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. 1981 Dec;15(12):1525-9.
doi: 10.1203/00006450-198112000-00015.

Type III group B streptococcal strain differences in susceptibility to opsonization with human serum

Type III group B streptococcal strain differences in susceptibility to opsonization with human serum

G W Fischer et al. Pediatr Res. 1981 Dec.

Abstract

Human serum opsonins to type III Group B streptococci (GBS) were studied in an in vitro opsonophagocytic assay. Two type III GBS test strains were susceptible (893 and IIINor) and two resistant (891 and 892) to opsonization by the majority of sera from 15 healthy adults. Four individuals with undetectable or low opsonic titers to the test strains were immunized with pneumococcal vaccine; immunization with pneumococcal vaccine induced a titer rise in all but one instance when susceptible GBS strains were tested. In contrast, only a single titer rise was detected when resistant GBS strains were employed in the test. These results indicate that immunization with a cross-reacting antigen (identical to core antigen of type III GBS) fails to induce opsonic antibody to all strains of type III GBS. A resistant strain was made highly susceptible to neutrophil killing in vitro by exposure to neuramindase prior to incubation with opsonic serum. Using a fluorescent lectin-binding assay, this enzyme appeared to remove surface sialic acid, suggesting that sialic acid is an antiphagocytic factor. However, the possibility that other surface moieties may act as antiphagocytic factors cannot be ruled out. Both opsonic susceptible and resistant strains absorbed opsonic antibody from serum, which suggests that the GBS antiphagocytic factors do not prevent binding of antibody to resistant bacteria. These findings indicate that demonstration of serum opsonic activity to one strain of type III GBS may not accurately depict opsonic activity to other strains. In addition, immunization with core antigen did not enhance opsonic activity against all GBS strains. These data also point out the need to use assays which measure functional antibody, since demonstration of antibody binding may not reflect its ability to facilitate bacterial phagocytosis and killing.

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