Strain specificity of opsonins for group B streptococci types II and III

Shigeoka, Ann O.; Hall, R T; Hill, Harry R.

doi:10.1128/iai.23.2.438-445.1979

Cited by 41 publications

(12 citation statements)

References 21 publications

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“…However, it is not known whether the proteins under investigation are toxins. It has been assumed that the type-specific carbohydrate of group B streptococci functions as a virulence factor by anti-phagocytic activity, and antibodies to these antigens are protective (1, 10,13). Whatever the mechanisms of protection by the antibodies to the Ibc proteins as demonstrated in the present study, the results support the notion that the Ibc proteins may function as an additional virulence factor in group B streptococci.…”

Section: Discussionsupporting

confidence: 85%

Mouse‐Protective Antibodies Against The Ibc Proteins of Group B Streptococci

Bevanger¹,

Néss²

1985

Acta Pathologica Microbiologica Scandinavica Series B: Microbio

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Antiserum to each of the α and β antigens of the Ibc protein fraction of group B streptococci was raised in rabbits. A possible protective effect of the antisera in mice challenged by group B streptococci was evaluated. Antiserum against each of the antigens significantly increased the survival rates of mice challenged by bacteria which produced the corresponding antigen, but not of those challenged by bacteria which produced only the heterologous antigen. Animals challenged with a strain which produced both of the α and β antigens were protected by antiserum to the β antigen but not by antiserum to the α antigen. In this case the effect of the anti‐α serum was a postponement of death of the animals. The antisera showed no protection of animals challenged by a group B streptococcal strain which did not produce any of the Ibc protein antigens.

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Section: Discussionsupporting

confidence: 85%

Mouse‐Protective Antibodies Against The Ibc Proteins of Group B Streptococci

Bevanger¹,

Néss²

1985

Acta Pathologica Microbiologica Scandinavica Series B: Microbio

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“…This low colonization-to-disease ratio suggests that a combination of bacterial virulence factors and altered neonatal defense mechanisms have to converge to culminate in a clinical case of GBBHS disease. The inoculum of maternal GBBHS colonization (19) and other features of the microorganism (10,16,21) have been proposed as bacterial virulence determinants. On the part of the host, the most important resistance factor appears to be the presence of adequate titers of transplacentally acquired anti-GBBHS opsonic antibody in the newborn (3).…”

mentioning

confidence: 99%

Bactericidal capacity of newborn phagocytes against group B beta-hemolytic streptococci

Becker

Robinson²,

Bazan³

et al. 1981

Infect Immun

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The bactericidal capacity of mononuclear and polymorphonuclear phagocytes obtained from normal newborn infants and from healthy adults was evaluated in vitro, using two group B beta-hemolytic streptococci (GBBHS) serotypes (GBBHS-Ia-SS-615/28 and GBBHS-III-SS-620/50) and uniform opsonic conditions. No intertype differences in bacteriolysis of these two serotypes were observed among leukocytes from newborns or adults. As group, only polymorphonuclear phagocytes from newborns disclosed a significantly lower mean bactericidal capacity than their adult cellular counterpart, and only with respect to GBBHS-III-SS-620/50. On the other hand, 4 or 16 polymorphonuclear samples from newborns tested revealed significantly low bactericidal capacities against both GBBHS serotypes, and an additional sample revealed a bactericidal capacity against GBBHS-III-SS-620/50 alone. Interstrain variations in the intrinsic bactericidal capacity of polymorphonuclear phagocytes from newborns against GBBHS-III may exist, as suggested by a single observation made by using four clinical isolates of GBBHS-III. Such deviant phagocytic capacities of polymorphonuclear phagocytes from newborns may constitute an additional selective risk factor in the genesis of GBBHS sepsis of the newborn.

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“…The quantity of type-specific capsular polysaccharide (2) and the production of neuraminidase (22), hyaluronidase (23), and proteases (28) have been proposed as possible GBS virulence factors, based on correlation with virulence in animal models, association with pathogenic strains, or analogy to other bacterial pathogens. These contentions have been contradicted, however, by other reports (12,19,26).…”

mentioning

confidence: 86%

Type-specific capsular antigen is associated with virulence in late-onset group B Streptococcal type III disease

Klegerman¹,

Boyer²,

Papierniak³

et al. 1984

Infect Immun

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Strain differences have been postulated to explain the observation that group B Streptococcus type III (GBS III) late-onset disease occurs in only a fraction of colonized infants. To determine the distribution of type-specific polysaccharide antigen (Ag) in GBS III, Ag was measured by rocket immunoelectrophoresis in both supernatant fluids and EDTA extracts and by radial immunodiffusion in multiple HCI extracts of the pellet from cultures of 10 strains of GBS III. Capsular Ag was defined as the sum of Ag in EDTA extracts + Ag in multiple HCI extracts. Both Ag in EDTA extracts and Ag in supernatant fluids correlated with capsular Ag (r = 0.94). GBS III strains were obtained from the blood of 19 infants with late-onset sepsis, from the cerebrospinal fluid or blood of 22 infants with late-onset meningitis, and from mucosal surfaces of both 18 infants and 12 mothers of infants with low levels of type-specific antibody and asymptomatic colonization. Mean values of Ag in supernatant fluids in strains from infants with late-onset sepsis (1.50 ± 0.08 ptg/ml) and late-onset meningitis (1.67 ± 0.09 pug/ml) were significantly greater than those in asymptomatic colonization strains (1.14 ± 0.05 ,ug/ml; P < 0.001). The number of organisms required for a 50% lethal dose in the chick embryo, determined in 29 strains, was inversely related to Ag in supernatant fluids (r =-0.60). The demonstration that the quantity of capsular Ag produced by GBS III strains is related to their virulence in chick embryos and to their invasiveness in susceptible infants supports the hypothesis that Ag is a virulence factor in humans.

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Strain specificity of opsonins for group B streptococci types II and III

Cited by 41 publications

References 21 publications

Mouse‐Protective Antibodies Against The Ibc Proteins of Group B Streptococci

Mouse‐Protective Antibodies Against The Ibc Proteins of Group B Streptococci

Bactericidal capacity of newborn phagocytes against group B beta-hemolytic streptococci

Type-specific capsular antigen is associated with virulence in late-onset group B Streptococcal type III disease

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