group b streptococcal infection group b streptococcal infection 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) (also 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. group b streptococcal infectionother namesgroup b streptococcal diseasestreptococcus agalactiae- gram stainspecialtypediatrics as other virulent bacteria, gbs harbours an important number of virulence factors, the most important are the capsular polysaccharide (rich in sialic acid), and a pore-forming toxin, β-haemolysin. the gbs capsule is probably the key virulence factor because it helps gbs escape from the host defence mechanisms interfering with phagocytic killing of gbs by human phagocytes. the gbs β-haemolysin is considered almost identical to the gbs pigment (granadaene). gbs was recognized as a pathogen in cattle by edmond nocard and mollereau in the late 1880s. it can cause bovine mastitis (inflammation of the udder) in dairy cows. the species name "agalactiae" meaning "no milk", alludes to this. its significance as a human pathogen was first described in 1938, when fry reported three fatal cases of puerperal infections caused by gbs. in the early 1960s, gbs was recognized as a main cause of infections in newborns. in general, gbs is a harmless commensal bacterium being part of the human microbiota colonizing the gastrointestinal and genitourinary tracts of up to 30% of healthy human adults (asymptomatic carriers). laboratory identification β-haemolytic colonies of streptococcus agalactiae, blood agar 18h at 36 °c positive camp test indicated by the formation of an arrowhead where s. agalactiae meets staphylococcus aureus (white middle streak) red colonies of s. agalactiae in granada agar, vagino-rectal culture 18h incubation 36 °c anaerobiosis as mentioned, s. 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. the camp test is also another important test for the identification of gbs. the camp factor acts synergistically with the staphylococcal β-haemolysin inducing enhanced haemolysis of sheep or bovine erythrocytes. gbs is also able to hydrolyse hippurate, and this test can also be used to identify gbs. haemolytic gbs strains produce an orange-brick-red nonisoprenoid polyene pigment (ornythinrhamnododecaene) (granadaene) when cultivated on granada medium that allows its straightforward identification. identification of gbs could also be carried out easily using modern methods as matrix-assisted laser desorption ionization-time of flight (maldi-tof) mass spectrometry. and nucleic acid amplification techniques (naats). additionally gbs colonies can be tentatively identified after their appearance in chromogenic agar media. nevertheless, gbs-like colonies that develop in chromogenic media should be confirmed as gbs using additional reliable tests (e.g.latex agglutination or the camp test) to avoid potential mis-identification. a summary of the laboratory techniques for gbs identification is depicted in ref 18. colonization versus infection gbs is found in the gastrointestinal and genitourinary tract of humans and is normal component of the intestinal and vaginal microbiota in some women. in different studies, 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. 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. though 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. pregnancy 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 chorioamnionitis (intra-amniotic infection or severe infection of the placental tissues) infrequently, postpartum infections (after birth) and it had been related with prematurity and fetal death. gbs urinary tract infections, more than 100.000 cfu (colony forming units) /ml, may induce labour in pregnant women and cause premature delivery (preterm birth) and miscarriage and requires antibiotic treatment. the presence of gbs in the urine of a pregnant woman, in any colony count, should be considered a marker of heavy gbs colonization and an indication for intra partum antibiotic prophylaxis (iap). newborns in the western world, gbs (in the absence of effective prevention measures) 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. 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 7 and 90 days after birth. roughly 50% of newborns of gbs colonized mothers are also gbs colonized and (without prevention measures) 1-2% of these newborns will develop gbs-eod. the most common clinical syndromes of gbs-eod are sepsis without apparent location, pneumonia, and less frequently meningitis. bacteremia without a focus occurs in 80-85%, pneumonia in 10-15%, and meningitis in 5-10% of cases. 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 is often necessary to rule out meningitis. colonization with gbs during labour is the primary risk factor for the 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; however, newborns who acquire gbs through this route can only become colonized, and these colonized infants usually do not develop gbs-eod. though maternal gbs colonization is the key determinant for gbs-eod, other factors also increase the risk. these factors are: onset of labour before 37 weeks of gestation (premature birth) prolonged rupture of membranes (longer duration of membrane rupture) (≥18 h before delivery) gbs bacteriuria during pregnancy intrapartum (during childbirth) fever (>38 °c, >100.4 °f) amniotic infections (chorioamnionitis) young maternal age maternal hiv-infection nevertheless, most babies who develop gbs-eod are born to colonized mothers without any of these risk factors. heavy gbs vaginal colonization may be 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 to women who were colonized prenatally, but had none of the aforementioned risk factors. presence of low levels of anticapsular antibodies against gbs in the mother are also of great importance for the development of gbs-eod. because of that, a previous sibling with gbs-eod is also an important risk factor for the development of the infection in subsequent deliveries, probably reflecting the lack of protective antibodies in the mother. 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. today, the mortality associated with gbs eod in the us is 2.1% among term newborns and 19.2% among preterm newborns. 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-lod 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. gbs-lod can not only be acquired through vertical transmission during delivery; it can also 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. s.agalactiae neonatal meningitis does not present with the hallmark sign of adult meningitis, a stiff neck; rather, it presents with nonspecific symptoms, such as fever, vomiting and irritability, and can consequently lead to a late diagnosis. hearing loss and mental impairment can be a long-term consequence of gbs meningitis. in contrast with gbs-eod, the incidence of gbs-lod has remained stable in the us at 0.31 per 1000 live births from 2006 to 2015. prevention of neonatal infection currently, the only reliable way to prevent gbs-eod is administration of intrapartum antibiotics before delivery, that is to say, intrapartum antibiotic prophylaxis (iap). iap interrupts vertical transmission of gbs from the mother to the newborn and decreases the incidence of gbs-eod. administration of intravenous (iv) antibiotics during labour. intravenous penicillin or ampicillin given at the onset of labour and then again every four hours until delivery to gbs colonized women have been proven to be very effective at preventing vertical transmission of gbs from mother to baby and gbs-eod (penicillin g, 5 million units iv initial dose, then 3 million units every 4 hours until delivery or ampicillin, 2 g iv initial dose, then 1 g iv every 4 hours until delivery). 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 (2 g iv initial dose, then 1 g iv every 8 hours until delivery) instead of penicillin or ampicillin. if the woman has a severe allergy to beta-lactams then intravenous vancomycin (1 g every 12 hours) is recommended. neither clindamycin nor erythromycin are recommended today because the high proportion of gbs resistance to erythromycin (up to 44.8%), testing for penicillin allergy and can be helpful for all gbs carrying pregnant women and will cancel the frequent use of other antibiotics for gbs-eod iap. neither oral nor intramuscular antibiotics are effective in reducing the risk gbs-eod. antibiotic susceptibility testing 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 (including inducible clindamycin resistance) 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. for women who are at risk of anaphylaxis after exposure to penicillin, the laboratory requisitions should indicate clearly the presence of penicillin allergy to ensure that the laboratory is aware for the need of testing gbs isolates for clindamycin susceptibility. vancomycin (20 mg/kg every 8 hours until delivery) is used to prevent gbs-eod in infants born to penicillin-allergic mothers. if appropriate iap in gbs colonized women starts as soon as possible once labour starts or waters have broken. when the first dose is given at least 4 hours before delivery, the risk of neonatal infection is reduced; when given between 2–4 hours before delivery the risk is partially reduced. true penicillin allergy is rare with an estimated frequency of anaphylaxis of one to five episodes per 10,000 cases of penicillin therapy. penicillin administered to a woman with no history of β-lactam allergy has a risk of anaphylaxis of 0.04 to 4 per 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. iaps 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. other strategies to prevent gbs-eod have been studied, and chlorhexidine intrapartum vaginal cleansing has been proposed to help preventing gbs-eod, nevertheless no evidence has been shown for the effectiveness of this approach. identifying candidates to receive iap two ways are used to