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• W12299610 abstract "Despite recommendations for universal screening and intrapartum antibiotic prophylaxis strategies for pregnant women, group B Streptococcus remains a major cause of neonatal disease.After completing this article, readers should be able to:Streptococcus agalactiae, or group B Streptococcus (GBS), was first recognized as a distinct entity in the 1930s by Rebecca Lancefield, who used immunologic typing of carbohydrate antigens as a means to classify streptococci. (1) Early studies by her group and others indicated that GBS was an uncommon cause of human disease and was more frequently isolated as an etiologic agent of bovine mastitis. Sporadic case reports from that time demonstrated the potential for GBS to cause invasive infections, especially in peripartum women, although such infections were believed to be infrequent. However, over the period of the 1950s to the early 1970s, GBS became the major cause of neonatal sepsis in the United States and worldwide.GBS asymptomatically colonizes the lower gastrointestinal and female genital tracts. Colonization rates exceed 20% in some populations. (2) Asymptomatic colonization may be transient or long-lived, and person-to-person transmission likely occurs from a colonized individual through close contact (sexual and fecal-oral transmission have both been hypothesized as mechanisms of spread).GBS has numerous features that facilitate evasion of the host immune system and, thus, promote colonization and/or invasive disease. As is the case for many pathogenic streptococci, GBS produces a polysaccharide capsule that likely inhibits opsonophagocytosis and dampens immune responses. The capsule is the major target of host antibody responses, but the presence of 10 known GBS capsular types (Ia, Ib, II-IX) makes the development of widely cross-protective responses (either through natural infection or vaccination) challenging. Certain GBS serotypes, especially types Ia, Ib, II, III, and V, cause the majority of neonatal disease. (3)(4) Direct targeting of human cells by GBS β-hemolysin/cytolysin, inhibition of oxidative killing by the GBS pigment, inactivation of complement components, and engagement of inhibitory immune receptors all contribute to the multipronged manipulation of human immunity by GBS. (5) Recent studies have also demonstrated the remarkable plasticity of the GBS genome, with transfer of large stretches of DNA driving GBS diversification over relatively short time periods. For example, the emergence of the sequence type-17 type III “hypervirulent” strain, which produces a distinct adhesin (HvgA) that facilitates binding and traversal of the gastrointestinal epithelial barrier, is believed to have contributed substantially to the rise of GBS as a cause of neonatal infection. (3)(6) Such transitions from asymptomatic colonization to invasive disease are important factors in the pathogenesis of human GBS infections, but a detailed understanding of such events has remained elusive.Most studies of GBS colonization and invasive disease originate from high-income countries such as the United States. More recently, data have become available from a broader sampling of populations, demonstrating a substantial burden of disease worldwide. (7) However, substantial gaps remain in our understanding of global GBS epidemiology. Expanding studies of GBS epidemiology to areas with limited data will be crucial to the development of prevention efforts that can extend across many nations (see the section on Prevention).Despite substantial variability among reports, several risk factors for GBS colonization in pregnancy have held up across multiple studies, including obesity, African American race, and known GBS colonization during a prior pregnancy. Among infants born to GBS-positive mothers, certain factors are associated with the risk of developing invasive GBS disease. Specific factors are discussed in subsequent sections of this article.Maternal gastrointestinal and/or genitourinary colonization represents the primary risk factor for neonatal GBS disease. Colonization is common but varies geographically, and reported prevalence rates may be influenced substantially by detection methods. Approximately 10% to 30% of pregnant women are colonized with GBS. Population-based colonization rates have remained stable over decades, and no effective interventions to eliminate GBS colonization are known. Before the institution of intrapartum antibiotic prophylaxis (IAP) guidelines (described in the section on Prevention), infants born to GBS-colonized mothers had an ∼50% rate of surface and/or gastrointestinal colonization, and 2% of those colonized infants would progress to early-onset (EO) invasive disease (age <7 days) that included pneumonia, bacteremia, and meningitis. Late-onset (LO) GBS (age ≥7 days) occurs less frequently and is believed to be associated with gastrointestinal colonization originating from either perinatal or postnatal exposure. Infants born to mothers with GBS bacteriuria during pregnancy are at higher risk for colonization as well as EO disease.Before widespread use of IAP, EO-GBS disease occurred in more than 1.5 per 1,000 live births in the United States and LO-GBS in ∼0.4 per 1,000. Overall EO-GBS rates have decreased significantly following widespread adoption of IAP (Fig 1). However, the burden of EO-GBS remains substantial and disproportionately affects preterm and African American infants. In addition, GBS is an emerging pathogen in non-neonatal groups, including peripartum women, elderly adults, and those with diabetes.Most EO-GBS disease occurs within the first 24 hours of birth, although the definition of EO-GBS includes disease with onset within the first postnatal week. GBS may ascend from the vaginal mucosa to the uterus during antepartum or intrapartum periods. This typically occurs following rupture of the amniotic membranes. However, GBS also appears to be capable of traversing intact membranes. Once in the amniotic fluid, GBS replicates and may be aspirated into the fetal lungs, causing invasive disease in utero. Alternatively, exposure to GBS may occur during parturition via direct contact between the infant and the vaginal mucosal surface.In the vast majority of cases, EO-GBS manifests as sepsis without a focus (83%). (8) Pneumonia (9%) and meningitis (7%) are less common. Several maternal risk factors have been associated with the development of EO-GBS in their offspring. These include GBS rectovaginal colonization, young maternal age, history of a prior infant with invasive GBS disease, intrapartum fever, intraamniotic infection, prolonged membrane rupture, low serum concentrations of anticapsular antibody, and human immunodeficiency virus (HIV) exposure.LO-GBS occurs after the first postnatal week. Multisite active surveillance in the United States indicates that LO-GBS currently occurs in 0.28 in 1,000 live births, surpassing EO-GBS as the most common presentation of invasive GBS disease during infancy. Risk factors for LO infection include maternal rectovaginal colonization, African American race, and prematurity. (9) In contrast to EO-GBS infection, there are currently no effective strategies to reduce the incidence of LO-GBS disease or to target specific at-risk populations.LO-GBS typically manifests as bacteremia without focal infection (65%), bone/soft-tissue infections (including osteomyelitis and septic arthritis), or meningitis (27%). (8) LO-GBS meningitis may lead to vascular complications, including arterial ischemic stroke and venous thrombosis, which may contribute to severe neurologic outcomes.Routes of transmission in LO-GBS infection are not well understood. Maternal rectovaginal colonization appears to be a major source; 50% of infants who develop LO disease are colonized around the time of birth by GBS that is the same serotype as that carried by their mothers. (10) Peripartum exposure may lead to surface or gastrointestinal colonization of the neonate, which progresses to LO-GBS disease through unknown mechanisms (translocation from intestinal sources to the bloodstream has been hypothesized as one potential means for GBS to access sterile sites). Some reports of GBS transmission via contaminated human milk (11) or environmental sources (12) (including health-care workers or caretakers) indicate that postnatal transmission may represent the source of infection in at least some cases of LO-GBS. A large prospective cohort study conducted in Italy revealed that most mothers (64%) were rectovaginally colonized with GBS at the time their infants were diagnosed with LO-GBS, and 6% had GBS mastitis. (13) Notably in that study, IAP was associated both with delayed presentation of symptoms and milder LO-GBS disease. Regardless of transmission route, the establishment of GBS intestinal colonization appears to be a critical precursor for invasive disease in the newborn.The development of invasive GBS disease in infants older than 3 months is often referred to as late, late-onset GBS (or very late-onset GBS). This typically presents as bacteremia without a focus, but central nervous system and soft-tissue/bone involvement may also occur. Based on retrospective case series, infants with late, late-onset GBS appear to have lower gestational ages and longer initial hospitalizations than infants with LO-GBS. An atypically late presentation has also been described in individuals with underlying immunodeficiencies such as HIV infection and interleukin-1 receptor-associated kinase-4 deficiency, (14) indicating that immune dysfunction may contribute to disease presentation beyond the typical interval observed for term infants.The risk of invasive GBS infection in the twin of an affected infant has been reported to be as high as 40%. This observation may be the result of concordant exposures and, potentially, shared genetic predispositions. Twins born to GBS-colonized mothers may be exposed to GBS perinatally, either in utero or during vaginal delivery. They may share inherent risk factors for invasive GBS disease, such as prematurity, low concentrations of circulating anti-GBS antibody, hereditary immunodeficiencies, or other genetic factors. (15) During infancy, twins are similarly exposed to other exogenous sources of GBS, including maternal, hospital, and household contacts. (16) A report describing synchronous LO-GBS recurrence in twins highlights the potential for transmission via infected human milk. (17) The simultaneous appearance of clinical symptoms in this particular case suggests a short incubation period after a shared enteral exposure rather than bacterial translocation in chronically colonized infants.Because of the high concordance rate for GBS sepsis in twins, careful observation and early empiric therapy if signs of illness develop are indicated for the birth mates of affected cases. (18)Most non-neonatal GBS disease in the United States occurs among nonpregnant adults. In this population, potentially immunocompromising conditions, including malignancy, diabetes, HIV, and age older than 65 years, raise a particular risk. Such patients most often present with bacteremia without a focus, although cellulitis, pneumonia, and bone/joint infections also occur. Mortality from GBS invasive disease exceeds 10% in elderly individuals. (19) Postpartum women have a more than 20-fold increased risk of invasive GBS infections compared to nonpregnant women. (20)Among infants, recurrence of GBS infection following treatment is rare (approximately 1% of cases), and the relevant mechanisms have not been delineated. Some infant cases have been attributed to human milk transmission because the mother’s milk has been found to harbor GBS, although such a link has not been definitively proven. Most commonly, recurrent infections are caused by the same GBS strain as the initial infection. Nonpregnant adults are also at risk for recurrent GBS invasive disease, particularly those who are immunocompromised. As with infants, the recurrent infection is typically caused by the same strain as the initial infection and can occur up to several months later.GBS colonization has traditionally been detected by culture of vaginorectal swabs obtained in late pregnancy (35-37 weeks’ gestation). Assessment of colonization within 5 weeks of delivery provides negative predictive values that exceed 95%. Inclusion of both vaginal and rectal sampling enhances detection of GBS and helps ensure appropriate delivery of IAP to infants born to colonized mothers. To optimize detection by culture, Centers for Disease Control and Prevention (CDC) guidelines (21) recommend use of a selective enrichment broth rather than direct agar plating of specimens. After growth in enrichment media, GBS may be subcultured to blood agar and presumptively identified using latex agglutination test or detection of the Christie, Atkins, Munch-Petersen (CAMP) factor. Rapid polymerase chain reaction (PCR) assays that allow for direct GBS identification are now available in many laboratories and are replacing traditional culture-based techniques.Detection of GBS in the setting of invasive disease generally requires culture of the organism from a normally sterile site (most often blood or cerebrospinal fluid [CSF]). Latex particle agglutination tests are rarely used due to suboptimal sensitivity. More recently, PCR-based testing of both blood and CSF for large panels of pathogens, including GBS, has become widely available and may lead to faster detection of invasive GBS disease.GBS is generally susceptible to penicillin G, ampicillin, first- and second-generation cephalosporins, and vancomycin. Whenever neonatal invasive GBS disease is suspected, empiric therapy should include ampicillin. Once GBS is confirmed, penicillin G is the preferred agent, although ampicillin remains an acceptable alternative. Gentamicin provides synergy and should be used during initial days of therapy and continued until repeat blood and/or CSF cultures are sterile.Uncomplicated GBS bacteremia and pneumonia require at least a 10-day course of intravenous antimicrobial therapy. For uncomplicated GBS meningitis, a 14-day course is generally adequate. Complicated cases of GBS meningitis (including the presence of seizures, ventriculitis, or intracranial abscess) should be treated for at least 21 days, although longer courses may be required. Repeat CSF analyses may be useful in guiding therapy for GBS meningitis. (18) GBS septic arthritis or osteomyelitis requires therapy for at least 21 to 28 days.As noted previously, penicillin and ampicillin are the drugs of choice for GBS prophylaxis and treatment. GBS remains universally sensitive to penicillin, although there have been reports of strains with elevated penicillin minimum inhibitory concentrations. In contrast, resistance to second-line drugs (including erythromycin and clindamycin) has increased substantially over time, limiting the utility of these agents in prophylaxis. CDC surveillance data have demonstrated rates of erythromycin resistance in GBS greater than 50%, and clindamycin resistance is present in ∼20% of isolates. (21) Alarmingly, 2 cases of vancomycin-resistant GBS infections in adults have recently been reported. (22)The overall case fatality rate (CFR) of EO-GBS is ∼5%. (21) LO-GBS has a CFR of 2% to 7%. (7) CFR for both EO- and LO-GBS is substantially higher among preterm infants.Considerable morbidity can be associated with GBS infections, especially those involving the central nervous system. Approximately 25% of infants with GBS meningitis die or have neurologic abnormalities detected at hospital discharge. (23) Long-term follow-up demonstrates that ∼25% have mild-to-moderate impairment and ∼20% have severe impairment. (24)During the 1980s, clinical studies revealed that administration of antibiotics to GBS-colonized women during labor could reduce vertical transmission to their newborns and subsequent EO sepsis. In 1996, the CDC issued the first guidelines recommending IAP. Candidates for prophylaxis were identified using either a risk-based approach or by performing rectovaginal screening culture for GBS during the third trimester. By 2002, the superiority of a universal culture-based screening method was recognized and endorsed for all pregnant women. The most recent guidelines for prevention were published in 2010 (21) and are summarized below.Routine screening of pregnant women occurs at 35 to 37 weeks’ gestation to detect vaginal and/or rectal carriage of GBS. Some women, including those who have had a prior infant with invasive GBS or those in whom GBS was isolated from the urine during pregnancy, do not require screening and should receive IAP.All women with positive GBS screening results should receive IAP during labor. If screening results are not available, IAP is indicated for women with prolonged (≥18 hours) membrane rupture, preterm (<37 weeks) gestation, or fever (temperature ≥100.4°F [38.0°C]). Treatment is not required for women undergoing cesarean delivery, if delivery is performed before the onset of labor with intact amniotic membranes. If labor or membrane rupture occurs before the planned cesarean delivery, GBS-colonized women should receive IAP.Penicillin is the drug of choice for IAP, although ampicillin is acceptable. Women who are allergic to penicillin but have no history of anaphylaxis or angioedema to penicillin or cephalosporin should receive cefazolin. Penicillin-allergic women at high risk for anaphylaxis should receive clindamycin only if their GBS isolate has been tested and demonstrated to lack intrinsic or inducible resistance to clindamycin. If the isolate is resistant to clindamycin or if susceptibility testing was not performed, such penicillin-allergic patients at high risk for anaphylaxis should receive vancomycin. IAP is most effective and may be considered “adequate” if administered at least 4 hours before delivery. Pharmacokinetic studies demonstrate that peak umbilical cord serum concentrations of penicillin are reached within 60 minutes of administration of maternal loading dose. Notably, the efficacy of clindamycin and vancomycin in prevention of neonatal EO-GBS has not been demonstrated definitively, and these agents do not constitute “adequate” IAP by CDC guideline definitions.Although the widespread implementation of universal maternal screening and IAP of GBS-colonized mothers has been an overwhelming public health success, there continue to be missed opportunities for prevention. A prospective observational study of nearly 400,000 infants from 2006 through 2009 highlights several of the limitations of the current “screen and treat” strategy to prevent EO-GBS. (25) Fifty-eight percent of the mothers whose infants developed EO-GBS were appropriately screened, and only 76% of mothers with a positive GBS screen received IAP. Of the women who had prenatal screening, the culture was negative for mothers of more than 80% of term and more than 25% of preterm infants with EO disease, reflecting false-negative screening or maternal acquisition of GBS colonization between screening and delivery.Any newborn who exhibits clinical signs of sepsis requires a diagnostic evaluation and intravenous antibiotic therapy. This is true for infants born to GBS-positive mothers, regardless of whether the mother received adequate IAP. Well-appearing infants, regardless of gestational age, whose mothers received adequate IAP may be observed for 48 or more hours without routine laboratory testing.The term (≥37 weeks’ gestation) well-appearing infant born to a mother who had an indication for IAP but received no or inadequate prophylaxis requires observation for 48 or more hours if the duration of membrane rupture is less than 18 hours, but routine diagnostic testing is not recommended. A well-appearing infant of less than 37 weeks gestational age or with membrane rupture of 18 or more hours should receive a limited laboratory evaluation (blood culture at birth and complete blood cell count with differential count at birth and/or at 6 to 12 hours following birth) and observation for 48 hours or more.The American Academy of Pediatrics Committee on Fetus and Newborn has proposed the following modifications to the previous CDC guidelines regarding the approach to management of infants born to mothers with inadequate GBS prophylaxis (Fig 2) (26):Initial concerns that widespread implementation of IAP would be accompanied by an increase in non-GBS EO sepsis have not been borne out. Large epidemiologic studies have thus far been reassuring. However, in specific at-risk populations (extremely low birthweight infants, preterm infants), some studies suggest that the incidence of Escherichia coli sepsis may be increasing. (27) The relationship of this secular trend to IAP remains unclear.More recently, several small studies have described perturbations in the gastrointestinal microbiota (“microbiome”) of infants born to mothers who have received IAP, but both longitudinal and outcome data are lacking. Thus, the long-term consequences of such alterations remain unclear. In considering the relevance of such changes in the microbiota, it is important not to lose sight of the substantial known benefits of IAP (decreased risk of invasive EO-GBS disease). Long-term studies of the clinical relevance of the neonatal gastrointestinal microbiota and the effect of IAP are needed to address such questions.Even if implementation were optimal, the approach of universal screening and targeted IAP has inherent limitations. Due to the timing of screening (35-37 weeks’ gestation) and the transient nature of GBS colonization, even perfect laboratory techniques cannot identify all infants at risk. Precipitous deliveries are also problematic with this approach because they do not allow adequate time to administer 4 or more hours of IAP before delivery. Recent clinical validation of rapid identification of GBS carriage by PCR could ameliorate some of these issues by allowing identification of colonized women at the time of presentation.Emergence of antibiotic resistance among GBS or other bacterial pathogens remains a concern with any prevention strategy that relies on IAP. Growing resistance of GBS to erythromycin and clindamycin has already led to changes in recommendations for IAP for women allergic to penicillin, and the eventual development of resistance to β-lactams remains a possibility. Furthermore, exposing mothers and infants to antibiotics has sparked concern about the potential effects this could have on the maternal and neonatal microbiota.Prevention of GBS disease by vaccination has been the subject of investigation for several decades. (28) A correlation between maternal serum anticapsular antibody titers and neonatal protection against EO-GBS has been established, providing a basis for the investigation of capsule-based vaccines. Ideally, such vaccines would lead to production of high titers of capsule-specific immunoglobulin G that would then cross the placenta, providing passive immunity for the fetus. Early studies of purified GBS capsular polysaccharide vaccines demonstrated safety but suboptimal immunogenicity in pregnant women. Protein-polysaccharide conjugate vaccines have demonstrated considerable promise, and multivalent GBS capsular polysaccharide-protein conjugate vaccines are currently in human trials. A vaccine targeting GBS serotypes Ia, Ib, II, III, and V would be estimated to protect against more than 85% of infant disease globally. However, the emergence of several GBS types (including type IV, which has increased in prevalence considerably in recent years) as well as the possibility of serotype replacement may limit the overall impact of conjugate vaccines based on a limited number of serotypes. Nonetheless, GBS vaccination remains an important goal that could eventually obviate the need for universal screening and IAP strategies." @default.
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• W12299610 title "Group B Streptococcal Infections" @default.
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