Group B streptococcal infection, also known as Group B streptococcal disease or just Group B strep, is the infection caused by the bacterium Streptococcus agalactiae (S. agalactiae).
It known as group B streptococcus or GBS.
GBS can colonize healthy adults with no clinical consequences, but may cause ill illness in newborns, young, infant, pregnant persons, and older adults.
The group B antigen is a polysaccharide structure that is linked to cell wall peptidoglycan and does not elicit a protective antibody response.
GBS commonly colonizes the human G.I. and genitourinary tracts and is the single most common bacterial cause of invasive infections among newborns in the United States.
GBS infection can cause serious illness and sometimes death, especially in newborns, the elderly, and people with compromised immune systems.
In infants younger than one year of age have the highest rates of group B streptococcal infection.
Neonatal Group B streptococcal infection is categorized as early onset disease when it occurs from birth to six days of age, and is late onset disease when it from 7 to 89 days of age.
Most cases of early onset disease (75%) parentheses are recognized on the date of birth, and up to 95% occur within 48 hours after birth.
In the pathogenesis of late onset disease in infants can acquire group B streptococcus from non-maternal sources.
Infant oropharyngeal and G.I. colonization are important factors in late onset pathogenesis, and late onset disease has been associated with maternal group B stretococcal mastitis.
GPS is the single most common pathogen, causing invasive infection among all newborns in the US and second most common among infants born pre-term.
Maternal rectal vaginal group be streptococcal colonization is the most important risk factor for neonatal early onset, disease.
GPS is neither a permanent nor a populous member of the G.I. and genital urinary flora of humans.
23% of pregnant persons in the US are colonized with GPS and approximately 18% are colonized worldwide.
Maternal GBS colonization in the US is associated with younger age, obesity, sexual activity, and tobacco smoking.
Early onset disease involves ascending GBS colonization from the maternal G.I. and lower genitourinary tracts to the upper genital tract, uterine compartment, and ultimately colonization of the fetus and newborn.
Fetal and neonatal mucosal and skin colonization, as well as aspiration or swallowing of infected amniotic fluid, can promote transition to invasive disease.
In the absence of intrapartum antibiotic prophylaxis, approximately half the infants born to colonized parturient persons, are colonized at surface sites, and invasive disease develops in 1 to 2%.
Worldwide in 2020 GBS caused approximately 400,000 infections among infants, 50 to 100,000 infant deaths, 40,000 infections among pregnant persons, and 40 to 50,000 stillbirths.
GBS harbours an important number of virulence factors: capsular polysaccharide, rich in sialic acid, and a pore-forming toxin, β-haemolysin.
The GBS capsule is the key virulence factor because it helps GBS escape from the host defense mechanisms interfering with phagocytic killing of GBS by human phagocytes.
GBS is usually a harmless commensal bacterium being part of the human microbiota colonizing the gastrointestinal and genitourinary tracts of up to 30% of healthy human adults.
S. agalactiae is a Gram-positive coccus with a tendency to form chains, beta-hemolytic, catalase-negative, and facultative anaerobe.
GBS grows readily on blood agar plates, surrounded by a narrow zone of β-hemolysis.
GBS’s cell wall of the group B antigen of the Lancefield classification that can be detected directly in intact bacteria using latex agglutination tests.
The CAMP test and its ability to hydrolyse hippurate, are test that can be used to identify GBS.
Hemolytic GBS strains produce an orange-brick-red pigment when cultivated on medium.
Identification of GBS could also be carried out by laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry and Nucleic Acid Amplification Techniques.
It known as group B streptococcus or GBS.
GBS infection can cause serious illness and sometimes death, especially in newborns, the elderly, and people with compromised immune systems.
Infants with early onset disease may present with nonspecific signs of illness – tachypnea, poor feeding, skin mottling, severe sepsis syndrome with metabolic acidoasis, pneumonitis, surfactant deficiency persistent pulmonary hypertension, or systemic hypotension and 10% of cases are complicated by meningitis.
Most deaths occur in preterm infants rather than in term infants.
GBS harbours an important number of virulence factors: capsular polysaccharide, rich in sialic acid, and a pore-forming toxin, β-haemolysin.
The GBS capsule is the key virulence factor because it helps GBS escape from the host defense mechanisms interfering with phagocytic killing of GBS by human phagocytes.
GBS is usually a harmless commensal bacterium being part of the human microbiota colonizing the gastrointestinal and genitourinary tracts of up to 30% of healthy human adults.
S. agalactiae is a Gram-positive coccus with a tendency to form chains, beta-hemolytic, catalase-negative, and facultative anaerobe.
GBS grows readily on blood agar plates, surrounded by a narrow zone of β-hemolysis.
GBS’s cell wall of the group B antigen of the Lancefield classification that can be detected directly in intact bacteria using latex agglutination tests.
The CAMP test and its ability to hydrolyse hippurate, are test that can be used to identify GBS.
Hemolytic GBS strains produce an orange-brick-red pigment when cultivated on medium.
Identification of GBS could also be carried out by laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry and Nucleic Acid Amplification Techniques.
GBS is found in the gastrointestinal and genitourinary tract of humans and is normal component of the intestinal and vaginal microbiota in some women.
GBS vaginal colonization rate ranges from 4 to 36%, with most studies reporting rates over 20%.
Vaginal or rectal colonization may be intermittent, transitory, or persistent.
GBS is an asymptomatic and harmless colonizer of the gastrointestinal human tract in up to 30% of otherwise healthy adults, including pregnant women.
This opportunistic harmless bacterium can, in some circumstances, cause severe invasive infections.
Though GBS colonization is asymptomatic and, in general, 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 intra-amniotic infection or severe infection of the placental tissues infrequently, postpartum infections and it had been related with prematurity and fetal death.
GBS urinary tract infections may induce labour in pregnant women and cause premature delivery and miscarriage and requires antibiotic treatment.
Neonates with meningitis often have an initial clinical presentation identical to presentation in those without meningeal invasion, and study of the cerebrospinal fluid is often necessary to rule out meningitis.
Colonization with GBS during labor is the primary risk factor for the development of GBS-early onset of disease, as it 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 from ascending infection or during birth, after rupture of membranes.
Additional factors for early onset disease include factors that support pathogenesis with longer duration of rupture of membranes, provide baseline vulnerability as preterm birth with poor neonatal immune defenses, or evidence that infection is developing with maternal fever.
Infants can also be infected during passage through the birth canal; but these colonized infants usually do not develop GBS-early onset of disease.
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.
GBS is the main cause of bacterial infections in newborns, such as sepsis, pneumonia, and meningitis, which can lead to death or long-term after effects, through 89 days of age.
The primary risk factor for invasive, Group B streptococcal disease in newborns is exposure to maternal rectovaginal Group B streptococcal colonization during delivery.
An ascending Group B streptococcal infection in the mother, can also affect the fetus before delivery, when intramniotic infection, premature labor, or stillbirth can occur.
Pregnant women undergo screening for Group B streptococcal colonization late in the third trimester, and intrapartum antibiotic prophylaxis is administered to those with positive results.
IAP does to not prevent all cases of GBS-EOD /early onset disease) its efficacy is estimated at 80%.
The risk-based prevention strategy does not prevent about 33% of cases with no risk factors.
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.
Where insufficient intravenous antibiotics are given before delivery, the baby may be given antibiotics immediately after birth, but evidence is inconclusive as to whether this practice is effective.
Approximately 10–30% of women are colonized with GBS during pregnancy.
During pregnancy, colonization can be temporary, intermittent, or continual.
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.
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.
Because of that, testing for GBS colonization in pregnant women is recommended by the CDC at 36–37 weeks of gestation.
The sample is collected by swabbing the lower vagina followed by the rectum.
The US Preventive Services Task Force and ACOG recommend routine urine screening for all pregnant women early in their pregnancies, even in the absence of urinary symptoms, in order to detect asymptomatic bacteriuria.
As with UTIs, any asymptomatic bacteriuria cases with high CFU/mL values have also been shown to induce pyelonephritis, low birth weight, and preterm deliveries.
Therefore, treatment of these asymptomatic cases at the time of diagnosis with antibiotics is just as important as treating symptomatic UTIs in pregnancy in order to reduce these risks.
GBS UTI and asymptomatic GBS bacteriuria with high CFU/mL, pregnant women with asymptomatic GBS bacteriuria, even with low CFU/mL counts at any time during the pregnancy, should receive intrapatrum antibiotics during birth to protect the newborn, regardless of the results of the recto-vaginal screen later in pregnancy.
GBS bacteriuria, even asymptomatic, at any CFU/mL is an indication of heavy ano-genital colonization.
No current culture-based test is both accurate enough and fast enough to be recommended for detecting GBS once labor starts.
Alternative methods to detect GBS in clinical samples are based on nucleic acid amplification tests, such as polymerase chain reaction (PCR) tests, and DNA hybridization probes.
Testing women for GBS colonization using vaginal or rectal swabs at 35–37 weeks of gestation and culturing them in an enriched media is not as rapid as a PCR test.
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.
The most missed opportunities for prevention of cases of GBS-EOD: 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.
GBS-early onset infections presented in infants whose mothers had been screened as GBS culture-negative may be caused by incorrect sample collection, delay in processing the samples, incorrect laboratory techniques, recent antibiotic use, or GBS colonization after the screening was carried out.
In the past, the incidence of GBS-EOD ranged from 0.7 to 3.7 per thousand live births in the US, and from 0.2 to 3.25 per thousand in Europe.
After widespread use of antenatal screening and intrapartum antibiotic prophylaxis, the Centers for Disease Control and Prevention in the United States reported an incidence of 0.28 cases of GBS-EOD per thousand live births in the US.
Intrapartum antibiotic prophylaxis is used to reduce the risk of Group B streptococcal disease among pregnant persons and newborns.
No strategies are available currently to prevent disease in later infancy or among non-pregnant adults.
Vaccines against group B streptococcal disease consists of capsular polysaccharides linked to protein antigens in development to provide a means of preventing disease for all at risk populations.
The estimate of the global incidence of GBS LOD is 0.26 cases per 1,000 live births.
It has been appraised that GBS infections cause at least 409.000 maternal/fetal/infant cases and 147.000 stillbirths and infant deaths worldwide annually.
The following are estimates of the chances that a baby will be infected with a GBS neonatal infection if no preventive measures are taken and no other risk factors are present:
One in 1,000 where the woman is not a known GBS carrier.
One in 400 where the woman carries GBS during the pregnancy
One in 300 where the woman carries GBS at delivery
One in 100 where the woman had a previous baby infected with GBS
If a woman who carries GBS is given IAP during labor, the baby’s risk is reduced significantly:
One in 8,000 where the mother carries GBS during pregnancy;
One in 6,000 where the mother carries GBS at delivery; and
One in 2,200 where the mother has previously had a baby infected with GBS
GBS is also an important infectious agent able to cause invasive infections in adults.
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.
GBS infections in adults include urinary tract infection, skin and soft-tissue infection bacteremia without focus, osteomyelitis, meningitis and endocarditis.
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.
Gentamicin plus penicillin (for antibiotic synergy) in patients with life-threatening GBS infections may be used.
Toxic shock syndrome (TSS) is an acute multisystem life-threatening disease resulting in multiple organ failure.
TSS is caused primarily by some strains of Staphylococcus aureus and Streptococcus pyogenes that produce exotoxins.
GBS infection can be infrequently complicated, by streptococcal toxic shock-like syndrome.
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 immune compromised individuals: compromised by diseases such as diabetes, cirrhosis and cancer.
GBS associated infections in adults include: urinary tract infection, skin and soft-tissue infection, a bacteremia without focus, osteomyelitis, meningitis and endocarditis.
GBS infection in adults can be serious, with mortality rates higher among adults than among neonates.
Penicillin is the antibiotic of choice for treatment of GBS infections.
GBS infection warrants immediate medical treatment.
Toxic shock is caused primarily by some strains of Staphylococcus aureus and Streptococcus pyogenes that produce exotoxins.
Low levels of maternal antibodies against the GBS capsular polysaccharide are correlated with susceptibility to GBS-EOD and GBS-LOD.
Maternal-specific antibodies, transferred from the mother to the newborn, are able to confer protection to babies against GBS infection.
GBS6 vaccine elicited, anti-capsular poly saccharide antibodies against Group B streptococcus in pregnant women that were transferred to infants at levels associated with reduce risk of invasive Group B streptococcal disease.
Patients with late onset disease in the US presented at a median of 34 days of age.
More than 40% of these cases occur among preterm infants.
Late onset disease is complicated by meningitis in approximately 30% of cases and less commonly by pneumonia, septic arthritis, osteomyelitis and peritonitis.
Unlike early onset disease, late onset disease commonly manifests with fever.
The US case fertility rate for late onset disease is approximately 5 to 6% with a greater incidence among preterm infants and in caseescomplicated by meningitis where it is approximately 8 to 10%.
Very late onset disease occurs in approximately 10 times less often as late on disease.
Neonatal and infant deaths from group B streptococcal infection are observed at higher rates in low and middle income countries, than in high income countries.
Extremely preterm infants with group B Streptococcus infection show that nearly 80% have death or survival with moderate to severe neurodevelopmental impairment.