Group B streptococcal infection

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Group B streptococcal infection
Classification and external resources
Specialty pediatrics
ICD-10 B95.1, P36.0
eMedicine article/229091

Group B streptococcus infection is the infection caused by the bacteria Streptococcus agalactiae (S. agalactiae) (also known as Group B streptococcus or GBS). Group B streptococcal infection can cause serious illness and sometimes death, especially in newborns, the elderly, and people with compromised immune systems. GBS was recognized as a pathogen in cattle by Edmond Nocard and Mollereau in the late 1880s, but its significance as a human pathogen was not discovered before the 1938 when Fry [1] described three fatal cases of puerperal infections caused by GBS. In the early 1960s GBS was recognized as a main cause of neonatal sepsis. [2]

In general, GBS is a harmless commensal bacterium being part of the human microbiota colonizing the gastrointestinal and genitourinary tract of up to 30% of healthy human adults (asymptomatic carriers). [3] [4] [5]

S. agalactiae is also a common veterinary pathogen, because it can cause bovine mastitis (inflammation of the udder) in dairy cows. The species name "agalactiae" meaning "no milk", alludes to this. [6] S. agalactiae is a gram-positive coccus (spherical bacteria) with a tendency to form chains (streptococcus), beta-haemolytic, catalase-negative, and facultative anaerobe. [7] [8] [9]

Streptococcus agalactiae- Gram stain
β-haemolytic colonies of Streptococcus agalactiae, blood agar 18h at 36°C

S. agalactiae is the species designation for streptococci belonging to the group B of the Rebecca Lancefield classification of streptococci (Lancefield grouping). GBS is surrounded by a bacterial capsule composed of polysaccharides (exopolysaccharides). GBS are subclassified into ten serotypes (Ia, Ib, II–IX) depending on the immunologic reactivity of their polysaccharide capsule. [5] [7] [10] As other virulent bacteria, GBS harbours an important number of virulence factors, [11] the most important are the capsular polysaccharide (rich in sialic acid), and a pore-forming toxin, β-haemolysin. [12] The GBS capsule is probably the key virulence factor because it helps GBS escape from host defence mechanisms interfering with phagocytic killing of GBS by human phagocytes. [5] [12] The GBS β-haemolysin is considered identical to the GBS pigment. [13] [14] [15] [16]

Identification of GBS in the laboratory[edit]

As mentioned, Streptococcus agalactiae is a gram-positive coccus with a tendency to form chains, beta-haemolytic, catalase-negative, and facultative anaerobe. GBS grows readily on blood agar plates as microbial colonies surrounded by a narrow zone of β-haemolysis. GBS is characterized by the presence in the cell wall of the group B antigen of the Lancefield classification (Lancefield grouping) that can be detected directly in intact bacteria using latex agglutination tests. [9] The CAMP test is also another important test for identification of GBS. The CAMP factor acts synergistically with the staphylococcal β-haemolysin inducing enhanced haemolysis of sheep or bovine erythrocytes. [9]

Positive CAMP test indicated by the formation of an arrowhead where Streptococcus agalactiae meets the Staphylococcus aureus (white middle streak)

GBS is also able to hydrolyse hippurate and this test can also be used to identify presumptively GBS. Haemolytic GBS strains produce an orange-brick-red non-isoprenoid polyene pigment (ornythinrhamnododecaene) (granadaene) when cultivated on granada medium that allows its straightforward identification. [17]

Red colonies of S.agalactiae in granada agar. Vagino-rectal culture 18h incubation 36°C anaerobiosis

Identification of GBS could also be carried out easily using modern methods for identifying bacteria as MALDI-TOF (Matrix-Assisted Laser Desorption Ionization-Time of Flight Mass Spectrometry). [18]

GBS colonization and infection[edit]

Almost always, GBS is an innocuous commensal bacterium that colonizes the gastrointestinal and genitourinary tract of humans. In different studies, GBS vaginal colonization rate ranges from 4 to 36%, with most studies reporting rates over 20%. These variations in the reported prevalence of asymptomatic (presenting no symptoms of disease) colonization could be related to the different detection methods used, and differences in populations studied. [19] [20] [21]

Though GBS is an asymptomatic colonizer of the gastrointestinal human tract in up to 30% of otherwise healthy adults, including pregnant women, [5] [19] this opportunistic harmless bacterium can, in some circumstances, cause severe invasive infections. [4]

GBS and pregnancy[edit]

Though GBS colonization is asymptomatic and, in general, in healthy women during pregnancy, does not cause problems it can sometimes cause serious illness for the mother and the baby during gestation and after delivery. GBS infections in the mother can cause chorioamnionitis (intra-amniotic infection or severe infection of the placental tissues) infrequently, and postpartum infections (after birth). GBS urinary tract infections (UTI) may induce labour and cause premature delivery (preterm birth). [5]


In the western world, GBS (in the absence of effective prevention measures) is the main cause of bacterial infections in newborns, such as septicemia, pneumonia, and meningitis, which can lead to death or long-term sequelae. [5] [22]

GBS infections in newborns are separated into two clinical types, early-onset disease (GBS-EOD) and late-onset disease (GBS-LOD). GBS-EOD manifests from 0 to 7 living days in the newborn, most of the cases of EOD being apparent within 24 h from birth. GBS-LOD starts between seven and 90 days after birth. [5] [21]

The most common clinical syndromes of GBS-EOD are septicemia without apparent location, pneumonia, and less frequently meningitis. Bacteremia without a focus occurs in 80-85%, pneumonia in 10% to 15% and meningitis in 5% to 10% of neonates suffering from GBS-EOD. The initial clinical findings are respiratory signs in more than 80% of cases. Neonates with meningitis often have an initial clinical presentation identical to presentation in those without meningeal affectation. An exam of the cerebrospinal fluid (CSF) is often necessary to rule out meningitis. [5] [23] [24]

Colonization with GBS during labour is the primary risk factor for development of GBS-EOD. GBS-EOD is acquired vertically (vertical transmission), through exposure of the fetus or the baby to GBS from the vagina of a colonized woman, either in utero (because of ascending infection) or during birth, after rupture of membranes. Infants can also be infected during passage through the birth canal, nevertheless, newborns that acquire GBS through this route can only become colonized, and these colonized infants usually do not develop GBS-EOD.

Roughly, 50% of newborns to GBS colonized mothers are also GBS colonized and (without prevention measures) 1% to 2% of these newborns will develop GBS-EOD. [25] In the past, the incidence of GBS-EOD ranged from 0.7 to 3.7 per thousand live births in the US, [5] and from 0.2 to 3.25 per thousand in Europe. [20] In 2008, after widespread use of antenatal screening and intrapartum antibiotic prophylaxis, the Centers for Disease Control and Prevention of United States (CDC) reported an incidence of 0.28 cases of GBS-EOD per thousand live births in the US. [26]

Though maternal GBS colonization is the key determinant for GBS-EOD, other factors also increase the risk. These factors comprise: [5] [21]—Onset of labour before 37 weeks of gestation (premature birth).

--Prolonged rupture of membranes (longer duration of membrane rupture) (≥18 h before delivery).

--Intrapartum (during childbirth) fever (>38 °C, >100.4 °F).

--Amniotic infections (chorioamnionitis).

--Young maternal age.

Nevertheless, most babies who develop GBS-EOD are born to GBS colonized mothers without any of these risk factors. [21] Heavy GBS vaginal colonization is also associated with a higher risk for GBS-EOD.

Women who had one of these risk factors but who are not GBS colonized at labour are at low risk for GBS-EOD compared with women who were colonized prenatally but had none of the aforementioned risk factors. [25]

Presence of low levels of anticapsular antibodies against GBS in the mother are also of great importance for the development of GBS-EOD. [27] [28] Because of that, a previous sibling with GBS-EOD is also an important risk factor for development of the infection in subsequent deliveries, probably reflecting the lack of protective antibodies in the mother. [21]

Overall, the case fatality rates from GBS-EOD have declined, from 50% observed in studies from the 1970s to between 2% and 10% in recent years, mainly as a consequence of improvements in therapy and management. Fatal neonatal infections by GBS are more frequent among premature infants. [5] [21] [29]

GBS-LOD affects infants from 7 days to 3 months of age and has a lower case fatality rate (1%-6%) than GBS-EOD. Clinical syndromes of GBS-EOD are bacteremia without a focus (65%), meningitis (25%), cellulitis, osteoarthritis, and pneumonia. Prematurity has been reported to be the main risk factor. Each week of decreasing gestation increases the risk by a factor of 1.34 for developing GBS-LOD. [30]

GBS-LOD is not acquired through vertical transmission during delivery, it can be acquired later from the mother from breast milk or from environmental and community sources. GBS-LOD commonly shows nonspecific signs, and diagnosis should be made obtaining blood cultures in febrile newborns. Hearing loss and mental impairment can be a long-term consequence of GBS meningitis. [5] [22]

Prevention of neonatal infection. Intrapartum antibiotic prophylaxis (IAP)[edit]

Currently, the only reliable way to prevent GBS-EOD is intrapartum antibiotic prophylaxis (IAP). That is to say administration of antibiotics during delivery. It has been proved that intravenous penicillin or ampicillin given at the onset of labour and then again every four hours until delivery to GBS colonized women are very effective at preventing vertical transmission of GBS from mother to baby and GBS-EOD (Penicillin G, 5 million units IV initial dose, then 2.5–3.0 million units every 4 hrs until delivery or Ampicillin, 2 g IV initial dose, then 1 g IV every 4 hrs until delivery). [5] [21]

It has been indicated that penicillin-allergic women without a history of anaphylaxis (angioedema, respiratory distress or urticaria) following administration of a penicillin or a cephalosporin (low risk of anaphylaxis) could receive cefazolin (2g IV initial dose, then 1 g IV every 8 hrs until delivery) instead of penicillin or ampicillin. [21]

Clindamycin (900 mg IV every 8 hrs until delivery), and vancomycin (1 g IV every 12 hrs until delivery) are used to prevent GBS-EOD in infants born to penicillin-allergic mothers. [21]

Erythromycin is not recommended for IAP under any circumstances today. [21]

Antibiotic susceptibility testing (AST) of GBS isolates is crucial for appropriate antibiotic selection for IAP in penicillin-allergic women, because resistance to clindamycin, the most common agent used (in penicillin-allergic women), is increasing among GBS isolates. Appropriate methodologies for testing are important, because resistance to clyndamicin (antimicrobial resistance) can occur in some GBS strains that appear susceptible (antibiotic sensitivity) in certain susceptibility tests. [21]

It has been shown that if appropriate IAP in GBS colonized women starts at least 2 hours before delivery the risk of neonatal infection is also somehow reduced. [31] [32] [33]

True penicillin-allergy is rare with an estimated frequency of anaphylaxis of 1 to 5 episodes per 10,000 cases of penicillin therapy. [34] Penicillin administered to a woman with no history of β-lactam allergy has a risk of anaphylaxis of 4/10,000 to 4/100,000. Maternal anaphylaxis associated with GBS IAP occurs, but any morbidity associated with anaphylaxis is offset greatly by reductions in the incidence of GBS-EOD. [21]

Home births are becoming increasingly popular in the UK. Recommendations for preventing GBS infections in newborns are the same for home births as for hospital births. Around 25% of women having home births probably carry GBS in their vagina at delivery without knowing. And it could be difficult to follow correctly the recommendations of IAP and to deal with the risk of a severe allergic reaction to the antibiotics outside of a hospital setting. [35]

IAP have been considered to be associated with the emergence of resistant bacterial strains and with an increase in the incidence of early-onset infections caused by other pathogens, mainly Gram-negative bacteria such as Escherichia coli. Nevertheless, most studies have not found an increased rate of non-GBS early-onset sepsis related to the widespread use of IAP. [21] [36] [37] [38]

Other strategies to prevent GBS-EOD have been studied, and chlorhexidine intrapartum vaginal cleansing has been proposed to help preventing GBS-EOD, nevertheless there is no evidence of the effectiveness of this approach. [21] [39] [40]

Identifying candidates to receive intrapartum antibiotic prophylaxis[edit]

There are two ways to select female candidates to IAP: the culture-based screening approach and the risk-based approach. [41] The culture-based screening approach identifies candidates using lower vaginal and rectal cultures obtained between 35 and 37 weeks of gestation, and IAP is administered to all GBS colonized women. The risk-based strategy identifies candidates to receive IAP by the aforementioned risk factors known to increase the probability of GBS-EOD without considering if the mother is or is not a GBS carrier. [5] [21] [42]

IAP is also recommended, when selecting candidates for IAP, for women with intrapartum risk factors if their GBS carrier status is not known at the time of delivery, and for women with GBS bacteriuria during their pregnancy, and for women who have had an infant with GBS-EOD previously. The risk-based approach is, in general, less effective than the culture-based approach, [43] because in most cases GBS-EOD develops among newborns who have been born to mothers without risk factors. [21] [25] [44]

IAP is not required for women undergoing planned caesarean section in the absence of labour and with intact membranes, irrespective of carriage of GBS. [21] [45]

Routine screening of pregnant women is performed in most developed countries such as the United States, France, Spain, Belgium, Canada, and Australia. And data have shown falling incidences of GBS-EOD following the introduction of screening-based measures to prevent GBS-EOD. [20] [44] [46]

The risk-based strategy is advocated, among other counties, in the United Kingdom, the Netherlands, New Zealand, and Argentina. [20]

In the UK, the Royal College of Obstetricians and Gynaecologists (RCOG) does not recommend bacteriological screening of pregnant women for antenatal GBS carriage. [45] [47] Instead, women are treated according to their risk in labour. IAP is given to women where GBS has been found from their urine or vaginal/rectal swabs taken during the pregnancy, and to women who have previously had a baby with GBS disease. Immediate induction of labour and IAP should be offered to all women with prelabour rupture of membranes at 37 weeks of gestation or more, to women whose membranes are ruptured more than 18 hours and to those who have fever in labour. Women who are pyrexial in labour should be offered broad-spectrum antibiotics including an antibiotic appropriate for preventing EOD-GBS. [45] [48]

The issue of cost-effectiveness of both strategies for identifying candidates for IAP is less clear-cut. And some studies have indicated that testing low risk women, plus IAP administered to high-risk women and those found to carry GBS is more cost-effective than the advocated current UK practice. [49] Other evaluations have also found the culture-based approach to be more cost-effective than the risk-based approach for the prevention of GBS-EOD. [50] [51]

It has been reported that IAP will not prevent all cases of GBS-EOD. IAP efficacy is estimated at 80%. The risk-based prevention strategy does not prevent about 33% of cases with no risk factors. [52]

It has also been proposed that testing pregnant women to detect GBS carriers, and giving IAP to those carrying GBS and to high-risk women, is significantly more cost-effective than the use of the risk-factor approach. One research paper calculated an expected net benefit to the UK Government of such an approach of around £37million a year, compared with the current RCOG approach. [49] [50]

In the UK, it has also been suggested that:

"For women known to carry GBS where it is not expected that the intravenous antibiotics can be given for at least 4 hours before delivery, an intramuscular injection of 4.8 MU (2.9 g) of Penicillin G at about 35 weeks of pregnancy may be useful in addition to intravenous antibiotics given from the onset of labour or membranes rupturing until delivery to try to eradicate GBS colonisation until after delivery". [53]

However, this recommendation IS NOT supported by the present guidelines. [21] [45]

It has also been pointed out that up to 90% of cases of GBS-EOD would be preventable if IAP were offered to all GBS carriers identified by universal screening late in pregnancy, plus to the mothers in higher risk situations. [54]

Where insufficient intravenous antibiotics are given before delivery, the baby may be given antibiotics immediately after birth, although evidence is inconclusive as to whether this practice is effective or not. [21] [55] [56] [57]

Falling incidence of EOD & LOD GBS disease in US-CDC

Screening for GBS colonization in pregnancy[edit]

Approximately 10%–30% of women are colonized with GBS during pregnancy. Nevertheless, during pregnancy colonization can be temporary, intermittent, or continual. [21]

Because the GBS colonization status of women can change during pregnancy, only cultures carried out ≤5 weeks before delivery predict quite accurately the GBS carrier status at delivery. In contrast, if the prenatal culture is carried out more than 5 weeks before delivery it is unreliable for accurately predicting the GBS carrier status at delivery. And because of that, testing for GBS colonization in pregnant women is recommended by the CDC guidelines at 35–37 weeks of gestation. [21] [58]

The clinical samples recommended for culture of GBS are swabs collected from lower vagina and rectum through the external anal sphincter. The sample should be collected swabbing the lower vagina (vaginal introitus) followed by the rectum (i.e., inserting the swab through the anal sphincter) using the same swab or two different swabs. Cervical, perianal, perirectal or perineal specimens are not acceptable, and a speculum should not be used for sample collection. [21] Samples can be taken by healthcare professionals, or by the mother herself with appropriate instruction. [59] [60] [61]

Instructions for the collection of a genital swab for the detection of GBS

Following the recommendations of the CDC these swabs should be placed into a non-nutritive transport medium. When feasible, specimens should be refrigerated and sent to the laboratory as soon as possible. [21] Appropriate transport systems are commercially available, and in these transport media GBS can remain viable for several days at room temperature. However, the recovery of GBS declines over one to four days, especially at elevated temperatures, which can lead to false-negative results. [21] [62]

Culture methods[edit]

Samples (vaginal, rectal or vagino-rectal swabs) should be inoculated into a selective enrichment broth, (Todd Hewitt broth with selective antibiotics, enrichment culture). This involves growing the samples in an enriched medium to improve the viability of the GBS and simultaneously impairing the growth of other naturally occurring bacteria. After incubation (18-24h, 35-37 °C), the enrichment broth is subcultured to blood agar plates and GBS-like colonies are identified by the CAMP test or using latex agglutination with GBS antisera. [21] [63] In the UK this is the method described by the Health Protection Agency (UK Standards for Microbiology Investigations. Detection of Carriage of Group B Streptococci). [64]

After incubation, the enrichment broth can also be subcultured to granada agar where GBS grows as pink-red colonies [17] [63] [65] [66] or to chromogenic agars, where GBS grows as coloured colonies. [21]

Today in the UK, the detection of GBS colonization using the enrichment broth technique is not offered from most laboratories serving the NHS. However, the implementation of this test seems to be a viable option. At present, culture for GBS (using enriched culture medium) at 35–37 weeks to define an at-risk group of women appears to be the most cost-effective strategy currently available. [50] [51]

The charitable organization Group B Strep Support have published a list of hospitals in the UK that offers the detection of GBS using the enrichment broth culture method (Enrichment culture medium, ECM). [67] This test is also available privately from around £35 per test for a home-testing pack, and it is offered by private clinics: "Where can I get the ECM test?" [67] The test is also available privately, for a UK-wide postal service. [68] [69]

It is also possible to inoculate directly the vaginal and rectal swabs or the vagino-rectal swab in a plate of an appropriate culture medium for GBS (blood agar, granada medium or chromogenic media). However, this method (bypassing the selective enrichment broth step) can lead to some false negative results, and this approach should be taken only in addition to, and not instead of, inoculation into selective broth. [21]

Point of care testing (POCT). PCR intrapartum testing[edit]

No current cultured based test is both accurate enough and fast enough to be recommended for detecting GBS once labour starts. Plating of swab samples requires time for the bacteria to growth, meaning that this is unsuitable as an intrapartum point-of-care test.

Alternative methods to detect GBS in clinical samples (as vagino-rectal swabs) rapidly have been developed, such are the methods based in nucleic acid amplification, nucleic acid amplification tests (NAAT), like polymerase chain reaction (PCR) tests, and DNA hybridization probes. These tests can also be used to detect GBS directly from broth media, after the enrichment step, avoiding the subculture of the incubated enrichment broth to an appropriate agar plate. [21] [70]

Testing women for GBS colonization using vaginal or rectal swabs at 35–37 weeks of gestation and culturing them in enriched media is not as rapid as a PCR test in labour that would check whether the pregnant woman is carrying GBS at delivery. And PCR tests, allow starting IAP on admission to the labour ward in those women in whom it is not known if they are GBS carriers or not. [21] PCR testing for GBS carriage could, in the future, be sufficiently accurate to guide IAP. However, the PCR technology to detect GBS must be improved and simplified to make the method cost-effective and fully useful as point of care testing (POCT) to be carried out in the labour ward (bedside testing), and these tests still cannot replace antenatal culture for the accurate detection of GBS carriers. [21] [71]

Missed opportunities for GBS early onset disease prevention[edit]

The important factors for successful prevention of GBS-EOD using IAP and the universal screening approach are: i) To reach most pregnant women for antenatal screens; ii) Proper sample collection; iii) Using an appropriate procedure for detecting GBS; and iv) Administering a correct IAP to GBS carriers.

Several studies have found that most cases of GBS-EOD occur in term infants born to mothers who screened negative for GBS colonization and in preterm infants born to mothers who were not screened. Though some false negative results observed in the GBS screening tests can be due to the test limitations and to the acquisition of GBS between the time of screening and delivery, these data show that improvement in specimen collection and processing methods for detecting GBS are still necessary in some settings. False negative screening test, along with failure to receive IAP in women delivering preterm with unknown GBS colonization status, and the administration of inappropriate IAP agents to penicillin-allergic women account for most missed opportunity for prevention of cases of GBS-EOD.

GBS-EOD infections presented in infants whose mothers had been screened as GBS culture-negative are particularly worrying, and may be caused by incorrect sample collection, by delay in processing the samples, by incorrect laboratory techniques, by recent antibiotic use, or by GBS colonization after the screening was carried out. [44] [72] [73] [74] [75]


In 2000–2001 the reported overall incidence of neonatal GBS infection in the UK was 0.72 per 1,000 live births, 0.47 per 1,000 for GBS-EOD and 0.25 per 1,000 for GBS-LOD. Very marked variations were observed, the incidence in Scotland was 0.42 per 1,000 whilst in Northern Ireland it was 0.9 per 1,000 live births. [76] [77]

Nevertheless, it has been suggested that it may be a serious underestimate of the real incidence of GBS infection in newborns. A plausible explanation of this is that a considerable number of infants with probable GBS-EOD had negative cultures as a result of a previous maternal antibiotic treatment that inhibits the growth of GBS in blood and cerebrospinal fluid cultures, but does not mask clinical symptoms. [78] [79]

Data collected prospectively for neonates who required a septic screen in the first 72 hrs of life in the UK, indicated a combined rate of definite and probable GBS-EOD infection of 3.6 per 1,000 live births. [80] Another study on the epidemiology of Invasive GBS infections in England and Wales, reported a rise in the incidence of GBS-EOD between 2000 and 2010 from 0.28 to 0.41 per 1,000 live births. Rates of GBS-LOD also increased between 1991 and 2010 from 0.11 to 0.29 per 1,000 live births in England and Wales. [81]

In the US, it has also been reported that the incidence of GBS-EOD decreased from 0.47 per 1,000 live births in 1999-2001 to 0.34 per 1,000 live births in 2003-2005. [46] And the CDC reported an incidence of GBS-EOD of 0.25 per 1,000 live births in 2010. In contrast the incidence of GBS-LOD has remained unchanged at 0.26 per 1,000 live births in the US. [82]

Falling incidence of GBS-EOD in Spain (Castrillo Group of Hospitals)

In Spain, the incidence of GBS vertical sepsis declined by 73.6%, from 1.25/1,000 live births in 1996 to 0.33/1,000 in 2008. [83] In the Barcelona area between 2004 and 2010, the incidence of GBS-EOD was 0.29 ‰ living newborns, with no significant differences along the years. The mortality rate was 8.16%. [44] [84]

In France, since 2001, it has also been reported a rapid decrease of incidence of the neonatal GBS infections after widespread use of IAP, from 0.7 to 0.2 per 1,000 births between 1997 and 2006. [85]

Recently (since 2012) the incidence of neonatal GBS infection has been estimated as 0.53 per 1,000 births in the European region, 0.67 in America and 0.15 in Australasia. Countries reporting no use of IAP had a 2.2-fold higher incidence of GBS-EOD compared with those reporting any use of IAP. [29] [77]

The following are estimates of the chances that a baby will be infected with a GBS neonatal infection if no preventative measures are taken and no other risk factors are present: [86]

  • 1 in 1,000 where the woman is not a known GBS carrier
  • 1 in 400 where the woman carries GBS during the pregnancy
  • 1 in 300 where the woman carries GBS at delivery
  • 1 in 100 where the woman had a previous baby infected with GBS

If a woman who carries GBS is given IAP during labour the baby’s risk is reduced significantly:

  • 1 in 8,000 where the mother carries GBS during pregnancy;
  • 1 in 6,000 where the mother carries GBS at delivery; and
  • 1 in 2,200 where the mother has previously had a baby infected with GBS.



Royal College of Obstetricians & Gynaecologists (RCOG)[edit]

The RCOG issued their Green Top Guideline No 36 "Prevention of early onset neonatal Group B streptococcal disease" in November 2003. [87] In this guideline it is clearly stated that:

Routine bacteriological screening of all pregnant women for antenatal GBS carriage is not recommended, and that

Vaginal swabs should not be taken during pregnancy unless there is a clinical indication to do so.

However, it is also stated that:

Intrapartum Antibiotic Prophylaxis should be offered if GBS is detected on a vaginal swab in the current pregnancy.

Nevertheless, this guidelines uses minimum incidence figures from a study undertaken in 2000-2001, [88] and therefore it could not only underestimate the true incidence of GBS infection, but it could also have underestimated the risks to babies from GBS infection. GBS infection in babies has increased in England, Wales and Northern Ireland since 2003 (when the guideline was introduced). Voluntarily reported cases from the CDR/HPA (Communicable Disease Report/Health Protection Agency) show 0.48 cases per 1,000 live births in 2003, which increased to 0.64 per 1,000 in 2009. [89]

In 2007, the RCOG published the findings of their audit to evaluate practice in the UK obstetric units against their recommendations. [90] The audit started out by comparing international guidelines for prevention of GBS-EOD: highlighting the fact that, in contrast to the UK and New Zealand guidelines, most of the other countries surveyed recommended identifying women for IAP by offering sensitive tests to all pregnant women. The audit reviewed hospitals’ protocols against GBS infection in newborns. And of the 161 UK units, which submitted their protocol, four units did not even have a protocol for GBS, of those that did, 35% did not mention the 2003 RCOG guideline, and only a minority of units had protocols that were entirely consistent with the guideline.

Further UK research published in 2010 looked at the opportunities for prevention of GBS-EOD following the introduction of the RCOG Guideline. They found that, in the 48 cases of GBS during 2004 to 2007 (0.52/1,000 live births), only 19% of the mothers in whom risk factors were present were given adequate IAP. And the researchers stated that: “if all women with risk factors received prophylaxis, 23 cases (48%) may have been prevented.[52]

The 2003 RCOG guideline was reviewed in July 2012, [45] but there were no substantial changes made, the most notable being the clarification of procedure when a woman carrying GBS has PROM and the clarification that oral antibiotics are not recommended in labour against GBS infection in the baby.

The review also dealt with a common misconception regarding vaginal cleansing, stating that there is no evidence showing that this procedure can reduce GBS infection in the baby. New evidence and guidance in this field were reviewed by the RCOG in 2014 and it was decided that revision of the guideline would be deferred to a later date. And in the mean time the version available on the website will remain valid until replaced. [47]

The second and final audit report into GBS (Audit of current practice in preventing early-onset neonatal group B streptococcal disease in the UK) has been published (RCOG, January 2016). As a result of the audit, the RCOG has recommend that the national guidelines for preventing GBS infection in newborns should be updated. [91]

NICE guidelines[edit]

The UK's National Institute for Health and Care Excellence (NICE) does not recommend routine testing for GBS, stating: “Pregnant women should not be offered routine antenatal screening for group B streptococcus because evidence of its clinical and cost effectiveness remains uncertain”. [92]

Nevertheless, the NICE Guideline "Neonatal infection: antibiotics for prevention and treatment" state that:

"Intrapartum Antibiotic Prophylaxis should be offered if group B streptococcal colonisation, bacteriuria or infection are detected in the current pregnancy". [93]

National Screening Committee[edit]

The UK National Screening Committee’s current policy position on GBS is that:

"screening should not be offered to all pregnant women". [94]

This policy was reviewed in 2012, and despite receiving 212 responses, of which 93% advocated screening, [95] the NSC decided to not recommend antenatal screening.

This decision was strongly criticized by the charity Group B Strep Support as ignoring both the wishes of the public and the rising incidence rates of GBS infection in the UK. [96]

In May 2006, the UK National Screening Committee launched their GBS online learning package. This learning package was developed to raise awareness of GBS amongst health care professionals. Developed by the Women’s Health Specialist Library (part of the National Library for Health), the learning package is based upon the current UK guidelines published by the RCOG. And it is divided into three sections – antenatal, delivery and postnatal. Within each section, there is the option to access an introduction to GBS, different clinical scenarios, a series of quiz questions to test knowledge and a FAQs section. [97]

Guidelines from the Centers for Disease Control and Prevention, CDC[edit]

Recommendations for IAP to prevent perinatal GBS disease were issued in 1996 by the CDC. In these guidelines it was recommended the use of one of two prevention methods, either a risk-based approach or a culture-based screening approach. [41]

The CDC issued updated guidelines in 2002. These CDC` 2002 guidelines recommended the universal culture-based screening of all pregnant women at 35–37 weeks’ gestation to optimize the identification of women who must receive IAP. CDC also recommended that women with unknown GBS colonization status at the time of delivery be managed according to the presence of intrapartum risk factors. Because of this strategy, the US has seen a major reduction in the incidence GBS-EOD. [98]

The CDC issued updated guidelines again in 2010. However, the foundations of prevention in the CDC`s 2010 guidelines remain unchanged. [21]

-The following were the main additions in the 2010 guidelines:

-Expanded options for laboratory detection of GBS, including use of pigmented media and PCR assays.

-A revised colony count threshold for laboratories to report GBS in the urine of pregnant women.

-Revised algorithms for GBS screening and use of IAP for women with threatened preterm delivery, including one algorithm for preterm labor and one for preterm premature rupture of membranes.

-Recommendations for IAP agents are presented in an algorithm format in an effort to promote use of the most appropriate antibiotic for penicillin-allergic women.

-A minor change has been made to penicillin dosing to facilitate implementation in facilities with different pre-packaged penicillin products.

-The neonatal management algorithm’s scope was expanded to apply to all newborns.

-Management recommendations that depend upon clinical appearance of the neonate and other risk factors such as maternal chorioamnionitis, adequacy of IAP if indicated for the mother, gestational age and duration of membrane rupture.

-Changes were made to the algorithm to reduce unnecessary evaluations in well appearing newborns at relatively low risk for GBS-EOD. [99]

Other guidelines[edit]

National guidelines in most developed countries advocate the use of universal screening of pregnant women late in pregnancy to detect GBS carriage and use of IAP in all colonized mothers. e.g. Canada, [100] Spain, [101] Switzerland, [102] Germany, [103] Poland, [104] Czech Republic, [105] France, [106] and Belgium. [107]

In contrast, risk factor-based guidelines were issued in the Netherlands, [108] New Zealand, [109] Argentina, [110] and Queensland. [111] Nevertheless, the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) does not recommend clearly one of both prevention strategies -either the risk-based or the screening based approach- to identify pregnant women for IAP, and allow practitioners to choose according jurisdictional guidelines. [112]

GBS infection in adults[edit]

GBS is also an important infectious agent able to cause invasive infections in adults. Serious life-threatening invasive GBS infections are increasingly recognized in the elderly and in individuals compromised by underlying diseases such as diabetes, cirrhosis and cancer. GBS infections in adults include urinary tract infection, skin and soft-tissue infection (skin and skin structure infection) bacteremia without focus, osteomyelitis, meningitis and endocarditis. [4] GBS infection in adults can be serious, and mortality is higher among adults than among neonates. In general, penicillin is the antibiotic of choice for treatment of GBS infections. Erythromycin or clindamycin should not be employed for treatment in penicillin-allergic patients unless susceptibility of the infecting GBS isolate to these agents is documented. Gentamicin plus penicillin (for antibiotic synergy) in patients with life-threatening GBS infections may be used. [113][114] [115]


Though the introduction of national guidelines to screen pregnant women for GBS carriage and the use of IAP has significantly reduced the burden of GBS-EOD disease, it has had no effect on preventing neither GBS-LOD in infants nor GBS infections in adults. [116]

Because of that, if an effective vaccine against GBS were available it would be an effective means of controlling not only GBS disease in infants but also GBS infections in adults. The capsular polysaccharide of GBS which is an important GBS virulence factor is also an excellent candidate for the development of an effective vaccine.

As early as 1976,[27] it was demonstrated that low levels of maternal antibodies against the capsular polysaccharide of GBS correlated with susceptibility to GBS-EOD and GBS-LOD. Maternal specific antibodies, transferred from the mother to the newborn, were able to confer protection to babies against GBS infection. [117] Vaccination is considered an ideal solution to prevent not only GBS-EOD and GBS-LOD but also GBS infections in adults at risk. Nevertheless, though research and clinical trials for the development of an effective vaccine to prevent GBS infections are underway, no vaccine is currently available in 2015. At present, the licensing of GBS vaccines is difficult because of the challenge in conducting efficacy clinical trials in humans due to the low incidence of GBS neonatal diseases. [20] [118] [119]

GBS infection in animals[edit]

GBS has been found in many mammals and other animals such as camels, dogs, cats, seals, dolphins, and crocodiles. [120]


In cattle, GBS causes mastitis, an infection of the udder. It can produce an acute febrile disease or a sub-acute, more chronic disease. Both lead to diminishing milk production (hence its name: agalactiae meaning "no milk"). Mastitis associated with GBS can have an important effect on the quantity and quality of milk produced, and are also associated with elevated somatic cell count and total bacteria count in the milk. Outbreaks in herds are common. And as this is of major significance for the dairy industry, programs to reduce the impact of GBS have been enforced in many countries. [121]


GBS it is also an important pathogen in a diversity of fish species, leading to serious economic losses in many species of fish worldwide. GBS causes severe epidemics in fish farmers causing septicemia and external and internal hemorrhages. GBS infection has been reported from wild and captive fish and has been involved in epizootics in many countries. [122][123]

Vaccines to protect fish against GBS infections are under development. [124]


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