Neonatal Group B Streptococcus Infection Research Articles

The Pediatric Investigators Collaborative Network on Infections in Canada (PICNIC) study of neonatal group B streptococcal infections in Canada

To determine the presentation and medical outcomes of neonatal group B streptococcus (GBS) disease in Canada, and describe maternal and obstetrical risk factors. Retrospective review of health records and laboratory databases using standardized data collection forms. All neonates diagnosed with GBS infections in 1992 at 13 Canadian paediatric centres. A total of 105 infants meeting the criteria for neonatal GBS disease were identified. The majority of cases (78 or 74.3%) had early-onset disease (EOD); 78.9% (60 of 76) of these cases presented within 24 h of delivery. Rates of EOD (less than seven days) varied from 0.44/1000 live births to 2.1/1000 live births, with an overall rate of 1.2/1000 live births. Pneumonia was the most common clinical illness (43.8%), followed by bacteremia without focus (23.8%) and meningitis (16.2%). At least one maternal risk factor for neonatal GBS disease was noted in 46 of 78 (59%) infants with EOD. A median of one dose (range one to 23 doses) of intrapartum antibiotics was given in 18 of 75 (24%) of the pregnancies. Overall, the mean gestational age at birth was 36.2+/-4.7 weeks, with 38 of 96 (39.6%) infants having a gestational age at birth younger than 37 weeks (31 of 73 [42.5%] EOD cases were born with a gestational age younger than 37 weeks). The median birth weight was 3099 g (range 610 g to 4830 g). Thirty of 94 (31.9%) infants had a birth weight less than 2500 g. Seventeen (16.2%) infants died. In 1992, neonatal GBS disease was a significant cause of morbidity and mortality in Canadian infants. More than half of the cases identified in this study could have been potentially preventable by the use of intrapartum antibiotics for women with known risk factors. There is a need for prospective studies to better define risk factors and preventative measures for neonatal GBS infections in Canada.

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.

Prevention of group B Streptococcus infection in neonates.

To review the epidemiology of group B Streptococcus (GBS) infection, risk factors for infection, and clinical manifestations of disease in the neonate, as well as the role of chemoprophylaxis and immunoprophylaxis in prevention of GBS disease and current recommendations for prevention. MEDLINE searchers (1976-1997) of the English-language literature. Despite clinical advances in health care in the past two decades, GBS remains a leading cause of serious neonatal infection. Most early-onset GBS infections can be prevented through the use of intrapartum antimicrobial chemoprophylaxis. Preventing GBS infection in neonates is more cost-effective than treating GBS infections, and implementing prevention programs can reduce morbidity and mortality resulting from GBS disease. Many proposals have been made regarding prevention strategies; however, they have not been implemented widely and consistently in the US. To coordinate both pediatric and obstetric supported strategies, the Centers for Disease Control and Prevention (CDC) recently published recommendations for prevention of neonatal GBS disease through two possible strategies. In the first strategy, intrapartum antibiotic chemoprophylaxis should be offered to all women identified by prenatal culture as colonized and those who develop premature membrane rupture or onset of labor at less than 37 weeks gestation. The second strategy involves administration of intrapartum antibiotics to all women who develop one or more risk factors at the time of membrane rupture or onset of labor. GBS is difficult to eradicate, causing many women to be colonized with the organism during pregnancy and labor, thereby infecting their infant. Prevention strategies have been published for more than 10 years without successful implementation. Although optimal prevention management has not been defined, following one of two strategies recommended by the CDC can prevent the majority of GBS infections in neonates.

Epidemiology of group B streptococcal infection in a special care neonatal unit.

Over the last two decades group B streptococci (GBS) have become a major cause of early-onset neonatal sepsis. The reported world-wide incidence of neonatal GBS infection ranges from 0.4–3.7 per 1000 live births. Some of the risk factors associated with infection include colonisation of maternal genital and lower gastrointestinal tracts and prematurity. A number of studies have considered preventive measures such as antibiotic prophylaxis given to mothers before delivery and to babies at risk post delivery.KeywordsStreptococcal InfectionLower Gastrointestinal TractTracheal SecretionVaginal ColonisationDecade GroupThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Restriction endonuclease analysis of group B streptococcal isolates from two distinct geographical regions

This study examined isolates of group B streptococci (GBS) by latex seroagglutination and restriction endonuclease analysis (REA). REA analysis was performed with high- and low-frequency cutting enzymes, and fragments were resolved by linear and pulsed-field gel electrophoresis (PFGE), respectively. GBS isolates were derived from a regional acute-care hospital and a tertiary referral obstetric hospital. The most common serotype isolated at the general hospital was serotype V (42%). A high incidence of this serotype V was associated with wound infections, but there was no predominant REA profile. Serotype III was the most common from the obstetric hospital (41%). The majority of these isolates were associated with neonatal GBS infection and there was a predominant restriction pattern. Analysis of restriction patterns of GBS isolated from individual mother/baby pairs revealed common patterns. These data extend the evidence for vertical transmission of GBS and clones of serotype III GBS with increased pathogenic potential.

Increased recovery of group B streptococcus by the inclusion of rectal culturing and enrichment

Detection of intrapartum carriage of group B streptococcus (GBS) and subsequent antibiotic prophylaxis may prevent GBS infections in neonates. Because the gastrointestinal tract is the primary source of this organism, detection of carrier status requires both rectal and vaginal swabs. Vaginal swabs from 651 obstetric outpatients were plated onto 5% sheep blood agar. A second vaginal and a rectal swab were collected and incubated overnight in an enrichment medium of Todd-Hewitt broth containing antibiotics. By at least one method, 110 (16.9%) patients were positive for GBS. Only 31.8% of these positive patients were detected by direct culture of vaginal swabs. The use of vaginal swabs directly plated onto blood agar identified only three carriers not detected by another method. Inoculation of an enrichment broth with the vaginal swab and subsequent subculture detected 70.9% of the total. The use of both vaginal and rectal swabs with enrichment detected 97.3% of total GBS carriers. A subset of enrichment broths inoculated with vaginal and rectal specimens from 279 patients was tested for GBS by direct latex agglutination (Streptex; Murex Diagnostics, Inc., Norcross, GA, USA). Of the 90 broths that grew GBS on subculture, only 59 (65.6%) were positive by the direct agglutination method. The use of this method, although reducing processing time by 1 day, gave false-negative results for one-third of the GBS-positive broths. An accurate detection of the GBS carrier state can only be achieved by a combination of vaginal and rectal swabs incubated in enrichment broth and subcultured on blood agar.

Group B Streptococcus (GBS) and Neonatal Infections

At the Royal Women's Hospital, Melbourne over an 8-year period (1981-1988) all public antenatal patients were screened at 32 weeks' gestation for group B streptococcus (GBS). In a total of 30,197 livebirths there were no early onset neonatal GBS infections in infants of treated asymptomatic carrier mothers. By contrast there were 27 infections with 8 deaths in an unscreened control group of private patients (total livebirths 26,915). It is recommended that GBS screening occur antenatally at 28 weeks and that intrapartum chemoprophylaxis be offered at least to those carriers with obstetric risk factors.

Group B Streptococcus (GBS) and Neonatal Infections: The Case for Intrapartum Chemoprophylaxis

At the Royal Women's Hospital, Melbourne over an 8-year period (1981-1988) all public antenatal patients were screened at 32 weeks' gestation for group B streptococcus (GBS). In a total of 30,197 livebirths there were no early onset neonatal GBS infections in infants of treated asymptomatic carrier mothers. By contrast there were 27 infections with 8 deaths in an unscreened control group of private patients (total livebirths 26,915). It is recommended that GBS screening occur antenatally at 28 weeks and that intrapartum chemoprophylaxis be offered at least to those carriers with obstetric risk factors.

Enhanced Killing of Group B Streptococci In Vitro by Penicillin and Opsonophagocytosis with Intravenous Immunoglobulin

Combined effects of intravenous immunoglobulin (IVIG) and antibiotics in killing bacteria are of interest with broadening clinical use of IVIG. Since the kinetics of killing by these agents differ and each may influence the outcome of the other, it is difficult to evaluate combination effects in vitro. Conditions were developed to measure killing of group B streptococci (GBS), type III strain M732, by an opsonic mixture with IVIG, fresh serum, and human polymorphonuclear leukocytes (PMNL) with or without penicillin. Bacterial killing was observed with the opsonic IVIG mixture, penicillin, and the opsonic IVIG mixture plus penicillin at 1 h. The effect of the combination was greater than the sum of the effects of two separate incubations. The enhanced killing was evident for up to 18 h. By 24 h, the killing by the combination was no greater than that by penicillin alone. A similar pattern of GBS killing was observed with cord blood PMNL, six different GBS type III strains, and pretreatment of GBS with either IVIG or penicillin. These effects suggest that the combination of IVIG and penicillin has potential for use in the treatment of neonatal GBS infections.

Immunoglobulin therapy of neonatal Group B streptococcal infections

Group B streptococci (GBS) are a major cause of sepsis and meningitis in newborn babies. Neonatal GBS infections are often rapidly progressive, suggesting that the immunity to GBS is deficient. Studies have shown that opsonic antibody is required for efficient phagocytosis and killing of GBS, and neonatal GBS infections have been associated with diminished levels of anti-GBS antibody. Intravenous immunoglobulin (IVIG) has been shown to provide protective immunity in experimental GBS infection models. However, lot to lot variation in opsonic antibody levels occurs in standard IVIG preparations. Recently hyperimmune anti-GBS IVIG has been prepared with high levels of opsonic and protective antibody to GBS. Hyperimmune IVIG preparations will allow physicians to give higher quantities of specific anti-GBS antibody without having to administer large fluid volumes or large amounts of nonspecific immunoglobulin. In addition specific immunoglobulin preparations will ensure that the IVIG contains reliable antibacterial activity. Although human studies are limited they suggest that IVIG therapy in neonates may be safe and effective in treating neonatal sepsis. However, further studies are necessary to determine the role of IVIG in preventing or treating neonatal infections.

Multiple Group B Streptococcal Infections in a Premature Infant: Eradication of Nasal Colonization With Rifampin

Sir .—Although group B streptococci (GBS) are uniformly sensitive to penicillin in vitro, penicillin treatment failures in neonatal GBS infection and recurrent neonatal GBS infection may occur. 1 Furthermore, attempts to eradicate GBS from colonized pregnant women or from colonized neonates have had limited success. 2,3 There are no published data that address the appropriate management of the infant who is colonized with GBS and who develops recurrent systemic GBS infections. We report the course of a premature infant, colonized with GBS from birth, who experienced multiple infections with GBS type III during his four-month nursery stay. Patient Report .—Twin A weighed 920 g at birth. The pregnancy was complicated by premature labor two days before delivery at 28 weeks and maternal fever to 38.8 °C (102 °F) shortly before delivery by caesarean section. At birth, twin A was limp and foul-smelling and required vigorous resuscitation (twin B died at

MONOCLONAL OR POLYCLONAL ANTIBODY-MEDIATED PROTECTION AGAINST GROUP B STREPTOCOCCI IS MARKEDLY ENHANCED BY FIBRONECTIN

Fibronectin (FN) is reported to enhance particle attachment to macrophages and PMNs. Our previous studies showed that cord plasma FN levels are decreased compared with adult levels and that the opsonic activity against group B streptococci (GBS) of such plasma can be increased by the addition of purified FN. The present studies were designed to determine the role of FN alone and in combination with antibody preparations in providing protection against experimental neonatal GBS infection in a rat model. FN administration alone did not protect against type III GBS infection (untreated 33% survival, n=18; vs treated 29%, n=17). When FN was combined with a polyclonal human IgG preparation modified for intravenous use (IGIV), increased protection was observed (untreated 24% survival, n=17; IGIV 29%, n=17; IGIV+FN 48%, n=31). The enhanced protection observed with a combination of FN and antibody was more impressive when a murine monoclonal type III specific IgG antibody was employed (untreated 0%, n=31; FN 14%, n=29; IgG 17%, n=24; FN+IgG 62%, n=29). FN also enhanced protection by low dose monoclonal IgM antibody (untreated 5%; FN 26%; IgM 18%; FN+IgM 78%). Surprisingly, FN also significantly enhanced protection mediated by an IgA type III monoclonal (untreated 36%, IgA 42%, FN+IgA 65%). These studies indicate that FN interacts with antibody of IgG, IgM and even IgA isotype in host defence. Optimal immunotherapy of neonatal group B disease may involve the adminstration of both antibody and FN.

Functional characteristics of a modified immunoglobulin preparation for intravenous administration: Summary of studies of opsonic and protective activity against group B streptococci

Group B streptococci (GBS) remains a major cause of morbidity and mortality in newborn babies, despite antibiotic therapy, Recent studies suggest that phagocytosis and killing of GBS is ineffective due to a deficiency in anti-GBS antibody. Using an opsonophagocytic bacterial assay and a suckling rat model of GBS sepsis, we analyzed a modified human immunoglobulin for opsonic and protective antibody. Immune globulin (IGIV) prepared for intravenous use (Gamimune, Cutter Laboratories, Inc.) was highly protective in this experimental GBS model. Using the opsonophagocytic assay, antibody activity to several strains of types Ia, II, and III GBS were also demonstrated with IGIV. To ensure that the IGIV activity was in fact antibody, globulin from IGIV was isolated and analyzed. Purified IgG retained opsonic activity in vitro and also provided protection in experimental GBS disease. Variation in the quantity of IgG necessary for protection was observed in different GBS strains. Since IGIV has opsonic and protective activity against several strains and serotypes of GBS, its intravenous administration may provide a valuable adjunct to standard antibiotic therapy for neonatal GBS infections.

Experimental group B streptococcal infection in the rhesus monkey: I. Disease production in the neonate

Group B streptococci (GBS) are responsible for serious infections of newborn infants. An experimental model for GBS infection was developed in the newborn rhesus monkey in order to obtain more information concerning the pathogenesis of such infections. A series of 29 newborn monkeys were inoculated with either type Ic or type III GBS or sterile broth. Fatal neonatal meningitis without associated pneumonia was produced consistently following intracerebral inoculation with either type Ic or type III; intracerebral inoculation with sterile broth produced no apparent disease. Variable disease production followed intravenous or intra-amniotic GBS inoculation, and clinical manifestations ranged from no apparent disease to fatal meningitis and pneumonia. This monkey model may be useful for further investigation of treatment and prevention of neonatal GBS infection.