Level of Maternal Antibody Required to Protect Neonates against Early‐Onset Disease Caused by Group B Streptococcus Type Ia: A Multicenter, Seroepidemiology Study

Lin, Feng-Ying C.; Philips, Joseph B.; Azimi, Parvin H.; Weisman, Leonard E.; Clark, Penny; Rhoads, George G.; Regan, Joan A.; Concepcion, Nelydia F.; Frasch, Carl E.; Troendle, James; Brenner, Ruth A.; Gray, Barry M.; Bhushan, Reva; Fitzgerald, G R; Moyer, Patricia; Clemens, John D.

doi:10.1086/323350

Cited by 111 publications

(82 citation statements)

References 39 publications

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“…The absence of passively derived maternal antibody such as that directed against Group B Streptococcus appears to be important (4,5). Indeed premature neonates of less than 32 wk of gestation have fetal IgG concentrations of less than 50% of maternal levels (6,7). Many elements of the acquired immune system are also either low or function sub-optimally (8,9).…”

Section: Espite Advances In Perinatal Care Neonatal Infection Re-mentioning

confidence: 99%

The Role of Mannose-Binding Lectin in Susceptibility to Infection in Preterm Neonates

et al. 2008

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Preterm neonates are susceptible to infection due to a combination of sub-optimal immunity and increased exposure to invasive organisms. Mannose-binding lectin (MBL) is a component of the innate immune system, which may be especially important in the neonatal setting. The objective of this study was to investigate the impact of MBL on susceptibility and severity of infection in preterm neonates during their first month of life. One hundred fifty eight preterm neonates were genotyped for MBL mutations by heteroduplex analyses. Consecutive serum MBL levels were measured by ELISA and clinical and laboratory data, including blood cultures, were collected for each baby. A third of the premature neonates had genetically determined MBL deficiency. In addition, MBL levels were also low in the first week of life and lower in neonates with a wild type genotype who were less than 28 wk gestation or a birth weight of less than 1000 g, thereby increasing the number of neonates with a low MBL level at birth. MBL deficiency was associated with an increased risk of sepsis (p Ͻ 0.01). This study indicates that MBL levels are low in neonates at birth and renders premature neonates to an increased risk of infection. (Pediatr Res 63: 680-685, 2008)

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Section: Espite Advances In Perinatal Care Neonatal Infection Re-mentioning

confidence: 99%

The Role of Mannose-Binding Lectin in Susceptibility to Infection in Preterm Neonates

et al. 2008

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“…Alternatively (though less desirably), surrogate immunological measures of clinical efficacy based on maternal and neonatal serotype-specific IgG antibody may be sufficient endpoints. 25,48 RECOMMENDATIONS What is the best preventive strategy for the UK? Table 7 summarizes estimates of the numbers of deaths and cases of serious disability estimated to be prevented by each of the three preventive strategies.…”

Section: Conducting a Trialmentioning

confidence: 99%

The prevention of neonatal group B streptococcal disease: a report by a working group of the Medical Screening Society

et al. 2005

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Streptococcus agalactiae, or Lancefield group B streptococcus (GBS), is the most frequent cause of serious bacterial sepsis, including neonatal meningitis, in UK neonates. Early-onset neonatal GBS infection, but not late-onset, can be prevented by screening to identify high-risk pregnancies and administering penicillin during delivery. A vaccine has been developed as an alternative means of prevention but it is awaiting a randomized trial before being available for general use. In this review we examine the published literature to assess the morbidity and mortality attributable to neonatal GBS infection, quantify the screening performance of the two alternative modes of screening (microbiological and risk factor based), review the evidence on the efficacy of the vaccine, and estimate the numbers of deaths and cases of serious disability that each strategy in turn might prevent in the UK, in order to assess the most effective means of prevention for the UK.

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“…Maternal serotype-specific immunoglobulin G (IgG) transferred to the fetus protects colonized neonates from invasive disease, but most neonates who are colonized with GBS at birth do not develop invasive disease despite lacking protective levels of serotype-specific IgG (19,20). Although serotype III-specific IgG concentrations correlate with the efficiency of opsonophagocytic killing by polymorphonuclear leukocytes (PMNs) in vitro, serum deficient in serotype-specific IgG still mediates significant opsonophagocytic killing by a process that involves activation of the complement pathway (8).…”

mentioning

confidence: 99%

L-Ficolin and Capsular Polysaccharide-Specific IgG in Cord Serum Contribute Synergistically to Opsonophagocytic Killing of Serotype III and V Group B Streptococci

et al. 2012

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ABSTRACTGroup B streptococci (GBS;Streptococcus agalactiae) are the most common cause of neonatal sepsis and meningitis. Serotype-specific IgG antibody is known to protect neonates against GBS infections by promoting opsonophagocytosis. The L-ficolin-mediated lectin pathway of the complement is also a potential mechanism for opsonization of GBS, because L-ficolin activates the complement after binding to serotype Ib, III, V, VI, and VIII GBS. In the present study, we investigated how L-ficolin and serotype-specific IgG in cord sera contribute to opsonophagocytic killing of GBS. Neither L-ficolin nor serotype-specific IgG concentrations correlated with C3b deposition on serotype Ib and VI GBS, suggesting L-ficolin- and serotype-specific IgG-independent mechanisms of complement activation. The percentage of serotype VIII GBS killed was high regardless of the concentration of L-ficolin and IgG. In contrast, L-ficolin and serotype-specific IgG can each initiate C3b deposition on serotype III and V GBS and promote phagocytosis by polymorphonuclear leukocytes, but L-ficolin and serotype-specific IgG together promote opsonophagocytic killing to a greater extent than does either alonein vitro. This synergy was observed when serotype III-specific IgG concentrations were between 1 and 6 μg/ml and when serotype V-specific IgG concentrations were between 2 and 5 μg/ml. Concentrations of serotype III-specific IgG in cord blood above 7 μg/ml are considered protective for neonates colonized with GBS, but most neonates with IgG levels of less than 7 μg/ml do not develop GBS infections. The data presented here suggest that L-ficolin enhances opsonophagocytosis of serotype III and V GBS when serotype-specific IgG alone is suboptimal for protection.

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Level of Maternal Antibody Required to Protect Neonates against Early‐Onset Disease Caused by Group B Streptococcus Type Ia: A Multicenter, Seroepidemiology Study

Cited by 111 publications

References 39 publications

The Role of Mannose-Binding Lectin in Susceptibility to Infection in Preterm Neonates

The Role of Mannose-Binding Lectin in Susceptibility to Infection in Preterm Neonates

The prevention of neonatal group B streptococcal disease: a report by a working group of the Medical Screening Society

L-Ficolin and Capsular Polysaccharide-Specific IgG in Cord Serum Contribute Synergistically to Opsonophagocytic Killing of Serotype III and V Group B Streptococci

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