An in vitro assay was used to study the adherence of Neisseria meningitidis to human buccal epithelial cells. Both unencapsulated and encapsulated, piliated isolates obtained from throats of asymptomatic carriers demonstrated significantly higher levels of adherence to buccal cells than encapsulated, piliated isolates obtained from the blood and cerebrospinal fluid of patients (P < 0.001). Meningococcal adherence to buccal cells could not be correlated to a specific capsular polysaccharide serogroup, outer membrane protein serotype, or quantitative differences in pili. However, the data suggested that capsular polysaccharide impedes the adherence of meningococci to buccal cells, and the significantly smaller amount of capsular polysaccharide extracted from carrier isolates compared with case isolates (P < 0.001) could explain differences in meningococcal adherence to buccal cells. Increased adherence may facilitate host colonization, promote nasopharyngeal carriage, and possible reflect altered pathogenicity.
We studied seven strains of group G streptococci isolated from clinically severe bacteremic infections in six intravenous drug abusers. These group G strains multiplied luxuriantly in fresh human blood. On electron microscopy, they exhibited surface fibrillae similar to those observed in M-protein-rich group A streptococci, but they were not serologically M typable with a battery of 39 M antisera. Rabbit antisera raised against two of the group G strains (1618 and 1750) opsonized the homologous but not the heterologous isolates and exhibited type-specific Ouchterlony immunoprecipitin reactions. Moreover, antisera raised against peptic extracts of strain 1750 also promoted phagocytic killing of that strain. Anti-1750 reacted in high titer in an enzyme-linked immunosorbent assay against peptic extracts of the homologous strain; these antibodies were removed by absorption with 1750 cells but not by absorption with heterologous strains. These studies represent, to our knowledge, the first analysis of virulence factors of group G streptococci isolated from invasive human disease. The seven epidemiologically related blood isolates of group G streptococci possess distinct type-specific, antiphagocytic surface virulence factors analogous to the M proteins of group A streptococci.
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