Introduction

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  Group B Streptococcus (GBS) is a harmless opportunistic commensal bacterium but has the potential to cause severe infections.

  
  
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  In adults, streptococcal A infections can cause necrotising fasciitis (Group A) or meningitis.¹

  
  
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  In neonates, GBS causes early- or late-onset neonatal infection. GBS is the common cause of life-threatening infections in neonates.²

  
  
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  GBS is also known to cause urinary tract infection, intra-amniotic infection and invasive disease during pregnancy and postpartum endometritis.

Prevalence and Incidence for Neonatal Infections

According to research led by the London School of Hygiene and Tropical Medicine, out of the 410 000 cases of GBS detected globally every year, 147 000 end in stillbirth or infant death. In 2015 Africa had the highest incidence of maternal and fetal morbidity and mortality, including infant death. The research found GBS was present all over the world, with an average of 25 per cent of pregnant women colonised with the bacteria (ranging from 11 per cent in eastern Asia to 35 per cent in the Caribbean).³

Since active prevention began in the mid-1990s, the rate of group B strep disease among newborns in the first week of life has declined by 80 per cent.

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  In the USA, where GBS is the leading infectious cause of morbidity and mortality among infants, the rate of early-onset infection has decreased from 1.7 cases per 1000 live births (1993) to 0.24 cases per 1000 live births in 2014.⁴

  
  
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  In the UK, the incidence of early-onset GBS (EOGBS) disease in 2015 was 0.57/1000 births (517 cases), a significant increase in incidence since previous surveillance undertaken in 2000 (0.48/1000).⁵

Microbiology

GBS has a bacterial capsule composed of polysaccharides and sub-classified into 10 serotypes (Ia, Ib, II–IX) depending on the immunologic reactivity of their polysaccharide capsule. Five of nine capsular serotypes, III, Ia, V, Ib and II, cause 95 per cent of invasive disease (in decreasing frequency). The most important virulent part of GBS is capsular polysaccharide which is rich in sialic acid and β-haemolysin and probably the key virulence factor.⁶

Pathophysiology

GBS is a gram-positive cocci identified by its β-haemolytic nature. GBS infection during pregnancy is associated with increased rates of preterm and neonatal complications. The precise pathophysiology is unknown. It has been possible to isolate numerous virulence factors that are required to overcome the local host defence, vaginal flora and invade the amniotic cavity.

GBS is thought to be transmitted from person to person via multiple routes, including faecal–oral, sexual and vertical transmission but it is not classified as a sexually transmitted disease (STD).

GBS normally colonises the intestine, vagina or rectum of healthy women. Due to the female anatomy, the proximity of the vagina and rectum allows for easier trafficking of the intestinal flora. Once the bacteria enter the vagina they are overcome by the hostile environment, including the physical mucus and epithelial barriers, low pH of the vagina, local immune factors including antimicrobial peptides and antibodies, as well as a vaginal microbiome dominated by lactobacilli.^{7, 8}

Once GBS has reached the amniotic sac, it adheres to the epithelial cell, inducing secretion of pro-inflammatory chemokines including TNFa, IL-1B and IL-6. While preterm birth is usually associated with severe microbial invasion, the induction of cytokines in the absence of invasive disease is sufficient to induce labour and fetal lung injury. GBS bacteraemia results when there is a failure in epithelial barrier function and immunological clearance, resulting in septicaemia and related consequences. Invasive disease of the fetus in utero can cause direct tissue damage, pneumonia, meningitis, sepsis and fetal death.

Adult Beta Streptococcus Infections: Signs and Symptoms

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  In adults, GBS is present in the bowels, vagina and lower urogenital tract (30–40 per cent) without any symptoms. This is ‘colonisation’ and the woman is then a ‘carrier’.

  
  
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  These women are asymptomatic and generally do not have problems and do not require treatment.

  
  
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  However, GBS colonisation may cause serious invasive illnesses:

  
  
  
  
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     1. Bloodstream infection (septicaemia)

     
     
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     2. Skin and soft tissue infection

     
     
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     3. Bone and joint infection

     
     
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     4. Pneumonia

     
     
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     5. Urinary tract infection

     
     
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     6. Meningitis

  
  

The rate of serious invasive group B strep disease among non-pregnant adults is about 10 cases out of every 100 000 non-pregnant adults.

Neonatal Transmission⁴

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  GBS is present in the bowel flora of 20–40 per cent of adults (colonisation).

  
  
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  During pregnancy, GBS colonisation is asymptomatic and generally does not cause problems and does not require treatment.

  
  
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  Vertical transmission occurs during intrapartum/labour from the time of membrane rupture to delivery of the baby.⁷

Risk Factors for EOGBS

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   1. Previous baby with GBS infection:

   
   

   If a woman has had a previous baby infected with GBS, she has a 10 times higher risk

   
   
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   2. Urinary tract infection or colonisation:

   
   

   The risk is four times higher if GBS is found in a woman’s urine during the current pregnancy

   
   
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   3. Raised temperature during labour:

   
   

   There is a four times higher risk if a woman’s temperature is raised during labour (37.5°C or higher)

   
   
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   4. Colonisation in a rectal or vaginal swab:

   
   

   The risk is three times higher if found on a vaginal or rectal swab during the current pregnancy

   
   
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   5. Premature rupture of membranes:

   
   

   The risk is three times higher if PROM occurs more than 18 hours before delivery¹¹

   
   
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   6. Preterm labour in known GBS carrier:

   
   

   There is a three times higher risk of preterm labour in a known GBS carrier

   
   
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   7. A classic prospective cohort study conducted during the 1980s revealed that pregnant women with GBS colonisation were >25 times more likely than pregnant women with negative prenatal cultures to deliver infants with EOGBS disease¹² [EL 2]

   
   
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   8. In the absence of any intervention, an estimated 1–2 per cent of infants born to colonised mothers develop EOGBS infections