Group B streptococcal infection

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 bacterium 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 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 infections. [2]

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). [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 bacterium) 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 10 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][13] 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. [5] [12] The GBS β-haemolysin is considered identical to the GBS pigment. [14] [15] [16] [17]

Identification of GBS in the laboratory

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. [9] 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. [9]

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

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. [18]

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 as matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry . [19]

GBS colonization and infection

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. [20] [21] [22]

Though GBS is an asymptomatic colonizer of the gastrointestinal human tract in up to 30% of otherwise healthy adults, including pregnant women, [5] [20] this opportunistic harmless bacterium can, in some circumstances, cause severe invasive infections. [4]

GBS and 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, and postpartum infections (after birth). GBS urinary tract infections may induce labour and cause premature delivery (preterm birth). [5]

Newborns

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 after effects. [5] [23]

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. [5] [22]

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 10-15%, 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. [5] [24] [25]

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, nevertheless, newborns who acquire GBS through this route can only become colonized, and these colonized infants usually do not develop GBS-EOD.

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. [26] 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. [21] In 2008, after widespread use of antenatal screening and intrapartum antibiotic prophylaxis, the Centers for Disease Control and Prevention of United States reported an incidence of 0.28 cases of GBS-EOD per thousand live births in the US. [27]

Though maternal GBS colonization is the key determinant for GBS-EOD, other factors also increase the risk. These factors are:[5][22]

Nevertheless, most babies who develop GBS-EOD are born to colonized mothers without any of these risk factors.[22] 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 to women who were colonized prenatally, but had none of the aforementioned risk factors. [26]

Presence of low levels of anticapsular antibodies against GBS in the mother are also of great importance for the development of GBS-EOD. [28] [29] 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. [22]

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] [22] [30]

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. [31]

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][23]

Prevention of neonatal infection

Currently, the only reliable way to prevent GBS-EOD is intrapartum antibiotic prophylaxis (IAP) - administration of antibiotics during delivery. 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 2.5–3.0 million units every 4 hours until delivery or ampicillin, 2 g IV initial dose, then 1 g IV every 4 hours until delivery).[5][22]

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.[22] Clindamycin (900 mg IV every 8 hours until delivery), and vancomycin (1 g IV every 12 hours until delivery) are used to prevent GBS-EOD in infants born to penicillin-allergic mothers.[22] Erythromycin is not recommended under any circumstances today.[22]

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 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. [22]

If appropriate IAP in GBS colonized women starts at least 2 hours before the delivery, the risk of neonatal infection is also somehow reduced.[32][33][34]

True penicillin allergy is rare with an estimated frequency of anaphylaxis of one to five episodes per 10,000 cases of penicillin therapy.[35] 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. [22]

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 vaginas 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.[36]

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. [22] [37] [38] [39]

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.[22][40][41]

Identifying candidates to receive IAP

Two ways are used to select female candidates to IAP: the culture-based screening approach and the risk-based approach.[42] 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][22][43]

IAP is also recommended 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, [44] because in most cases, GBS-EOD develops among newborns who have been born to mothers without risk factors.[22][26][45]

IAP is not required for women undergoing planned caesarean section in the absence of labour and with intact membranes, irrespective of the carriage of GBS.[22][46]

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.[21][45] [47]

The risk-based strategy is advocated, among other counties, in the United Kingdom, the Netherlands, New Zealand, and Argentina.[21]

In the UK, the Royal College of Obstetricians and Gynaecologists does not recommend bacteriological screening of pregnant women for antenatal GBS carriage.[46] [48] 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.[46] [49]

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 to those found to carry GBS is more cost-effective than the current UK practice. [50] 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.[51][52]

IAP has been reported to not prevent all cases of GBS-EOD; its efficacy is estimated at 80%. The risk-based prevention strategy does not prevent about 33% of cases with no risk factors.[53]

Testing pregnant women to detect GBS carriers has also been proposed, 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.[50][51]

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". [54] However, this recommendation IS NOT supported by the present guidelines.[22][46]

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.[55]

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.[22][56][57][58]

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

Screening for GBS colonization in pregnancy

About 10–30% of women are colonized with GBS during pregnancy. Nevertheless, during pregnancy, colonization can be temporary, intermittent, or continual.[22] 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. Because of that, testing for GBS colonization in pregnant women is recommended by the CDC at 35–37 weeks of gestation.[22][59]

The clinical samples recommended for culture of GBS are swabs collected from the 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.[22] Samples can be taken by healthcare professionals, or by the mother herself with appropriate instruction. [60][61][62]

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.[22] 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.[22][63]

Culture methods

Samples (vaginal, rectal, or vaginorectal 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 (18–24 hours, 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 antiserum.[22][64] In the UK, this is the method described by the Health Protection Agency [65]

After incubation, the enrichment broth can also be subcultured to granada agar where GBS grows as pink-red colonies[18][64][66] [67] or to chromogenic agars, where GBS grows as coloured colonies.[22]

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.[51][52]

The charitable organization Group B Strep Support have published a list of hospitals in the UK that offer the detection of GBS using the enrichment broth culture method (enrichment culture medium, ECM).[68] This test is also available privately from around £35 per test for a home-testing pack, and it is offered by private clinics.[68] The test is also available privately, for a UK-wide postal service.[69] [70]

Inoculating directly the vaginal and rectal swabs or the vaginorectal swab in a plate of an appropriate culture medium (blood agar, granada medium or chromogenic media) is also possible. 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.[22]

Point-of-care testing

No current culture-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 grow, meaning that this is unsuitable as an intrapartum point-of-care test.

Alternative methods to detect GBS in clinical samples (as vaginorectal swabs) rapidly have been developed, such are the methods based on nucleic acid amplification tests, such as 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.[22][71]

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 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.[22] 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]] to be carried out in the labour ward (bedside testing). These tests still cannot replace antenatal culture for the accurate detection of GBS carriers.[22][72]

Missed opportunities for GBS EOD prevention

The important factors for successful prevention of GBS-EOD using IAP and the universal screening approach are:

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 improvements 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 opportunities 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, delay in processing the samples, incorrect laboratory techniques, recent antibiotic use, or GBS colonization after the screening was carried out.[45][73][74][75][76]

Epidemiology

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. [77][78]

Nevertheless, it may be a serious underestimation of the real incidence of GBS infections 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.[79][80]

Data collected prospectively for neonates that 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. [81] 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.[82]

In the US, the incidence of GBS-EOD has also been reported to have decreased from 0.47 per 1,000 live births in 1999-2001 to 0.34 per 1,000 live births in 2003-2005,[47] 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.[83]

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.[84] In the Barcelona area between 2004 and 2010, the incidence of GBS-EOD was 0.29 per thousand living newborns, with no significant differences along the years. The mortality rate was 8.16%.[45][85]

In France since 2001, a rapid decrease in the incidence of the neonatal GBS infections has also been reported after widespread use of IAP, from 0.7 to 0.2 per 1,000 births between 1997 and 2006.[86]

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.[30][78]

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: [87]

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

Guidelines

UK

Royal College of Obstetricians and Gynaecologists

The Royal College of Obstetricians and Gynaecologists (RCOG) issued their Green Top Guideline No 36 "Prevention of early onset neonatal Group B streptococcal disease" in November 2003.[88] The guideline clearly states: "Routine bacteriological screening of all pregnant women for antenatal GBS carriage is not recommended, and vaginal swabs should not be taken during pregnancy unless there is a clinical indication to do so." But, "Intrapartum antibiotic prophylaxis should be offered if GBS is detected on a vaginal swab in the current pregnancy."

Nevertheless, this guideline uses minimum incidence figures from a study undertaken in 2000-2001, [89] so it could not only have underestimated 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 Communicable Disease Report/Health Protection Agency show 0.48 cases per 1,000 live births in 2003, and this figure increased to 0.64 per 1,000 in 2009.[90]

In 2007, the RCOG published the findings of their audit to evaluate practice in the UK obstetric units against their recommendations.[91] 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 recommended identifying women for IAP by offering sensitive tests to all pregnant women. The audit reviewed hospitals’ protocols against GBS infection in newborns. 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 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. The researchers stated: "if all women with risk factors received prophylaxis, 23 cases (48%) may have been prevented."[53]

The 2003 RCOG guideline was reviewed in July 2012,[46] but no substantial changes were 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 no evidence shows 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.[48]

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.[92] As a result of the audit, the RCOG have recommended that the national guidelines for preventing GBS infection in newborns should be updated.[93]

NICE guidelines

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."[94]

Nevertheless, the NICE guideline "Neonatal infection: antibiotics for prevention and treatment" states: "Intrapartum Antibiotic Prophylaxis should be offered if group B streptococcal colonisation, bacteriuria or infection are detected in the current pregnancy".[95]

National Screening Committee

The UK National Screening Committee’s current policy position on GBS is: "screening should not be offered to all pregnant women."[96] This policy was reviewed in 2012, and despite receiving 212 responses, of which 93% advocated screening,[97] 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.[98] 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, the option exists to access an introduction to GBS, different clinical scenarios, a series of quiz questions to test knowledge, and a FAQs section.[99]

Guidelines from the Centers for Disease Control and Prevention

Recommendations for IAP to prevent perinatal GBS disease were issued in 1996 by the CDC. In these guidelines, the use of one of two prevention methods was recommended, either a risk-based approach or a culture-based screening approach.[42] The CDC issued updated guidelines in 2002; these 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 of GBS-EOD. [100]

The CDC issued updated guidelines again in 2010. However, the foundations of prevention in the CDC`s 2010 guidelines remain unchanged.[22] The following were the main additions in the 2010 guidelines:

Other guidelines

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, [102] Spain,[103] Switzerland,[104] Germany,[105] Poland,[106] Czech Republic,[107] France,[108] Norway, and Belgium.[109]

In contrast, risk factor-based guidelines were issued in the Netherlands, [110] New Zealand,[111] Argentina,[112] and Queensland. [113] Nevertheless, the Royal Australian and New Zealand College of Obstetricians and Gynaecologists does not recommend clearly one of both prevention strategies -either the risk-based or the culture-based approach to identify pregnant women for IAP, and allow practitioners to choose according jurisdictional guidelines.[114]

Nevertheless, in Argentina, it has been established by law, in 2008, the realization of GBS screening to all pregnant women between weeks 35 and 37, but this law is not regulated as of February 2016.[115]

GBS infection 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 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 used 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.[116][117][118]

Vaccination

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 either GBS-LOD in infants or GBS infections in adults.[119] Because of this, if an effective vaccine against GBS were available, it would be an effective means of controlling not only GBS disease in infants, but also infections in adults. The capsular polysaccharide of GBS, which is an important virulence factor, is also an excellent candidate for the development of an effective vaccine. As early as 1976,[28] low levels of maternal antibodies against the capsular polysaccharide were shown to be 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.[120] Vaccination is considered an ideal solution to prevent not only GBS-EOD and GBS-LOD, but also 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 available in 2016.[121] 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.[21][122][123]

Group B Strep Awareness Month

July has been recognised as Group B Strep Awareness Month,[124] a time when information about group B Strep aimed at families and health professionals is shared, predominantly in the UK and the US. In the UK, this is led by Group B Strep Support [125]

GBS infection in animals

GBS has been found in many mammals and other animals such as camels, dogs, cats, seals, dolphins, and crocodiles.[126]

Cattle

In cattle, GBS causes mastitis, an infection of the udder. It can produce an acute febrile disease or a subacute, 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 is 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.[127]

Fish

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 farmed fish, 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.[128][129] Vaccines to protect fish against GBS infections are under development.[130]

References

  1. ↑ Fry RM. (1938). "Fatal infections by haemolytic streptococcus group B.". Lancet. 1938:1: 199–201.
  2. ↑ Eickhoff TC, Klein JO, Kathleen Daly A, David Ingall, Finland M. (1964). "Neonatal Sepsis and Other Infections Due to Group B Beta-Hemolytic Streptococci". N Eng J Med. 271: 1221–1228. doi:10.1056/NEJM196412102712401.
  3. ↑ "Group B Strep Infection.". MedicineNet.com. Retrieved 10 January 2016.
  4. 1 2 3 Edwards MS, Baker CJ. (2010). Streptococcus agalactiae (group B streptococcus). Mandell GL, Bennett JE, Dolin R (eds) Principles and practice of infectious diseases. Vol 2, (7th. ed.). Elsevier. pp. Chapter 202. ISBN 978-0-443-06839-3.
  5. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Edwards MS, Nizet V. (2011). Group B streptococcal infections. Infectious Diseases of the Fetus and Newborn Infant (7th. ed.). Elsevier. pp. 419–469. ISBN 978-0-443-06839-3.
  6. ↑ Keefe GP. (1997). "Streptococcus agalactiae mastitis: a review. Can Vet J. 38: 199–204." (PDF). Can Vet J. 38: 199–204. PMC 1576741Freely accessible. PMID 9220132.
  7. 1 2 Whiley RA, Hardie JM. (2009). Genus I. Streptococcus Rosenbach 1884. Bergey's Manual of Systematic Bacteriology: Vol 3: The Firmicutes. (2nd. ed.). Springer. pp. 655–657. ISBN 978-0-387-95041-9.
  8. ↑ Ryan KJ, Ray CG, et al, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 286–288. ISBN 0-8385-8529-9.
  9. 1 2 3 Tille P. (2014). Bailey & Scott's Diagnostic Microbiology (13th. ed.). Elsevier. ISBN 978-0-323-08330-0.
  10. ↑ Slotved HC, Kong F, Lambertsen L, Sauer S, Gilbert GL. (2007). "Serotype IX, a proposed new Streptococcus agalactiae serotype" (PDF). J Clin Microbiol. 45: 2929–2936. doi:10.1128/jcm.00117-07.
  11. ↑ Maisey HC, Doran KS, Nizet V. (2009). "Recent advances in understanding the molecular basis of group B Streptococcus virulence" (PDF). Expert Rev Mol Med. 10: e27. doi:10.1017/S1462399408000811. PMC 2676346Freely accessible. PMID 18803886.
  12. 1 2 Rajagopal L. (2009). "Understanding the regulation of Group B Streptococcal virulence factors." (PDF). Future Microbiol. 4: 201–221. doi:10.2217/17460913.4.2.201. PMC 2691590Freely accessible. PMID 19257847.
  13. ↑ Leclercq SY, Sullivan MJ, Ipe DS, Smith JP, Cripps AW, Ulett GC. (2016). "Pathogenesis of Streptococcus urinary tract infection depends on bacterial strain and β-hemolysin/cytolysin that mediates cytotoxicity, cytokine synthesis, inflammation and virulence". Sci Rep. doi:10.1038/srep29000.
  14. ↑ Whidbey C, Harrell MI, Burnside K, Ngo L, Becraft AK, Iyer LM, Aravind L, Hitti J, Waldorf KM, Rajagopal L. (2013). "A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta." (PDF). J Exp Med. 210: 1265–1281. doi:10.1084/jem.20122753.
  15. ↑ Rosa-Fraile M, Dramsi S, Spellerberg B. (2014). "Group B streptococcal haemolysin and pigment, a tale of twins." (PDF). FEMS Microbiol Rev. 38.: 932–946.
  16. ↑ Whidbey C, Vornhagen J, Gendrin C, Boldenow E, Samson JM, Doering K, Ngo L, Ezekwe EA Jr, Gundlach JH, Elovitz MA, Liggitt D, Duncan JA, Adams Waldorf KM, Rajagopal L. (2015). "A streptococcal lipid toxin induces membrane permeabilization and pyroptosis leading to fetal injury." (PDF). EMBO Mol Med. 7: 488–505. doi:10.15252/emmm.201404883. PMC 4403049Freely accessible. PMID 25750210.
  17. ↑ Christopher-Mychael Whidbey (2015). Characterization of the Group B Streptococcus Hemolysin and its Role in Intrauterine Infection (PDF). University of Washington.
  18. 1 2 Rosa-Fraile M, Rodriguez-Granger J, Cueto-Lopez M, Sampedro A, Biel Gaye E, Haro M , Andreu A. (1999). "Use of Granada medium to detect group B streptococcal colonization in pregnant women" (PDF). J Clin Microbiol. 37.: 2674–2677.
  19. ↑ Binghuai L, Yanli S, Shuchen Z, Fengxia Z, Dong L, Yanchao C. (2014). "Use of MALDI-TOF mass spectrometry for rapid identification of group B Streptococcus on chromID Strepto B agar". International Journal of Infectious Diseases. 27: 44–48. doi:10.1016/j.ijid.2014.06.023.
  20. 1 2 Barcaite E, Bartusevicius A, Tameliene R, Kliucinskas M, Maleckiene L, Nadisauskiene R. (2008). "Prevalence of maternal group B streptococcal colonisation in European countries". Acta Obstet Gynecol Scand. 87: 260–271. doi:10.1080/00016340801908759. PMID 18307064.
  21. 1 2 3 4 5 Rodriguez-Granger J, Alvargonzalez JC, Berardi A, Berner R, Kunze M, Hufnagel M, Melin P, Decheva A, Orefici G, Poyart C, Telford J, Efstratiou A, Killian M, Krizova P, Baldassarri L, Spellerberg B, Puertas A, Rosa-Fraile M. (2012). "Prevention of group B streptococcal neonatal disease revisited. The DEVANI European project.". Eur J Clin Microbiol Infect Dis. 31: 2097–2114. doi:10.1007/s10096-012-1559-0.
  22. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 Verani JR, McGee L, Schrag SJ. 59(RR-10): 1–32. (2010). "Prevention of perinatal group B streptococcal disease: revised guidelines from CDC." (PDF). MMWR Recomm Rep. 59(RR-10):.
  23. 1 2 Libster R, Edwards KM, Levent F, Edwards MS, Rench MA, Castagnini LA, Cooper T, Sparks RC, Baker CJ, Shah PE. (2012). "Long-term outcomes of group B streptococcal meningitis" (PDF). Pediatrics. 130: e8–15. doi:10.1542/peds.2011-3453.
  24. ↑ Polin RA. (2012). "Management of Neonates With Suspected or Proven Early-Onset Bacterial Sepsis" (PDF). Pediatrics. 129: 1006–1015. doi:10.1542/peds.2012-0541.
  25. ↑ Martinez E, Mintegi S, Vilar B, Martinez MJ, Lopez A, Catediano E, Gomez B. (2015). "Prevalence and predictors of bacterial meningitis in young infants with fever without a source.". Pediatr Infect Dis J. 34: 494–498. doi:10.1097/inf.0000000000000629.
  26. 1 2 3 Boyer KM, Gotoff SP. (1985). "Strategies for chemoprophylaxis of GBS early-onset infections". Antibiot. Chemother. 35: 267–280.
  27. ↑ CDC. "Group B Strep (GBS)-Clinical Overview". Retrieved 10 January 2016.
  28. 1 2 Baker CJ, Kasper DL. (1976). "Correlation of maternal antibody deficiency with susceptibility to neonatal infection with group B Streptococcus.". N Eng J Med. 294: 753–756. doi:10.1056/nejm197604012941404. PMID 768760.
  29. ↑ Baker CJ, Edwards MS, Kasper DL. (1981). "Role of antibody to native type III polysaccharide of group B Streptococcus in infant infection.". Pediatrics. 68: 544–549. PMID 7033911.
  30. 1 2 Edmond KM, Kortsalioudaki C, Scott S, Schrag SJ, Zaidi AK, Cousens S, Heath PT. (2012). "Group B streptococcal disease in infants aged younger than 3 months: systematic review and meta-analysis" (PDF). Lancet. 279: 547–556.
  31. ↑ Lin FYC, Weisman LE ,Troendle J, Adams K. (2003). "Prematurity Is the Major Risk Factor for Late-Onset Group B Streptococcus Disease" (PDF). The Journal of Infectious Diseases. 188: 267–271. doi:10.1086/376457.
  32. ↑ Lin, F; Brenner, RA; Johnson, YR; Azimi, PH; Philips Jb, 3rd; Regan, JA; Clark, P; Weisman, LE; et al. (2001). "The effectiveness of risk-based intrapartum chemoprophylaxis for the prevention of early-onset neonatal group B streptococcal disease". American Journal of Obstetrics and Gynecology. 184 (6): 1204–10. doi:10.1067/mob.2001.113875. PMID 11349189.
  33. ↑ De Cueto, M; Sanchez, MJ; Sampedro, A; Miranda, JA; Herruzo, AJ; Rosa-Fraile, M (1998). "Timing of Intrapartum Ampicillin and Prevention of Vertical Transmission of Group B Streptococcus". Obstetrics & Gynecology. 91 (1): 112–4. doi:10.1016/S0029-7844(97)00587-5. PMID 9464732.
  34. ↑ Berardi A, Rossi C, Biasini A, Minniti S, Venturelli C, Ferrari F, Facchinetti F. (2011). "Efficacy of intrapartum chemoprophylaxis less than 4 hours duration.". J Matern Fetal Neonatal Med. 24: 619–625. doi:10.3109/14767058.2010.511347.
  35. ↑ Bhattacharya S. (2010). "The facts about Penicillin Allergy: A Review". J Adv Pharm Technol Res. 1: 11–17. PMC 3255391Freely accessible. PMID 22247826.
  36. ↑ GROUP B STREP SUPPORT. "FAQs35. Carrying GBS and home birth?". Retrieved 11 January 2016.
  37. ↑ Baltimore RS, Huie SM, Meek JI, Schuchat A, O'Brien KL (2001). "Early-onset neonatal sepsis in the era of group B streptococcal prevention.". Pediatrics. 108: 1094–1098. doi:10.1542/peds.108.5.1094.
  38. ↑ Sutkin G, Krohn MA, Heine RP, Sweet RL. (2005). "Antibiotic prophylaxis and non-group B streptococcal neonatal sepsis.". Obstet Gynecol. 105: 581–586. doi:10.1097/01.aog.0000153492.30757.2f.
  39. ↑ Schrag SJ, Hadler JL, Arnold KE, Martell-Cleary P, Reingold A, Schuchat A. (2006). "Risk factors for invasive, early-onset Escherichia coli infections in the era of widespread intrapartum antibiotic use.". Pediatrics. 118: 560–566. doi:10.1542/peds.2005-3083. PMID 16882809.
  40. ↑ Cutland, Clare L; Madhi, Shabir A; Zell, Elizabeth R; Kuwanda, Locadiah; Laque, Martin; Groome, Michelle; Gorwitz, Rachel; Thigpen, Michael C; et al. (2009). "Chlorhexidine maternal-vaginal and neonate body wipes in sepsis and vertical transmission of pathogenic bacteria in South Africa: A randomised, controlled trial". The Lancet. 374 (9705): 1909–16. doi:10.1016/S0140-6736(09)61339-8. PMID 19846212.
  41. ↑ Ohlsson, A; Shah, VS; Stade, BC (14 December 2014). "Vaginal chlorhexidine during labour to prevent early-onset neonatal group B streptococcal infection.". The Cochrane database of systematic reviews. 12: CD003520. doi:10.1002/14651858.CD003520.pub3. PMID 25504106.
  42. 1 2 CDC (1996). "Prevention of Perinatal Group B Streptococcal Disease: A Public Health Perspective". MMWR. 45-RR7: 1–24.
  43. ↑ Clifford V, Garland SM, Grimwood K. (2011). "Prevention of neonatal group B streptococcus disease in the 21st century.". J Paediatr Child Health. 48: 808–815. doi:10.1111/j.1440-1754.2011.02203.x.
  44. ↑ Schrag SJ, Zell ER, Lynfield R, Roome A, Arnold KE, Craig AS, Harrison LH, Reingold A, Stefonek K, Smith G, Gamble M, Schuchat A; Active Bacterial Core Surveillance Team. (2002). "A population-based comparison of strategies to prevent early-onset group B streptococcal disease in neonates.". N Engl J Med. 347: 233–239. doi:10.1056/nejmoa020205.
  45. 1 2 3 4 Giménez M, Sanfeliu I, Sierra M, Dopico E, Juncosa T, Andreu A, Lite J, Guardià C, Sánchez F, Bosch J., Article in Spanish. (2015). "Evolución de la sepsis neonatal precoz por Streptococcus agalactiae en el área de Barcelona (2004-2010). Análisis de los fallos del cumplimiento del protocolo de prevención. Group B streptococcal early-onset neonatal sepsis in the area of Barcelona (2004-2010). Analysis of missed opportunities for prevention." (PDF). Enf Infect Microbiol Clin. 33: 446–450. doi:10.1016/j.eimc.2014.10.015.
  46. 1 2 3 4 5 Royal College of Obstetricians and Gynaecologists. "The Prevention of Early-onset Neonatal Group B Streptococcal Disease.Green–top Guideline No. 36 2nd edition.2012" (PDF). Retrieved 11 January 2016.
  47. 1 2 Phares CR, Lynfield R, Farley MM, Mohle-Boetani J, Harrison LH, Petit S, Craig AS, Schaffner W, Zansky SM, Gershman K, Stefonek KR, Albanese BA, Zell ER, Schuchat A, Schrag SJ; Active Bacterial Core surveillance/Emerging Infections Program Network. (2008). "Epidemiology of Invasive Group B Streptococcal Disease in the United States, 1999-2005". JAMA. 299: 2056–2065. doi:10.1001/jama.299.17.2056.
  48. 1 2 Royal College of Obstetricians and Gynaecologists RCOG. "Group B Streptococcal Disease, Early-onset (Green-top Guideline No. 36. Update December 2014)". Retrieved 20 November 2015.
  49. ↑ Smaill, Fiona M. (2010). "Cochrane Database of Systematic Reviews: Intrapartum antibiotics for Group B streptococcal colonisation". Cochrane Database of Systematic Reviews (2): CD000115. doi:10.1002/14651858.CD000115.pub2. PMID 10796138.
  50. 1 2 Colbourn, T; Asseburg, C; Bojke, L; Philips, Z; Claxton, K; Ades, AE; Gilbert, RE (2007). "Prenatal screening and treatment strategies to prevent group B streptococcal and other bacterial infections in early infancy: Cost-effectiveness and expected value of information analyses". Health technology assessment. 11 (29): 1–226, iii. doi:10.3310/hta11290. PMID 17651659.
  51. 1 2 3 Colbourn, T. E; Asseburg, C.; Bojke, L.; Philips, Z.; Welton, N. J; Claxton, K.; Ades, A E; Gilbert, R. E (2007). "Preventive strategies for group B streptococcal and other bacterial infections in early infancy: Cost effectiveness and value of information analyses". BMJ. 335 (7621): 655. doi:10.1136/bmj.39325.681806.AD. PMC 1995477Freely accessible. PMID 17848402.
  52. 1 2 Kaambwa B, Bryan S, Gray J, Milner P, Daniels J, Khan KS, Roberts TE. (2010). "Cost-effectiveness of rapid tests and other existing strategies for screening and management of early-onset group B streptococcus during labour.". BJOG. 117: 1616–1627. doi:10.1111/j.1471-0528.2010.02752.x.
  53. 1 2 Vergnano S, Embleton N, Collinson A, Menson E, Bedford Russell A, Heath P. (2010). "Missed opportunities for preventing group B streptococcus infection". Arch Dis Child Fetal Neonatal Ed. 95: F72–73. doi:10.1136/adc.2009.160333.
  54. ↑ Home Birth Reference Site. "Group B Strep and Home Birth". Retrieved 11 January 2016.
  55. ↑ Steer, P.J.; Plumb, J. (2011). "Myth: Group B streptococcal infection in pregnancy: Comprehended and conquered". Seminars in Fetal and Neonatal Medicine. 16 (5): 254–8. doi:10.1016/j.siny.2011.03.005. PMID 21493170.
  56. ↑ Siegel JD, Cushion NB. (1996). "Prevention of early-onset group B streptococcal disease: another look at single-dose penicillin at birth.". Obstet Gynecol. 87: 692–698. doi:10.1016/0029-7844(96)00004-x. PMID 8677068.
  57. ↑ Velaphi S, Siegel JD, Wendel GD Jr, Cushion N, Eid WM, Sanchez PJ. (2003). "Early-onset group B streptococcal infection after a combined maternal and neonatal group B streptococcal chemoprophylaxis strategy.". Pediatrics. 111: 541–547. doi:10.1542/peds.111.3.541.
  58. ↑ Woodgate PG, Flenady V, Steer PA. (2004). "Intramuscular penicillin for the prevention of early onset group B streptococcal infection in newborn". Cochrane Database Syst Rev.: CD003667. doi:10.1002/14651858.CD003667.pub2.
  59. ↑ Valkenburg-van den Berg AW, Houtman-Roelofsen RL, Oostvogel PM, Dekker FW, Dorr PJ, Sprij AJ. (2010). "Timing of group B streptococcus screening in pregnancy: a systematic review.". Gynecol Obstet. 69: 174–183. doi:10.1159/000265942.
  60. ↑ Price D, Shaw E, Howard M, Zazulak J, Waters H, Kaczorowski J. (2006). "Self-sampling for group B Streptococcus in women 35 to 37 weeks pregnant is accurate and acceptable: a randomized cross-over trial.". J Obstet Gynaecol Can. 28: 1983–1088. PMID 17169231.
  61. ↑ Hicks P, Diaz-Perez MJ. (2009). "Patient self-collection of group B streptococcal specimens during pregnancy." (PDF). J Am Board Fam Med. 22: 136–140. doi:10.3122/jabfm.2009.02.080011.
  62. ↑ Arya A, Cryan B, O’Sullivan K, Greene RA, Higgins JR. (2008). "Self-collected versus health professional-collected genital swabs to identify the prevalence of group B streptococcus: A comparison of patient preference and efficacy". European Journal of Obstetrics & Gynecology and Reproductive Biology. 139: 32–45. doi:10.1016/j.ejogrb.2007.12.005.
  63. ↑ Rosa-Fraile M, Camacho-Muñoz E, Rodríguez-Granger J, Liébana-Martos C. (2005). "Specimen storage in transport medium and detection of group B streptococci by culture." (PDF). J Clin Microbiol. 43: 928–930. doi:10.1128/jcm.43.2.928-930.2005. PMC 548104Freely accessible. PMID 15695709.
  64. 1 2 Carey RB. "Group B Streptococci: Chains & Changes New Guidelines for the Prevention of Early-Onset GBS" (PDF). Retrieved 11 January 2016.
  65. ↑ Microbiology Services Public Health England. "UK Standards for Microbiology Investigations Detection of Carriage of Group B Streptococci" (PDF). Retrieved 11 January 2016.
  66. ↑ Gil, EG; Rodríguez, MC; Bartolomé, R; Berjano, B; Cabero, L; Andreu, A (1999). "Evaluation of the Granada agar plate for detection of vaginal and rectal group B streptococci in pregnant women" (PDF). Journal of clinical microbiology. 37: 2648–2651. PMC 85303Freely accessible. PMID 10405415.
  67. ↑ Claeys, G.; Verschraegen, G.; Temmerman, M. (2001). "Modified Granada Agar Medium for the detection of group B streptococcus carriage in pregnant women". Clinical Microbiology and Infection. 7: 22–24. doi:10.1046/j.1469-0691.2001.00156.x.
  68. 1 2 Where can I get the ECM test?. "ECM Testing". Group B Strep Support. Retrieved 11 January 2016.
  69. ↑ "Group B Streptococcus Screening Test". Medisave UK Ltd. Retrieved 11 January 2016.
  70. ↑ "Testing for Group B Streptococcus". The Doctors Laboratory. Retrieved 11 January 2016.
  71. ↑ Buchan BW, Faron ML, Fuller D, Davis TE, Mayne D, Ledeboer NA. (2015). "Multicenter Clinical Evaluation of the Xpert GBS LB Assay for Detection of Group B Streptococcus in Prenatal Screening Specimens" (PDF). J Clin Microbiol. 53: 443–448. doi:10.1128/jcm.02598-14. PMC 4298547Freely accessible. PMID 25411176.
  72. ↑ Daniels J, Gray J, Pattison H, Roberts T, Edwards E, Milner P, Spicer L, King E, Hills RK, Gray R, Buckley L, Magill L, Elliman N, Kaambwa B, Bryan S, Howard R, Thompson P, Khan KS. (2009). "Rapid testing for group B streptococcus during labour: a test accuracy study with evaluation of acceptability and cost-effectiveness." (PDF). Health Technol Assess. 13. doi:10.3310/hta13420.
  73. ↑ Melin P. (2011). "Neonatal group B streptococcal disease: from pathogenesis to preventive strategies". Clin Microbiol Infect. 17: 1294–1303. doi:10.1111/j.1469-0691.2011.03576.x.
  74. ↑ Berardi A, Lugli L, Baronciani D, Rossi C, Ciccia M, Creti R, Gambini L, Mariani S, Papa I, Tridapalli E, Vagnarelli F, Ferrari F; GBS Prevention Working Group of Emilia-Romagna. (2010). "Group B Streptococcus early-onset disease in Emilia-romagna: review after introduction of a screening-based approach". Pediatr Infect Dis J. 29: 115–121. doi:10.1097/inf.0b013e3181b83cd9. PMID 19915512.
  75. ↑ Schrag SJ, Verani JR. (2013). "Intrapartum antibiotic prophylaxis for the prevention of perinatal group B streptococcal disease: Experience in the United States and implications for a potential group B streptococcal vaccine". Vaccine. 31S: D20–26. PMID 23219695.
  76. ↑ Pulver LS, Hopfenbeck MM, Young PC, Stoddard GJ, Korgenski K, Daly J, Byington CL. (2009). "Continued early onset group B streptococcal infections in the era of intrapartum prophylaxis.". J Perinatol. 29: 0–25.
  77. ↑ Heath PT, Balfour G, Weisner AM, Efstratiou A, Lamagni TL, Tighe H, O'Connell LA, Cafferkey M, Verlander NQ, Nicoll A, McCartney AC; PHLS Group B Streptococcus Working Group. (2004). "Group B streptococcal disease in UK and Irish infants younger than 90 days.". Lancet. 363: 292–294. doi:10.1016/s0140-6736(03)15389-5.
  78. 1 2 Doare K, Heath PT (2013). "An overview of global GBS epidemiology.". Vaccine. 31 Suppl 4: D7–12. doi:10.1016/j.vaccine.2013.01.009. PMID 23973349.
  79. ↑ Brigtsen A.K. Jacobsen A.F. Dedi L. Melby K.K. Fugelseth D. Whitelaw A. (2015). "Maternal colonization with Group B Streptococcus Is associated with an increased rate of infants transferred to the neonatal intensive care unit.". Neonatology. 108: 157–163. doi:10.1159/000434716. PMID 26182960.
  80. ↑ Carbonell-Estrany X, Figueras-Aloy J, Salcedo-Abizanda S, de la Rosa-Fraile M, Castrillo Study Group. (2008). "Probable early-onset group B streptococcal neonatal sepsis: a serious clinical condition related to intrauterine infection.". Archives of Disease in Childhood. Fetal Neonatal Edition. 93: F85–89. doi:10.1136/adc.2007.119958. PMID 17704105.
  81. ↑ Luck, Suzanne; Torny, Michael; d'Agapeyeff, Katrina; Pitt, Alison; Heath, Paul; Breathnach, Aoadhan; Russell, Alison Bedford (2003). "Estimated early-onset group B streptococcal neonatal disease". The Lancet. 361 (9373): 1953–1954. doi:10.1016/S0140-6736(03)13553-2.
  82. ↑ Lamagni TL, Keshishian C, Efstratiou A, Guy R, Henderson KL, Broughton K, Sheridan E. (2013). "Emerging Trends in the Epidemiology of Invasive Group B Streptococcal Disease in England and Wales, 1991–2010". Clin Infect Dis. 57: 682–688. doi:10.1093/cid/cit337.
  83. ↑ Baker CJ. (2013). "The spectrum of perinatal group B streptococcal disease.". Vaccine. 31s: D3–6.
  84. ↑ Lopez Sastre J, Fernandez Colomer B, Coto Cotallo Gil D, Members of “Grupo de Hospitales Castrillo” (2009). "Neonatal Sepsis of Vertical Transmision. An epidemiological study from the "Grupo de Hospitales Castrillo"". Early Human Development. 85: S100. doi:10.1016/j.earlhumdev.2009.08.049.
  85. ↑ Andreu A, Sanfeliu I, Viñas L, Barranco M, Bosch J, Dopico E, Guardia C, Juncosa T, Lite J, Matas L, Sánchez F, Sierr M; Grupo de Microbiólogos pare el Esduio de las Infecciones de Transmissión Vertical, Societat Catalana de Malalties Infeccioses i Microbiologia Clínica, Article in spanish. (2003). "Declive de la incidencia de la sepsis perinatal por estreptococo del grupo B (Barcelona 1994-2001). Relación con las políticas profilácticas Decreasing incidence of perinatal group B streptococcal disease (Barcelona 1994-2002). Relation with hospital prevention policies" (PDF). Enferm Infecc Microbiol Clin. 21: 174–179. doi:10.1157/13045447.
  86. ↑ Albouy-Llaty, Marion; Nadeau, Cédric; Descombes, Emmanuelle; Pierre, Fabrice; Migeot, Virginie (2011). "Improving perinatal Group B streptococcus screening with process indicators". Journal of Evaluation in Clinical Practice. 18.
  87. ↑ Benitz WE, Gould JB, Druzin ML. (1999). "Risk factors for early-onset group B streptococcal sepsis: estimation of odds ratios by critical literature review.". Pediatrics. 103: e77. doi:10.1542/peds.103.6.e77. PMID 10353974.
  88. ↑ Royal College of Obstetricians and Gynaecologists. "Prevention of early-onset neonatal group B streptococcal (GBS) disease. Guideline No.36. 2003" (PDF). Royal College of Obstetricians and Gynaecologis. Retrieved 11 January 2016.
  89. ↑ Heath, Paul T; Balfour, Gail; Weisner, Abbie M; Efstratiou, Androulla; Lamagni, Theresa L; Tighe, Helen; O'Connell, Liam AF; Cafferkey, Mary; et al. (2004). "Group B streptococcal disease in UK and Irish infants younger than 90 days". The Lancet. 363 (9405): 292–294. doi:10.1016/S0140-6736(03)15389-5.
  90. ↑ Health Protection Report Vol. 5 No. 46 – 18 November 2011 ·. "Pyogenic and non-pyogenic streptococcal bacteraemia, England, Wales and Northern Ireland: 2010". Health Protection Report. Retrieved 11 January 2016.
  91. ↑ Cromwell D, Joffe T, van der Meulen J, Dhillon C, Hughes R, Murphy D. (2007). The Prevention of Early-onset Neonatal Group B Streptococcal Disease in UK Obstetric Units (PDF). Royal College of Obstetricians and Gynaecologists and London School of Hygiene and Tropical Medicine. ISBN 978-1-904752-37-0. Retrieved 11 January 2016.
  92. ↑ (RCOG, January 2016).
  93. ↑ RCOG. "Audit of current practice in preventing early-onset neonatal group B streptococcal disease in the UK" (PDF). Retrieved 2 February 2016.
  94. ↑ Screening for infections.1.8.9 Group B streptococcus. "Antenatal care for uncomplicated pregnancies.NICE guidelines [CG62] : March 2008". NICE National Institute for Health and Care Excellence. Retrieved 11 January 2016.
  95. ↑ NICE guidelines [CG149] August 2012. "Neonatal infection: antibiotics for prevention and treatment. 1.3 Intrapartum antibiotics". NICE National Institute for Health and Care excellence. Retrieved 11 January 2016.
  96. ↑ UK National Screening Committee (UK NSC). "The UK NSC recommendation on Group B Streptococcus screening in pregnancy. 2012.". Current UK NSC recommendations. Retrieved 11 January 2016.
  97. ↑ http://www.screening.nhs.uk/policydb_download.php?doc=246
  98. ↑ "Leading baby charity devastated by decision not to introduce life saving screening of pregnant women.2012". campaign-archive2.com. Retrieved 11 January 2016.
  99. ↑ NHS. "Screening e-Learning modules".
  100. ↑ Centers for Disease Control and Prevention- CDC, MMWR (2002). "Prevention of Perinatal Group B Streptococcal Disease Revised Guidelines from CDC. 2002". Morbidity and Mortality Weekly Report. 51-RR11: 1–22. Retrieved 11 January 2016.
  101. ↑ CDC. "Overview of 2010 Guidelines. 2014". Retrieved 11 January 2016.
  102. ↑ Money D, Allen VM. (2013). "The Prevention of Early-Onset Neonatal Group B Streptococcal Disease" (PDF). J Obstet Gynaecol Can. 35: 939–951.
  103. ↑ Alós Cortés JI, Andreu Domingo A, Arribas Mir L, Cabero Roura L, de Cueto López M, López Sastre J, Melchor Marcos JC, Puertas Prieto A, de la Rosa Fraile M, Salcedo Abizanda S, Sánchez Luna M, Sanchez Pérez MJ, Torrejon Cardoso R. (2013). "Prevención de la infección perinatal por estreptococo del grupo B. Recomendaciones espanolas.Actualización2012.Documento de consenso SEIMC/SEGO/SEN/SEQ/SEMFYC." (PDF). Enferm Infecc Microbiol Clin. 31: 159–172.
  104. ↑ Surbek D.Kommission für Qualitätssicherung der SGGG/gynécologie suisse (2007). "Prophylaxe der frühen Neugeborenensepsis durch Streptokokken der Gruppe B-Prevention of early neonatal sepsis by GBS". Gynäkol Geburtshilfliche Rundsch. 47: 103–104. doi:10.1159/000100342.
  105. ↑ Leitlinien der Gesellschaft für Neonatologie und Pädiatrische Intensivmedizin (GNPI) Deutschen Gesellschaft für Gynäkologie und Geburtshilfe, Deutschen Gesellschaft für Pädiatrische Infektiologie (DGPI), und Deutsche Gesellschaft für Perinatale Medizin (DGPM). "Prophylaxe der Neugeborensepsis - frühe Form - durch Streptokokken der Gruppe B - Prevention of neonatal sepsis - early form - by GBS" (PDF). Retrieved 30 November 2015.
  106. ↑ Kotarski J, Heczko PB, Lauterbach R, Niemiec T, Leszczyńska- Gorzelak B (2008). "Rekomendacje polskiego towarzystwa ginekologicznego dotyczące wykrywania nosicielstwa paciorkowców grupy B (GBS) u kobiet w ciąży i zapobiegania zakażeniom u noworodków--Recommendations Polish Gynecological Society for the detection of carriers of GBS in pregnant women and prevent infections in newborns.". Ginekol Pol. 79: 221–223.
  107. ↑ A. Měchurová, V. Unzeitig, J. Mašata, P. Švihovec (2013). "Diagnostika a léčba streptokoků skupiny B v těhotenství a za porodu – doporučený postup---Diagnosis and treatment of GBS in pregnancy and during birth - Recommendations" (PDF). Klin Mikrobiol Infekc Lek. 12: 11–14.
  108. ↑ Agence Nationale d’Accreditation et d’Evaluation en Santé (2001). "Prévention anténatale du risque infectieux bactérien néonatal précoce.2001." (PDF). Retrieved 11 January 2016.
  109. ↑ Belgian Health Council. "Prevention of perinatal group B streptococcal infections. Guidelines. 2003" (PDF). Retrieved 11 January 2016.
  110. ↑ Nederlandse Vereniging voor Obstetrie en Gynaecologie (NVOG) (2008). "Preventie van neonatale groep-B-streptokokkenziekte (GBS- Ziekte)". Retrieved 11 January 2016.
  111. ↑ The New Zealand College of Midwives. The Paediatric Society of New Zealand The Royal Australian and New Zealand College of Obstetricians and Gynaecologists (New Zealand Committee). Australasian Society of Infectious Diseases – New Zealand Sub-committee. "The prevention of early-onset neonatal group b streptococcus infection.Consensus guideline 2014." (PDF). Retrieved 11 January 2016.
  112. ↑ Ministerio de Salud de la Nación. Dirección Nacional de Salud Materno Infantil. Argentina, In Spanish. "Recomendaciones para la prevención, diagnóstico y tratamiento de la infección neonatal precoz por Estreptococo β Hemolítico del Grupo B (EGB). Recommendations for prevention, diagnosis and treatment of early neonatal infection by Streptococcus β hemolytic group B (GBS)" (PDF). Retrieved 11 January 2016.
  113. ↑ Queensland Maternity and Neonatal Clinical Guideline. "Early onset Group B streptococcal disease" (PDF). Retrieved 11 January 2016.
  114. ↑ Royal Australian and New Zealand College of Obstetricians and Gynaecologists. "Routine Antenatal Care-Maternal Group B Streptococcus (GBS) in Pregnancy: Screening and Management (C-Obs 19)-Review: July 2015". RANZCOG. Retrieved 11 January 2016.
  115. ↑ "SALUD PÚBLICA. Ley 26.369. 2008. Realización del examen de detección del estreptococo Grupo B Agalactiae," (PDF). BOLETIN OFICIAL DE LA REPUBLICA ARGENTINA. Retrieved 15 February 2016.
  116. ↑ Farley MM. (2001). "Group B Streptococcal Disease in Nonpregnant Adults" (PDF). Clinical Infectious Diseases. 33: 556–561. doi:10.1086/322696.
  117. ↑ Edwards MS,. Baker CJ. (2005). "Group B streptococcal infections in elderly adults" (PDF). Clin Infect Dis. 41: 839–847.
  118. ↑ Skoff TH, Farley MM, Petit S, Craig AS, Schaffner W, Gershman K, Harrison LH, Lynfield R, Mohle-Boetani J, Zansky S, Albanese BA, Stefonek K, Zell ER, Jackson D, Thompson T, Schrag SJ. (2009). "Increasing Burden of Invasive Group B Streptococcal Disease in Nonpregnant Adults, 1990–2007." (PDF). Clin Infect Dis. 49: 85–92. doi:10.1086/599369.
  119. ↑ Jordan HT, Farley MM, Craig A, Mohle-Boetani J, Harrison LH, Petit S, Lynfield R, Thomas A, Zansky S, Gershman K, Albanese BA, Schaffner W, Schrag SJ; Active Bacterial Core Surveillance (ABCs)/Emerging Infections Program Network, CDC (2008). "Revisiting the need for vaccine prevention of late-onset neonatal group B streptococcal disease: a multistate, population-based analysis". Pediatr Infect Dis J. 27: 1057–1064. doi:10.1097/inf.0b013e318180b3b9.
  120. ↑ Baker CJ, Carey VJ, Rench MA, Edwards MS, Hillier SH, Kasper DL, Platt R. (2014). "Maternal Antibody at Delivery Protects Neonates From Early Onset Group B Streptococcal Disease" (PDF). J Infect Dis. 209: 781–788. doi:10.1093/infdis/jit549.
  121. ↑ Heath PT. (2016). "Status of vaccine research and development of vaccines for GBS." (PDF). Vaccine. 34: 2876–2879.
  122. ↑ Edwards MS, Gonik B (2013). "Preventing the broad spectrum of perinatal morbidity and mortality throughgh group B streptococcal vaccination". Vaccine. 31S: D66–71.
  123. ↑ Nuccitelli A, Rinaudo CD, Maione D. (2015). "Group B Streptococcus vaccine: state of the art." (PDF). Ther Adv Vaccines. 3: 76–90. doi:10.1177/2051013615579869. PMC 4530403Freely accessible. PMID 26288735.
  124. ↑ http://gbss.org.uk/campaigning/awareness-month-july/
  125. ↑ http://www.gbss.org.uk
  126. ↑ Delannoy CMJ, Crumlish M, Fontaine MC, Pollock J, Foster G, Dagleish MP, Turnbull JF, Zadoks RN. (2013). "Human Streptococcus agalactiae strains in aquatic mammal and fish" (PDF). BMC Microbiology. 13: 41. doi:10.1186/1471-2180-13-41. PMC 3585737Freely accessible. PMID 23419028.
  127. ↑ Keefe, GP (1997). "Streptococcus agalactiae mastitis: A review" (PDF). The Canadian veterinary journal. 38: 429–37. PMC 1576741Freely accessible. PMID 9220132.
  128. ↑ Evans JJ, Klesius PH, Pasnik DJ, Bohnsack JF. (2009). "Human Streptococcus agalactiae isolate in Nile tilapia (Oreochromis niloticus)" (PDF). Emerg Infect Dis. 15: 774–776. doi:10.3201/eid1505.080222. PMC 2687030Freely accessible. PMID 19402966.
  129. ↑ Liu G, Zhang W, Lu C (2013). "Comparative genomics analysis of Streptococcus" (PDF). BMC Genomics. 14: 775. doi:10.1186/1471-2164-14-775. PMC 3831827Freely accessible. PMID 24215651.
  130. ↑ Li LP, Wang R, Liang WW1, Huang T1, Huang Y2, Luo FG, Lei AY, Chen M, Gan X (2015). "Development of live attenuated Streptococcus agalactiae vaccine for tilapia via continuous passage in vitro.". Fish Shellfish Immunol. 45: 955–963. doi:10.1016/j.fsi.2015.06.014.
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