Group B Streptococcal Infections in Neonates

1979 ◽  
Vol 1 (1) ◽  
pp. 5-15
Author(s):  
Carol J. Baker

β-Hemolytic streptococci of Lancefield group B have been causally linked to neonatal disease since 1938, but only in the last decade has the group B Streptococcus become the leading etiologic agent for bacteremia and/or meningitis occurring during the first two months of life. Neither the reasons for the emergence of this organism nor the shifts over the past 40 years in the prevalence of various bacteria responsible for neonatal infection has been adequately explained. However, the importance of the group B Streptococcus as a frequent cause of neonatal mortality and morbidity demands a thorough understanding of the epidemiology and pathogenesis, clinical features, diagnostic methods, and management of these infections by physicians caring for newborn infants. INCIDENCE The common occurrence of neonatal group B streptococcal septicemia and meningitis in several geographically distant centers since 1970 has allowed the relatively precise determination of attack rates for early onset type (≤5 days) infection. Reported attack rates have been surprisingly uniform, varying from 1.3/1,000 to 4.0/1,000 live births (Table 1). Because the attack rates for serious neonatal infections associated with Escherichia coli and other maternally acquired coliform organisms have been constant since 1960, the appearance of the group B Streptococcus resulted in an absolute increase in the incidence of neonatal bacterial disease during the past decade in many hospitals in this country.

2020 ◽  
Vol 14 (04) ◽  
pp. 332-340
Author(s):  
Jeane Zanini da Rocha ◽  
Jéssica Feltraco ◽  
Vanessa Radin ◽  
Carla Vitola Gonçalves ◽  
Pedro Eduardo Almeida da Silva ◽  
...  

Introduction: Considering that Group B Streptococcus (GBS) persists as an important cause of neonatal morbidity and mortality, the objective of this study was to evaluate the frequency of maternal colonization by GBS, comparing the culture by the Granada broth with the GeneXpert real-time PCR diagnostic methods and the impact of chemoprophylaxis in high-risk pregnant women. Methodology: A prospective cohort of 110 pregnant women hospitalized for gestational complications was formed and recruited following interview and collection of rectovaginal swabs. Results: The frequency of maternal colonization was 28.2% and statistically associated with Capurro> 37 weeks (p = 0.030) and neonatal infection (p = 0.008). Chemoprophylaxis was offered to 80% of those colonized. Among the pregnant women treated, a fivefold reduction in the rate of prematurity and rate of neonatal infection was observed. The sensitivity was 76.6% and 86.6% in culture and PCR, respectively, with an optimal index of agreement between the methods (K = 0.877). Grenade culture was considered an easy and low-cost method, while GeneXpert presented higher cost and error rate of 10%. However, 23.3% of the pregnant women were diagnosed exclusively by GeneXpert and the results were obtained in two hours. Conclusions: This study showed a significant prevalence of maternal colonization for GBS and that both culture and molecular methods had peculiarities that allow different applicability, with the culture being feasible for antenatal screening and in the hospital for high-risk pregnant women with no sign of imminent delivery and GeneXpert being prioritized for situations of preterm birth.


PEDIATRICS ◽  
1978 ◽  
Vol 62 (4) ◽  
pp. 620-621
Author(s):  
Gerald W. Fischer ◽  
James W. Bass ◽  
George H. Lowell ◽  
Martin H. Crumrine

The article by Bortolussi et al. on pneumococcal septicemia and meningitis in the neonat (Pediatrics 60:352, September 1977) was of great interest to us, since we have been analyzing the effect of antibody directed against Streptococcus pneumoniae on group B Streptococcus type III. We have recently shown (unpublished data) that antibody directed against S. pneumoniae type 14 precipitates the hot hydrochloric acid-extracted polysaccharide antigen of group B Streptococcus type III. Further studies have shown that this antibody is opsonic for group B Streptococcus type III in an in vitro bactericidal assay and protective in a suckling rat model of group B Streptococcus type III sepsis.1


PEDIATRICS ◽  
1969 ◽  
Vol 44 (1) ◽  
pp. 49-57 ◽  
Author(s):  
John H. Dossett ◽  
Ralph C. Williams ◽  
Paul G. Quie

The bactericidal capacity of newborn infants' whole blood for E. coli was deficient compared to the mothers, and attempts were made to identify cellular or humoral factors responsible for this deficiency. Separated polymorphonuclear leukocytes from newborn infants were found to be similar to polymorphs from mothers in capacity to engulf and kill E. coli and other bacteria so that cellular deficiency was not evident. Comparison of the serum opsonic capacity of newborn infants' and mothers' sera revealed deficient opsonic capacity for E. coli in newborn sera. The mean opsonic titer for E. coli was 46.7 in mothers and 4.3 in neonates. Serum opsonic titers for Staph. aureus and group B streptococcus were similar. The opsonic capacity for all bacterial species was decreased when the sera were heated or decomplemented with immune complexes indicating the phagocytosis amplifying role of complement. The newborn-maternal difference in opsonic capacity for E. coli was presumably a result of deficient 19S antibodies, the primary opsonic antibodies for this organism. Maternal 19S serum fractions alone, however, showed no opsonic capacity for E. coli. Addition of a complement source (newborn serum absorbed with E. coli) revealed the opsonic capacity of these 19S maternal serum fractions for E. coli. Antibodies in 19S serum fractions therefore are efficient opsonins for E. coli; however, complement is necessary to demonstrate their opsonic potential.


PEDIATRICS ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 40-44 ◽  
Author(s):  
Sambasivarao Voora ◽  
Gopal Srinivasan ◽  
Lawrence D. Lilien ◽  
Tsu F. Yeh ◽  
Rosita S. Pildes

Over a period of 18 months, 100 full-term newborns developed an axillary or a rectal temperature ≥37.8 C during the first four days of postnatal life. These febrile term newborns represented 1% of all full-term newborns in the normal nursery. Of the febrile newborns, 10% had culture-proven bacterial disease (BD). Fever developed in 54%, 27%, 13%, and 6% on the first, second, third, and fourth days, respectively. In 17 newborns fever developed within the first hour of life; 13 of these had mothers with fever and two others were under a radiant warmer in the birth room. Fever occurring on the third day of postnatal life had a significantly higher chance of being associated with BD than fever occurring at any other time in the first four days of postnatal life. Newborns with temperature ≥39 C had a significantly higher incidence of BD than newborns with temperature <39 C. The incidence of fever among breast-fed newborns (0.98%) was similar to that of formula-fed newborns (1.01%). Of the 100 febrile newborns, 45 had other symptoms compatible with BD, and eight of these had proven BD (group B Streptococcus in five, group D Streptococcus in one, Shigella D in one, and Propionibacterium species in one). The two other febrile newborns with proven BD had no other symptoms of infection (group B Streptococcus and Escherichia coli). Mean WBC count of febrile newborns with BD was significantly lower than that of febrile newborns without BD. Only three febrile newborns had WBC count <5,000/cu mm and two of them had proven BD. Febrile newborns should be evaluated and treated with antibiotics when they have symptoms of infection other than fever or when the fever persists or recurs.


PEDIATRICS ◽  
1977 ◽  
Vol 60 (3) ◽  
pp. 352-355
Author(s):  
Robert Bortolussi ◽  
Theodore R. Thompson ◽  
Patricia Ferrieri

Five infants with pneumococcal sepsis presented with respiratory distress and clinical signs of infection in the first day of life. Although there was no apparent epidemiological relationship among the patients, four of the five were seen within a 12-month period. Pneumonia, prolonged rupture of fetal membranes, and prematurity were features in these patients. Three infants died, two within 12 hours of diagnosis. Streptococcus pneumoniae was isolated from the vagina of three of the mothers; in two, the serotype was identical to that recovered from their infants. Clinical features of neonatal pneumococcal sepsis are similar to those of early-onset group B streptococcal infection. Like the group B Streptococcus, S. pneumoniae acquired from the maternal vagina is a potential life-threatening pathogen in the newborn period.


2000 ◽  
Vol 46 (10) ◽  
pp. 1583-1587 ◽  
Author(s):  
Marcello Assumma ◽  
Fabrizio Signore ◽  
Lucia Pacifico ◽  
Naila Rossi ◽  
John F Osborn ◽  
...  

Abstract Background: The reported sensitivities and specificities of procalcitonin (PCT) concentrations for the diagnosis of neonatal infection vary widely. A postnatal increase of PCT has been observed in healthy term newborns with a peak at ≈24 h of age, and many questions remain regarding maternal and perinatal factors that may influence the normal PCT kinetics during the immediate postnatal period. Methods: We prospectively investigated the association between the serum PCT values obtained from 121 mothers at delivery and serum PCT in their healthy, term offspring at birth as well as at 24 and 48 h of age. We also analyzed whether obstetric and perinatal factors would alter maternal and neonatal PCT response. Results: PCT concentrations in the babies at birth were significantly higher than in the mothers (P <0.0001), with even larger differences at 24 and 48 h of age. None of the variables identified from maternal and perinatal histories had a significant effect on maternal PCT response. In the healthy neonate, the variables that significantly affected the concentration of PCT at birth were the mothers’ PCT (P <0.01), maternal group B streptococcus colonization (P <0.05), and rupture of membranes ≥18 h (P <0.01). The coefficient of linear correlation between the mother’s PCT concentration and that of the baby at birth was 0.32 (P <0.01). The only variable that significantly altered the PCT concentration at both 24 (P <0.01) and 48 (P <0.01) h of age was rupture of membranes ≥18 h. Nonetheless, the PCT response observed during the 48-h period after birth among healthy babies born to mothers with risk factors for infection was well below that reported previously among age-matched neonates with sepsis. Conclusions: The postnatal increase of PCT observed in the healthy neonate with peak values at 24 h of age most likely represents endogenous synthesis. In estimating the sensitivities and specificities of PCT for diagnosis of sepsis throughout the initial 48 h of life, it is important to consider the normal PCT kinetics and the pattern(s) of PCT response in the healthy neonate.


2003 ◽  
Vol 71 (12) ◽  
pp. 6857-6863 ◽  
Author(s):  
Elisabeth E. Adderson ◽  
Shinji Takahashi ◽  
Yan Wang ◽  
Jianling Armstrong ◽  
Dylan V. Miller ◽  
...  

ABSTRACT Group B Streptococcus agalactiae bacteria (group B streptococci [GBS]) are the most common cause of serious bacterial infection in newborn infants. The majority of serotype III-related cases of neonatal disease are caused by a genetically related subgroup of bacteria, restriction fragment digest pattern (RDP) type III-3, suggesting that these strains possess unique genes contributing to virulence. We used genomic subtractive hybridization to identify regions of genomic DNA unique to virulent RDP type III-3 GBS strains. Within one of these III-3-specific regions is a 1,506-bp open reading frame, spb1 (surface protein of group B streptococcus 1). A mutant type III GBS strain lacking Spb1 was constructed in virulent RDP type III-3 strain 874391, and the interactions of the wild-type and spb1 isogenic mutant with a variety of epithelial cells important to GBS colonization and infection were compared. While adherence of the spb1 isogenic mutant to A549 respiratory, C2Bbe1 colonic, and HeLa cervical epithelial cells was slightly lower than that of the 874391 strain, invasion of the Spb1− mutant was significantly reduced with these cell lines compared to what was seen with 874391. The defect in epithelial invasion was corrected by supplying spb1 in trans. These observations suggest that Spb1 contributes to the pathogenesis of neonatal GBS infection by mediating internalization of virulent serotype III GBS and confirm that understanding of the population structure of bacteria may lead to insights into the pathogenesis of human infections.


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