Intravenous administration of human IgG to newborn infants: changes in serum antibody levels to group B streptococci

1984 ◽  
Vol 143 (2) ◽  
pp. 123-127 ◽  
Author(s):  
K. K. Christensen ◽  
P. Christensen ◽  
H. U. Bucher ◽  
G. Duc ◽  
C. H. Kind ◽  
...  
1984 ◽  
Vol 142 (2) ◽  
pp. 86-88 ◽  
Author(s):  
K. K. Christensen ◽  
P. Christensen ◽  
G. Duc ◽  
P. H�ger ◽  
C. Kind ◽  
...  

PEDIATRICS ◽  
1977 ◽  
Vol 60 (4) ◽  
pp. 473-476 ◽  
Author(s):  
Margaret R. Hammerschlag ◽  
Carol J. Baker ◽  
Susan Alpert ◽  
Dennis L. Kasper ◽  
Ingrid Rosner ◽  
...  

Cultures from the vagina, pharynx, and anal canal of 100 healthy girls, 2 months through 15 years of age, were examined for the presence of group B streptococci. Of the 100 participants, 20% were colonized at one or more of these three sites. Pharyngeal colonization was detected in 15% of the girls under 11 years of age and in 5% of those over 11 years of age. Colonization at anogenital sites was observed in 19% of participants under 3 years of age, in 25% of those 11 years of age and older, and in only 4% of those between the ages of 3 and 10 years (P < .025). The concentration of serum antibody directed against the polysaccharide capsular antigen isolated from type III, group B Streptococcus appeared, in part, to be related to increasing age.


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.


Author(s):  
Leslie C. Benchetrit ◽  
Sergio E.L. Fracalanzza ◽  
Heloiza Peregrino ◽  
Alipio Augusto Camelo ◽  
Leonardo A.L.R. Sanches

1982 ◽  
Vol 7 (2) ◽  
pp. 99-101 ◽  
Author(s):  
Daiel V. Lim ◽  
Keith S. Kanarek ◽  
Mary E. Peterson

2003 ◽  
Vol 77 (3) ◽  
pp. 121-126 ◽  
Author(s):  
Shigemi TERAKUBO ◽  
Yoshitoshi ICHIMAN ◽  
Hiromu TAKEMURA ◽  
Hiroyuki YAMAMOTO ◽  
Jingoro SHIMADA ◽  
...  

PEDIATRICS ◽  
1981 ◽  
Vol 68 (4) ◽  
pp. 544-549 ◽  
Author(s):  
Carol J. Baker ◽  
Morven S. Edwards ◽  
Dennis L. Kasper

The role of maternally acquired antibody to native type III polysacchande of group B Streptococcus as a determinant of susceptibility for infant systemic infection was investigated. Sera from 11 1 acutely ill infants with type III group B streptococcal bacteremia and/or meningitis and their mothers, and cord sera from 45 healthy neonates and their mothers who had type III group B streptococcal vaginal colonization at delivery were studied. Sera from each of 111 acutely ill infants contained very low levels ofantibody (sjlt 1.7 µg/ml, median 0.4 µg/ml), and a significant correlation with maternal levels was tested for early onset infection (median 0.6 µg/ml; r = .76; P sjlt .01). Women whose infants remained well had antibody levels sjgt 2 µg/ml in their sera (73%) more often than those whose infants developed symptomatic infection (17%) (P sjlt .001), and the median level in their sera (12.6 µg/ml) was considerably higher. Study of sera obtained during convalescence from 86 surviving infants indicated a poor antibody response to infection. In contrast, high levels of antibody were detected in sera from each of five convalescent women with postpartum bacteremia. These data extend earlier observations suggesting the correlation between low levels of type-specific antibody in serum and risk for systemic infection with type III strains of group B streptococci.


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