infection recommend universal culture-based screening for all pregnant women for vaginal and rectal GBS colonization in order to determine which women should receive intrapartum GBS chemoprophylaxis. CDC recommended that women with unknown GBS colonization status at the time of delivery be managed according to the presence of intrapartum risk factors. CDC‘s guidelines recommend screening for vaginal and rectal GBS colonization at 35-37 weeks’ gestation. Swabbing both the lower vagina and rectum (through the anal sphincter) increases the culture yield substantially compared with sampling the cervix or the vagina without also swabbing the rectum.^[1] Routine screening for asymptomatic bacteriuria is recommended in pregnant women, and laboratories should screen urine culture specimens for the presence of GBS in concentrations of 104 colony-forming units (cfu)/ml or greater.^[1]

CDC’s guidelines recommend universal culture-based screening for all pregnant women for vaginal and rectal GBS colonization (class A, level of evidence II) in order to determine which women should receive intrapartum GBS chemoprophylaxis. CDC recommended that women with unknown GBS colonization status at the time of delivery be managed according to the presence of intrapartum risk factors.^[1]

CDC’s guidelines recommend screening for vaginal and rectal GBS colonization at 35-37 weeks’ gestation.^[1]

Because GBS colonization status can change over the course of a pregnancy, the timing of specimen collection for determination of colonization status is important. Because colonization can be transient, colonization early in pregnancy is not predictive of early-onset GBS disease.^[2] Late third trimester colonization status has been used as a proxy for intrapartum colonization.^[3] The negative predictive value of GBS cultures performed ≤5 weeks before delivery is 95%-98%; however, the clinical utility decreases when a prenatal culture is performed more than 5 weeks before delivery because the negative predictive value declines.^[4]

Shown below is an algorithm for screening for group B streptococcal (GBS) colonization and use of intrapartum prophylaxis for women with preterm labor (gestational age <37 weeks) among whom no previous screening was performed based on the 2010 revised CDC guidelines.^[1]

* At <37 weeks and 0 days’ gestation.

† If patient has undergone vaginal-rectal GBS culture within the preceding 5 weeks, the results of that culture should guide management. GBS-colonized women should receive intrapartum antibiotic prophylaxis. No antibiotics are indicated for GBS prophylaxis if a vaginal-rectal screen within 5 weeks was negative.

¶ Patient should be regularly assessed for progression to true labor; if the patient is considered not to be in true labor, discontinue GBS prophylaxis.

** If GBS culture results become available prior to delivery and are negative, then discontinue GBS prophylaxis.

†† Unless subsequent GBS culture prior to delivery is positive.

§ A negative GBS screen is considered valid for 5 weeks. If a patient with a history of PTL is re-admitted with signs and symptoms of PTL and had a negative GBS screen >5 weeks prior, she should be rescreened and managed according to this algorithm at that time.

Shown below is an algorithm for screening for group B streptococcal (GBS) colonization and use of intrapartum prophylaxis for women with preterm (gestational age <37 weeks) premature rupture of membranes (pPROM) among whom no previous screening was performed based on the 2010 revised CDC guidelines.^[1]

* At <37 weeks and 0 days’ gestation.

† If patient has undergone vaginal-rectal GBS culture within the preceding 5 weeks, the results of that culture should guide management. GBS-colonized women should receive intrapartum antibiotic prophylaxis. No antibiotics are indicated for GBS prophylaxis if a vaginal-rectal screen within 5 weeks was negative.

§ Antibiotics given for latency in the setting of pPROM that include ampicillin 2 g intravenously (IV) once, followed by 1 g IV every 6 hours for at least 48 hours are adequate for GBS prophylaxis. If other regimens are used, GBS prophylaxis should be initiated in addition.

** GBS prophylaxis should be discontinued at 48 hours for women with pPROM who are not in labor. If results from a GBS screen performed on admission become available during the 48-hour period and are negative, GBS prophylaxis should be discontinued at that time.

†† Unless subsequent GBS culture prior to delivery is positive.

§ A negative GBS screen is considered valid for 5 weeks. If a patient with pPROM is entering labor and had a negative GBS screen >5 weeks prior, she should be rescreened and managed according to this algorithm at that time.

Early guidelines recommended the use of one of two approaches to identifying women who should receive intrapartum antibiotic prophylaxis: a risk-based approach or a culture-based screening approach.^[5] A large population-based study conducted during 1998-1999 demonstrated the superiority of culture-based screening over the risk-based approach to prevention of early-onset GBS disease.^[6] The study found that culture-based screening resulted in the identification of a greater proportion of women at risk for transmitting GBS to their newborns.^[1]

Swabbing both the lower vagina and rectum (through the anal sphincter) increases the culture yield substantially compared with sampling the cervix or the vagina without also swabbing the rectum.

Although a small number of studies have examined the ability of perianal or vaginal-perianal cultures to detect GBS colonization, the available data on their performance compared with vaginal-rectal cultures are limited.

Studies have indicated that when women in the outpatient clinic setting collect their own vaginal-rectal screening specimens, with appropriate instruction, GBS yield is similar to when specimens are collected by a health-care provider.

The use of appropriate transport media can help sustain the viability of GBS in settings where immediate laboratory processing is not possible. GBS isolates can remain viable in transport media for several days at room temperature; however, the recovery of isolates declines during 1-4 days, particularly at high temperatures. Even when appropriate transport media are used, the sensitivity of culture is greatest when the specimen is stored at 4°C before culture and processed within 24 hours of collection.^[1]

* Patients with a history of any of the following after receiving penicillin or a cephalosporin are considered to be at high risk for anaphylaxis: anaphylaxis, angioedema, respiratory distress, or urticaria.

Regardless of the test selected to identify GBS, use of an enrichment broth improves detection substantially. When direct agar plating is used instead of selective enrichment broth, as many as 50% of women who are GBS carriers have false-negative culture results. Examples of selective enrichment broths include Todd-Hewitt broth supplemented either with gentamicin (8 µg/ml) and nalidixic acid (15 µg/ml) [TransVag broth] or with colistin (10 µg/ml) and nalidixic acid (15 µg/ml) [Lim broth]. Although TransVag and Lim broth media are often available without blood, the addition of 5% sheep blood can increase the recovery of GBS . Selective enrichment broth also can contain chromogenic substrates that provide for a change in color in the setting of beta-hemolytic GBS. Such broths can facilitate the identification of beta-hemolytic GBS; however, non-hemolytic isolates will not be detected by these broths alone.^[1]

Following enrichment, the conventional means for identifying GBS is through isolation on subculture to blood agar plates and presumptive identification by the CAMP test or serologic identification using latex agglutination with group B streptococcal antisera. More recently, chromogenic agars that undergo color change in the presence of beta-hemolytic colonies of GBS have become available. As with pigmented enrichment broths, these chromogenic agars can facilitate detection of beta-hemolytic GBS, but the majority will not detect non-hemolytic strains. In addition more rapid techniques for identifying GBS directly from enrichment broth, or after subculture have been developed, including DNA probes and nucleic acid amplification tests (NAAT) such as polymerase chain reaction.^[1]

Despite the availability of NAAT for GBS, utility of such assays in the intrapartum setting remains limited. Although a highly sensitive and specific test with rapid turnaround time could be used to assess intrapartum GBS colonization and therefore obviate the need for antenatal screening, data on currently available assays do not support their use in replacement of antenatal culture or risk-based assessment of women with unknown GBS status on admission for labor. The additional time required for enrichment of samples makes it not feasible for intrapartum testing, and the sensitivity of assays in the absence of enrichment is not adequate in comparison to culture. In addition, concerns remain regarding real-world turnaround time, test complexity, availability of testing at all times, staffing requirements, and costs. In settings that can perform NAAT, such tests might prove useful for the limited circumstance of a woman at term with unknown colonization status and no other risk factors. Even optimal NAAT would have drawbacks in the intrapartum setting, including a delay in administration of antibiotics while waiting for the result, and no antimicrobial susceptibility testing for penicillin-allergic women. Other rapid tests in addition to NAAT have been developed to detect GBS rapidly from non-enriched samples, including optical immunoassays and enzyme immunoassays; however, none is sufficiently sensitive when used on a direct specimen to detect GBS colonization reliably in the intrapartum setting.^[1]

Antimicrobial susceptibility testing of GBS isolates is crucial for appropriate antibiotic prophylaxis selection for penicillin-allergic women who are at high risk for anaphylaxis because resistance to clindamycin, the most common agent used in this population, is increasing among GBS isolates.^[1]

In addition, appropriate methodologies for susceptibility testing are important because inducible clindamycin resistance can occur in some strains that appear susceptible in broth susceptibility tests. D-zone testing using the double-disk diffusion method has been used to identify isolates that are erythromycin-resistant and clindamycin-susceptible, yet have inducible resistance to clindamycin. Isolates that are D-zone positive are considered to have inducible clindamycin resistance and are presumed to be resistant although the clinical significance of this resistance is not clear.^[1]

Routine screening for asymptomatic bacteriuria is recommended in pregnant women, and laboratories should screen urine culture specimens for the presence of GBS in concentrations of 104 colony-forming units (cfu)/ml or greater.^[1]

Laboratories should identify GBS when present at ≥104 cfu/ml in pure culture or mixed with a second microorganism.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [3]

Group B Streptococcus (GBS) is the leading infectious cause of morbidity and mortality among infants in the United States, particularly among preterm neonates.^[1][2][3] Most newborns with early-onset disease have symptoms on the day of birth. Babies who develop late-onset disease may appear healthy at birth and develop symptoms of GBS disease after the first week of life.

Most newborns with early-onset disease have symptoms on the day of birth. Babies who develop late-onset disease may appear healthy at birth and develop symptoms of group B strep disease after the first week of life. Infants with early-onset GBS disease generally present with respiratory distress, apnea, or other signs of sepsis within the first 24 to 48 hours of life.^[4] The most common clinical syndromes of early-onset disease are sepsis and pneumonia; less frequently, early-onset infections can lead to meningitis.

• Disseminated intravascular coagulation (DIC)
• Hypoglycemia
• Respiratory failure
• Neurological complications of meningitis
  • Brain infarction
  • Cerebral edema
  • Cerebritis
  • Elevated intracranial pressure
  • Hydrocephalus
  • Subdural effusion
  • Subdural empyema
  • Ventriculitis
• Death

GBS is the leading infectious cause of morbidity and mortality among infants in the United States. The case-fatality ratio of early-onset disease has declined from as high as 50% in the 1970s^[1] to 4%-6% in recent years, primarily because of advances in neonatal care.^[2][3]

Mortality is higher among preterm infants, with case-fatality rates of approximately 20% and as high as 30% among those ≤33 weeks of gestation, compared with 2%–3% among full-term infants.^[2][3]

GBS colonization during pregnancy can be transient, intermittent, or persistent. Although some women with GBS colonization during a pregnancy will be colonized during subsequent pregnancies, a substantial proportion will not.^[5][6] In the absence of any intervention, an estimated 1%-2% of infants born to colonized mothers develop early-onset GBS infections.^[7][8]

Pregnant women who are colonized by GBS are most commonly asymptomatic. Some pregnant women develop serious conditions as a result of the infection, such as endometritis, chorioamnionitis, urinary tract infections, and preterm delivery.

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