Invasive Group B Streptococcus Infection Research Articles

Group B Streptococcus Early-Onset Disease in Emilia-Romagna: Review After Introduction of a Screening-Based Approach

Group B Streptococcus (GBS) is a leading cause of neonatal bacterial infections. Early-onset infections have decreased in recent years but, despite considerable efforts poured into prevention, cases continue to occur. To analyze trends and identify determining factors for the persistence of the GBS infections. To evaluate the impact of antenatal screening and intrapartum chemoprophylaxis on the clinical presentation of the infection. A prospective cohort, population-based study has been ongoing in Emilia-Romagna (Italy) since 2003. Invasive GBS infections, observed between 2003 and 2008 in infants aged < 7 days were analyzed. Among 214,120 live births, 61 early-infections were observed. Fourteen infants (23.0%) were born preterm. Among 47 infants who were delivered at term, 28 were born to mothers who had no risk factors and 7 were born to mothers who had none other than GBS colonization. Forty-one women at term had been screened prenatally; among them, only 10 were documented as GBS culture-positive.Disease severity was highest in infants at lower gestational ages, but most meningitis cases were observed in term infants born to mothers who were GBS culture-negative at screening.Nine newborns had culture-proven infection despite having received intrapartum antibiotics. They were born to mothers with > or =1 obstetrical risk factors and 5 mothers had been treated during labor with macrolides. Most infections presented in infants whose mothers had been screened as GBS culture-negative. Missed opportunities for prevention contributed more than prophylaxis failures to the early-onset disease burden.

ステロイド療法中の10 歳女児に発症した B 群レンサ球菌による菌血症の1 例

Group B streptococcus (GBS), a major cause of neonate and pediatric sepsis and meningitis, rarely causes invasive infection beyond infancy. We report the case of a 10-year-old girl developing GBS bacteremia during corticosteroid therapy for chronic idiopathic thrombocytopenic purpura. Brought to the emergency room due to sudden high fever and abdominal pain, she was in compensated shock. White blood cell count was 19,600/mm3 and C-reactive protein 0.18 mg/dL. She was diagnosed with sepsis and admitted for evaluation. Cefotaxime (100 mg/kg/day) administration and fluid replacement were begun immediately after blood culture. Her condition improved over the next 6 hours and she was afebrile by the next day. GBS isolated from blood had a serotype of Ib. Based on routine susceptibility testing, this strain was susceptible to penicillin, cephem, carbapenem, erythromycin, clindamycin, and vancomycin, but resistant to quinolone, including levofloxacin (MIC > or = 8.0 microg/mL) and gatifloxacin (MIC > or = 4.0 microg/mL). She was discharged on hospital day 8. This is, to our knowledge, the first report of pediatric meningitis-free GBS bacteremia in Japan. Physicians should therefore be aware of the possibility of invasive GBS infection such as bacteremia in this age group, especially during immunosuppressive therapy, because epidemiological studies in the US have showed significant mortality in those aged 1 to 14 years old with invasive GBS.

Outbreak of late-onset group B Streptococcus in a neonatal intensive care unit

In September 2007, the Tennessee Department of Health was notified of a cluster of late-onset group B streptococcal (GBS) infections in a neonatal intensive care unit (NICU). Outbreaks of late-onset GBS are rare. A case was defined as culture-confirmed invasive GBS infection in a neonate aged > or =7 days, identified in hospital A during August 23 to September 6, 2007. We reviewed medical records; examined NICU microbiology reports; and performed serotyping, pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing (MLST) on invasive isolates. Maternal GBS screening, prophylaxis, and infection control policies were reviewed and staff practices observed. Five cases of late-onset GBS were identified. None of the mothers of the infants received optimal GBS prophylaxis. Patient isolates were of 2 serotypes, 3 PFGE patterns, and 2 MLST patterns. Three isolates were indistinguishable on subtyping. These 3 cases were clustered in time. No common health care providers were identified. Infection control deviations in the NICU were observed. We identified a multiclonal cluster of 5 late-onset GBS cases. Multiple factors likely contributed to the outbreak, including nosocomial transmission of GBS. Further efforts to prevent late-onset GBS disease are necessary.

Clinical aspects of invasive infections with Streptococcus dysgalactiae ssp. equisimilis in Japan: differences with respect to Streptococcus pyogenes and Streptococcus agalactiae infections

Streptococcus dysgalactiae ssp. equisimilis (SDSE) is increasingly being identified as a pathogen responsible for invasive and non-invasive infections. We compared the clinical features of invasive SDSE infections with those of invasive infections caused by Streptococcus pyogenes (group A streptococcus (GAS)) and Streptococcus agalactiae (group B streptococcus (GBS)). Active surveillance for invasive SDSE, GAS and GBS was maintained over 1 year at 142 medical institutions throughout Japan. Clinical information was collected together with isolates, which were characterized microbiologically. Two hundred and thirty-one invasive SDSE infections were identified, 97 other patients had infections with GAS, and 151 had infections with GBS. The median age of the SDSE patients was 75 years; 51% were male and 79% had underlying diseases. Forty-two SDSE patients (19%) presented to the emergency department. Among the 150 patients (65%) for whom follow-up was completed, 19 (13%) died and eight (5%) had post-infective sequelae (poor outcome). Insufficient white blood cell responses (<5000 cells/microL) and thrombocytopenia on admission each suggested significantly higher risk of poor outcome (ORs 3.6 and 4.5, respectively). Of 229 isolates, 55 (24%) showed an stG6792 emm type, which was significantly associated with poor outcome (OR 2.4). Clinical manifestations of invasive SDSE infections were distinct from those of invasive GBS infections. Primary-care doctors should consider invasive SDSE infections when treating elderly patients.

Spot diagnosis: An ominous rash in a newborn

Purpura fulminans (PF) is an ominous cutaneous condition usually associated with meningococcemia. PF in the newborn is rarely reported. We report the case of a female preterm infant with extensive PF due to group B streptococcus (GBS) septicemia. She developed multi-organ system failure despite neonatal intensive care support and succumbed 9 days later. GBS, sensitive to penicillin, was isolated from the blood cultures of the mother and the infant. Invasive early GBS infection is common in the newborn and is empirically treated with prompt institution of intravenous antibiotics. PF associated with GBS is a rare cutaneous sign that must not be missed. Mortality remains high despite aggressive treatment and ICU support.

Alpha C protein-specific immunity in humans with group B streptococcal colonization and invasive disease

Alpha C protein, found in 76% of non-type III strains of group B Streptococcus (GBS), elicits antibodies protective against alpha C-expressing strains in experimental animals, making it an appealing carrier for a GBS conjugate vaccine. We determined whether natural exposure to alpha C elicits antibodies in women. Geometric mean concentrations of alpha C-specific IgM and IgG were similar by ELISA in sera from 58 alpha C GBS strain colonized and 174 age-matched non-colonized women (IgG 245 and 313 ng/ml; IgM 257 and 229 ng/ml, respectively), but acute sera from 13 women with invasive alpha C-expressing GBS infection had significantly higher concentrations (IgM 383 and IgG 476 ng/ml [p=0.036 and 0.038, respectively]). Convalescent sera from 5 of these women 16-49 days later had high alpha C-specific IgM and IgG concentrations (1355 and 4173 ng/ml, respectively). In vitro killing of alpha C-expressing GBS correlated with total alpha C-specific antibody concentration. Invasive disease but not colonization elicits alpha C-specific IgM and IgG in adults.

Real-Time Polymerase Chain Reaction for the Rapid Detection of Group B Streptococcal Colonization in Neonates

Group B streptococcal (GBS) infection remains a leading cause of neonatal sepsis. Currently, the management guidelines of neonates born to women with unknown GBS status at delivery are unclear. In this cohort, who undergo at least a 48-hour observation, a rapid method of detection of GBS colonization would allow targeted evaluation and treatment, as well as prevent delayed discharge. The goal of this research was to evaluate the validity of rapid fluorescent real-time polymerase chain reaction in comparison with standard culture to detect GBS colonization in infants born to women whose GBS status is unknown at delivery. Neonates at >32 weeks' gestation born to women whose GBS status was unknown at delivery were included. Samples were obtained from the ear, nose, rectum, and gastric aspirate for immediate culture and real-time polymerase chain reaction after DNA extraction using the LightCycler. Melting point curves were generated, and confirmatory agar gel electrophoresis was performed. The study population (n = 94) had a mean +/- SD gestational age of 38 +/- 2 weeks and birth weight of 3002 +/- 548 g. The rates of GBS colonization by culture were 17% and 51% by real-time polymerase chain reaction. The 4 surface sites had comparable rates of GBS. The overall sensitivities, specificities, and positive and negative predictive values of real-time polymerase chain reaction were: 90%, 80.3%, 28%, and 98.9%. Real-time polymerase chain reaction resulted in a threefold higher rate of detection of GBS colonization and had an excellent negative predictive value in a cohort of neonates with unknown maternal GBS status at delivery. Thus, real-time polymerase chain reaction would be a useful clinical tool in the management of those infants potentially at risk for invasive GBS infection and would allow earlier discharge for those found to be not at risk.

Group B Streptococcal Infections in Elderly Adults

Elderly adults account for >40% of persons with invasive group B streptococcal (GBS) disease and for >50% of GBS-associated deaths in the United States. The prevalence of colonization among healthy elderly adults (approximately 25%) is similar to that among women of childbearing age. Delineating contributions of comorbid conditions, altered integrity of anatomical barriers, and abnormalities in immune responses caused by immune senescence to pathogenesis require further investigation. Delayed clinical recognition of illness may contribute to poor outcome. Skin and soft-tissue infections and bacteremia with no identified focus are common manifestations of infection in elderly adults and younger nonpregnant adults. Urinary tract infection and pneumonia are presentations more often encountered in elderly persons than in younger adults. The safety and immunogenicity of GBS serotype V-tetanus toxoid conjugate vaccine in healthy elderly persons suggest the potential for vaccination as an approach to prevention of invasive GBS infections in elderly persons.

Invasive group B streptococcal disease in infants: a 19-year nationwide study. Serotype distribution, incidence and recurrent infection

During the period 1984-2002, 472 cases of invasive group B streptococcal (GBS) disease in infants aged 0-90 days in Denmark were registered. The overall incidence was 0.4/1000 live births. Most infants (73%) had early-onset GBS infection with 53% registered within the first day. Serotype III predominated (59%) with other serotypes as follows: Ia (16%), Ib (8%), NT (7%), II (6%), other serotypes (5%). Recurrence of GBS infection was registered in six infants, and the interval with no antibiotic therapy varied from 2 to 39 days. The serotypes of the isolates obtained from first and second episodes were identical (serotype III in five, and serotype Ia in one infant). Paired isolates were indistinguishable by PFGE and antibiotic susceptibility testing. Invasive GBS infections in infants are still a problem in Denmark, and recurrent infections are registered in 1% of these infants.

Group B Streptococcus necrotizing fasciitis: an emerging disease?

Necrotizing fasciitis is perhaps the most severe form of soft tissue infection primarily involving the superficial fascia and subcutaneous tissue. This condition is associated with severe sepsis, a fulminant course and high mortality. While group A Streptococcus (GAS) remains the most common etiologic agent in necrotizing fasciitis due to a single organism [1], we have recently noted an emergence of group B Streptococcus (GBS) or Streptococcus agalactiae as a causative agent. This report describes our recent experience with GBS necrotizing fasciitis seen in Singapore between the years 2000 and 2002. Five patients with monomicrobial necrotizing fasciitis caused by GBS were identified during this time period. All patients were female, with ages ranging from 38 to 66 years. Diabetes mellitus was a frequent association and was noted in four of the patients. Early aggressive surgical debridement is the cornerstone management of necrotizing fasciitis and was performed in all cases. The procedure was repeated until all necrotic and non-viable tissues were excised. Two to three debridements were necessary to achieve this. The group B streptococci isolated from all five patients were susceptible to penicillin, ampicillin and erythromycin. Table 1 summarizes the clinical presentation, antimicrobial therapy and outcome of the five cases. At our hospital, we generally treat patients with severe GBS soft tissue infections with high-dose parenteral penicillin once the organism has been isolated. Highdose intravenous penicillin is the drug of choice since resistance to penicillin is not an issue with GBS. Once the infection has been controlled, the parenteral regimen is replaced by an oral β-lactam agent such as penicillin or amoxicillin. Antimicrobial therapy is continued for 4–6 weeks, until all wounds are covered with split thickness skin grafts. However, in the five cases reported here there were some variations in the antimicrobial therapy administered because of the preferences of individual treating physicians. Some authors have advocated the use of clindamycin in combination with penicillin in cases of GBS necrotizing fasciitis [2, 3], and there is now growing in vitro and in vivo evidence that clindamycin may be the preferred agent for treating streptococcal necrotizing fasciitis. While not used to treat our patients, the combination of clindamycin and penicillin may be superior to penicillin alone and should be considered in the treatment of future cases of invasive GBS infections [2, 3]. Skin and soft tissue infections are the most common manifestations of invasive GBS infection [4, 5]. However, monomicrobial necrotizing fasciitis caused by GBS in non-pregnant adults is extremely rare, with just over ten cases being reported in the English-language medical literature to date [2, 3, 6–9]. The addition of the five cases we observed make clear that GBS is capable of causing necrotizing fasciitis. While the virulence factors that enable GBS to cause necrotizing fasciitis have not yet been established, this emerging clinical entity has been reported increasingly in recent years [2, 3, 6–9]. All five of our cases occurred during a relatively short period of time, between 2000 and 2002. Horizontal transfer of DNA encoding virulence factors (such as M1 or M3 surface proteins) among different strains of GAS have been demonstrated previously [10, 11]. Gardam et al. [2] postulated that a similar process may have occurred between group A and B streptococci, conferring the mutant strain of GBS with increased ability to spread through tissue planes, resulting in rapid tissue necrosis. This theory is supported by a report of the isolation of a 12,000-kD pyrogenic toxin similar to that found in GAS from a GBS strain in a case of toxic shock syndrome caused by this organism [12]. This sharing of C.-H. Wong (*) . K.-C. Tan Department of Plastic Surgery, Singapore General Hospital, Outram Road, Singapore, Singapore, 169608 e-mail: wchinho@hotmail.com Tel.: +65-63214686 Fax: +65-62209340

Alpha C Protein of Group B Streptococcus Binds Host Cell Surface Glycosaminoglycan and Enters Cells by an Actin-dependent Mechanism

Group B Streptococcus (GBS) colonizes mucosal surfaces of the human gastrointestinal and gynecological tracts and causes disease in a wide range of patients. Invasive illness occurs after organisms traverse an epithelial boundary and enter deeper tissues. Previously we have reported that the alpha C protein (ACP) on the surface of GBS mediates GBS entry into ME180 cervical epithelial cells and GBS translocation across layers of these cells. We now demonstrate that ACP interacts with host cell glycosaminoglycan (GAG); the interaction of ACP with ME180 cells is inhibited if cells are pretreated with sodium chlorate, an inhibitor of sulfate incorporation, or with heparitinases. The interaction is also inhibited in the presence of soluble heparin or heparan sulfate or host cell-derived GAG. In addition, ACP binds soluble heparin specifically in inhibition and dot blot assays. After interaction with host GAG, soluble ACP enters ME180 cells and fractionates to the eukaryotic cell cytosol. These events are inhibited in cells pretreated with cytochalasin D or with Clostridium difficile toxin B. These data indicate that full-length ACP interacts with ME180 cell GAG and enters the eukaryotic cell cytosol by a mechanism that involves Rho GTPase-dependent actin rearrangements. We suggest that these molecular interactions drive ACP-mediated translocation of GBS across epithelial barriers, thereby facilitating invasive GBS infection.

Prevalence of group B streptococcal type VI capsular IgG antibodies in Japan.

Multiple studies have highlighted the importance of group B Streptococcus (GBS) as a major pathogen for neonates [1]. GBS is classified into serotypes based on specific capsular polysaccharides (CPSs). Type VI GBS was first isolated in 1977 by Wilkinson [2] at the Centers for Disease Control, Atlanta, Georgia, and was originally designated as NT6. Since the mid 1980s, strains of this new type have frequently been isolated in Japan, and they currently rank second both in the carriage rate among pregnant women [3] and in the incidence of isolation from early-onset neonatal disease [4]. Given the numerous factors predicting invasive neonatal GBS infection, the single most important determinant is deficient maternal IgG antibody directed against the CPS of the GBS [1]. Protective antibody levels, however, may differ among CPS types, ranging from 0.5 to 2 g/ml [1]. In this study, we investigated the distribution of IgG antibodies to serotype VI GBS in healthy Japanese patients defined by colonization status. The subjects were comprised of the same study population previously investigated in seroepidemiologic studies of serotype VIII [5], i.e., 583 pregnant women attending the Department of Obstetrics and Gynecology, Nishi-Kobe Medical Center, between June 1999 and May 2000 and their 461 newborns. Specimens from the distal vagina of pregnant women at 28 weeks’ gestation were cultured on selective Todd-Hewitt medium broth [3]. Sera were collected from pregnant women at 28 weeks’ gestation and from neonatal cord blood at birth. A prototype strain of type VI, designated as B114877, was obtained from the Czech National Collection of Type Cultures (Prague, Czech Republic). Serotype VI CPS antigen was purified as described previously [5]. The type specificity of CPS antigen was determined by the Ouchterlony method using commercially available antisera (Denka Seiken, Japan). Assays to measure IgG antibodies for serotype VI CPS were performed using enzyme-linked immunosorbent assay identical to those described for serotypes Ia-III, and VIII [5], except for the antigen used. The lower limit of measurable IgG antibodies was 0.005 g/ml. Antibody concentrations of two groups were compared using the Mann-Whitney U test. Spearman’s rank correlation was used to determine the correlation between the antibody levels in maternalcord serum pairs. The proportion of women with positive antibody levels was compared by Fisher’s exact test. The statistical tests were two-sided, and P<0.05 was considered significant. Of the 583 women enrolled, 48 (8.2%) were colonized with GBS. The serotypes consisted of VIII (n=13), VI (n=9), Ib (n=6), III (n=5), Ia, II and nontypeable (4 each), and V (n=3). The type VI IgG antibody levels of the 583 women’s sera in association with their colonization status are shown in Fig. 1. The antibody levels of pregnant women colonized with type VI (1.80€8.63 g/ml, geometric mean€standard error, n=9) were significantly higher than those of noncolonized women (0.41€0.23 g/ ml, n=535, P<0.05), but not significantly different from those of women colonized with GBS serotypes other than type VI (0.71€2.23 g/ml, n=39). These findings indicated that type VI colonization induced a systemic immune response in pregnant women, concordant with previous studies on the prevalence of type-specific antibodies for serotypes Ia-V, and VIII [5, 6, 7, 8, 9]. We analyzed the correlation of serum type VI IgG antibody levels between paired sera of neonates and their mothers. The serum antibody levels of both term neonates (n=448, r=0.92, P<0.001, y=0.89x+0.01) and preterm neonates (n=13, r=0.90, P<0.001, y=0.53x+0.13) were highly correlated with those of their mothers (y, neonatal antibody level; x, maternal antibody level). The mean of K. Matsubara ()) · K. Baba · H. Nigami · H. Harigaya Department of Pediatrics, Nishi-Kobe Medical Center, 5-7-1 Kojidai, Nishi-ku, Kobe 651-2273, Japan e-mail: kskmatsu@portnet.ne.jp Tel.: +81-78-9972200 Fax: +81-78-9933728

Population-based active surveillance for neonatal group B streptococcal infections in Alberta, Canada: implications for vaccine formulation.

Knowledge of circulating serotypes of group B Streptococcus (GBS) is important for formulation of vaccines. There are no Canadian data on the serotype distribution of neonatal GBS isolates. Using a retrospective laboratory and health record survey between 1993 and 1994 (before introduction of Canadian prevention guidelines) and prospective active laboratory-based surveillance from 1995 to 1999 of all laboratories in Alberta, we identified 168 cases of invasive neonatal GBS infections including stillbirths among 262,398 total births; 118 of 123 (96%) isolates from 1995 to 1999 were serotyped, and the corresponding neonatal health records were reviewed. The average annual incidence was 0.64 of 1000 total births/year. Of these 95 (57%) had early onset disease (EOD), 15 (9%) were still births and 58 (34%) had late onset disease (LOD). Eighty-one percent of EOD cases were caused by serotypes Ia, Ia/c, Ia/c/R, III, III/R and V, V/R, whereas 81% of LOD cases were caused by serotypes III and III/R. GBS serotypes containing the C protein along with serotypes III and V as a group constituted 91% (107 of 118) of all GBS cases in our population. The most common clinical presentation was bacteremia without focus (74%) followed by meningitis (14%) and pneumonia (12%). During 1995 to 1999, in addition to 13 stillbirths, there were 6 of 64 (9%) neonatal deaths among EOD cases and 1 of 46 (2%) neonatal death among LOD cases. In this population-based study stillbirths account for a proportion of cases that are not routinely counted and represent a group for which intrapartum antibiotics would likely not be effective, but potentially preventable by vaccination. Inclusion of serotypes Ia, III and V in a conjugate vaccine or serotypes III and V conjugated with the C protein in a GBS vaccine could theoretically provide protection against the majority of GBS invasive disease in Alberta neonates.

Neonatal group B streptococcal disease in Finland: a ten-year nationwide study.

Group B Streptococcus (GBS) is the most common cause of invasive infections in newborns. GBS bacteria are typed on the basis of capsular polysaccharides or surface-localized proteins. Both polysaccharides and protein antigens have been suggested as potential vaccine candidates. A prospective nationwide laboratory-based study of invasive GBS infections in children younger than 3 months of age was conducted in 1985 through 1994. Isolates were serotyped by immunodiffusion in agar gel with HCl extracts and rabbit antisera. Clinical diagnoses and case fatalities were verified from the patient records or the national hospital discharge register. There were 485 cases registered during the 10-year period. The incidence of disease was 0.76/1000 live births. The case fatality rate was 8.0%. Of the 485 cases 398 (83%) were early onset and 87 (17%) late onset infections. The most common clinical diagnosis was bacteremia (77%) without an identified focus of infection. Other diagnoses included meningitis (17%), pneumonia (3%), osteomyelitis or septic arthritis (2%), pyelonephritis or cellulitis. Serotyping of 395 isolates revealed that 47% were of serotype III or III/R, 23% of Ia/c, 11% of Ib, 6% of II/R, 8% of IV, 1% of V and 7% were nontypable. The clinical picture of GBS disease and serotype distribution are similar to what has been reported from other countries. Serotypes III and III/R dominated (47% of all infections), especially in late onset disease. On the basis of these results a GBS vaccine including at least the Ia, Ib, II and III components would provide coverage against 88% of GBS serotypes causing neonatal disease in Finland.

Prevalence of antibodies against group B streptococcal capsular polysaccharides in healthy Chinese neonates.

Prevalence of antibodies against group B streptococcal capsular polysaccharides in healthy Chinese neonates.

The Rib and alpha proteins define a family of group B streptococcal surface proteins that confer protective immunity.

The group B Streptococcus (GBS) is the major cause of septicemia and meningitis in the neonatal period. Many children are exposed to this bacterium at birth, when the child may be colonized by GBS present in the normal vaginal flora. In most cases such colonization does not cause disease, but a minority of newborns fall seriously ill after birth, due to invasive GBS infection. Other children are born ill, due to an ascending infection starting during the later part of the pregnancy.1

Recurrent group B streptococcal infections in infants: Clinical and microbiologic aspects

Objective: To describe the potential for recurrence of group B streptococcal (GBS) infection in infants, using pulsed-field gel electrophoresis as an epidemiologic tool. Design: Retrospective review of cases identified by laboratory records and review of the literature. Setting: Neonatal nurseries of a county hospital system. Methods: Retrospective review of infants with second episodes of GBS bacteremia or meningitis. Digestion of chromosomal DNA with the restriction enzyme Sma I and separation of fragments by use of contour-clamped homogeneous electric field. Results: Nine cases of recurrent GBS infection were identified during a 14-year period. Eight of the nine infants were born at 25 to 36 weeks of gestation, and one was born at term. The first episode of invasive GBS infection occurred at a mean age of 10.4 days (median, 3 days; range, 1 to 27 days). Parenteral antibiotic therapy was administered for a mean of 13.9 days (median, 14 days; range, 10 to 21 days). Recurrence occurred at a mean age of 42.3 days (median, 48 days; range, 23 to 68 days). One patient died during the second episode; eight infants survived to discharge home. Of seven sets of isolates analyzed from first and second GBS episodes, five were confirmed to be the same genotypically. Conclusion: Recurrence of GBS disease in infants may be associated with the original infecting strain or a second acquired strain. (J P EDIATR 1994;125:931-8)

Effectiveness of Intrapartum Penicillin Prophylaxis in Preventing Early-Onset Group B Streptococcal Infection

OBJECTIVE: To determine the effectiveness of intrapartum penicillin prophylaxis in preventing early-onset group B streptococcal (GBS) infection in neonates of women whose birth canals are colonized by group B streptococci. DATA SOURCES: Articles published between 1966 and 1992 identified from MEDLINE, EMBASE, the Science Citation Index and the Oxford Perinatal Database; the bibliographies of primary studies, textbooks and review articles and published abstracts from major conferences and symposia. DATA SELECTION: Studies were selected if four criteria were met: (a) the target population was intrapartum women and neonates, (b) the intervention was penicillin prophylaxis, (c) invasive early-onset GBS infection was an outcome measure, and (d) the studies were controlled trials or cohort studies. Seven primary studies were identified, four of which were randomized controlled trials. DATA EXTRACTION: Explicit methodologic criteria were used by two of the authors to assess independently the study quality; one of the reviewers was blind as to author, institution and journal. The baseline characteristics of the population, intervention and outcome were summarized twice and checked for accuracy by two of the authors. DATA SYNTHESIS: Five of the studies showed a trend toward a beneficial effect of penicillin prophylaxis, and two showed a statistically significant effect. The pooled odds ratio indicated a 30-fold reduction (95% confidence interval 0.0013 to 0.17) in the incidence of early-onset GBS infection with intrapartum penicillin prophylaxis. Subgroup analyses did not change these results. The magnitude of improvement observed did not differ between women with prenatal risk factors (premature rupture of the membranes and premature labour) and those without these risk factors. CONCLUSIONS: There is accumulative evidence that intrapartum penicillin prophylaxis is effective in preventing early-onset GBS infection. Such therapy is beneficial to women whose birth canals are colonized with group B streptococci. Further studies are needed to determine the optimum timing and method of detecting vaginal colonization during pregnancy.

Detection of group B streptococcal antigen in body fluids by a latex-coupled monoclonal antibody assay

A commercially available latex agglutination reagent, Directigen (Hynson, Westcott & Dunning, Div. Becton Dickinson & Co., Baltimore, Md.), in which a murine monoclonal antibody to group B streptococcal (GBS) antigen is the active component, was evaluated by using body fluid specimens from 94 sick infants. Antigen was detected in one or more admission specimens from 18 of 19 (94.7%) infants with symptomatic GBS infection. In 15 patients with GBS meningitis, cerebrospinal fluid, serum, and 10-fold-concentrated urine specimens were positive in 87, 50, and 100%, respectively. GBS antigen was detected in 50% of unconcentrated urines, but in no sera from infants with nonmeningitic GBS sepsis. Among specimens from 27 infants with invasive infection due to organisms other than GBS and from 48 culture-negative sick infants, false-positive latex agglutination reactions occurred in only 4 (9.5%) urine specimens and in no cerebrospinal fluid or serum specimens. The 94.7% sensitivity and specificity of the Directigen GBS test indicate that it is a useful reagent for the rapid diagnosis of invasive GBS infection in young infants.