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

Abstract

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.

Phenotypic evaluation of acapsular transposon mutants of Vibrio vulnificus

“…An increase in the degree of encapsulation for other bacterial species correlates with a decrease in hydrophobicity (1,8,15). We were able to detect differences in cell surface hydrophobicity by examining the relative solubility of isolates in ammonium sulfate.…”

Identification of a genetic locus essential for capsule sialylation in type III group B streptococci

“…That type III strains are disproportionately prevalent among GBS associated with invasive disease suggested that the type III capsule serves as a virulence factor. This hypothesis was supported by the observation that type III isolates from the blood or cerebrospinal fluid of ill infants were more highly encapsulated than were colonizing strains (16). More direct evidence for the role of the type III capsule in virulence came from our studies of an unencapsulated mutant strain of type III GBS: loss of capsule expression was associated with loss of virulence in a neonatal rat model of GBS infection (26).…”

“…The type III capsular polysaccharide of GBS has been shown to be an important virulence determinant (1,6,16,26). The presence of sialic acid residues on the surface of the organisms inhibits activation of the alternative pathway of complement.…”

Serotypes and clinical manifestations of invasive group B streptococcal infections in western Sweden 1998-2001

“…Serotypes Ia, Ib, II and III have predominated in many parts of the world [6,12], but serotype V has emerged as an increasingly important pathogen [5,7]. Serum antibodies against the capsular polysaccharide provide type-specific protection against invasive GBS infections [13][14][15][16]. The high morbidity and mortality of invasive GBS infections has made the development of a multivalent conjugate polysaccharide vaccine a major focus for research [17][18][19][20][21][22][23].…”