Bacterial genetics and human immunity to group B streptococci

Serotype III group B Streptococcus agalactiae (GBS) are the most common cau se of neonatal sepsis and meningitis. We have classified type III GBS by re striction digest patterns of chromosomal DNA and demonstrated that a subgro up of genetically related strains (RDP type III-3) causes the majority of t ype III GBS neonatal infection. Genetic differences between type III GBS st rains contribute significantly to differences in virulence and host immune responses. While 100% of less virulent RDP type III-1 and III-2 organisms e xpress C5a-ase, an inhibitor of neutrophil chemotaxis, only 63% of virulent RDP type III-3 isolates have functional C5a-ase, Functional differences in type III GBS C5a-ase are attributable to a shared genetic polymorphism, su pporting our genetic classification. The mean capsular sialic acid content of virulent RDP type III-3 strains is significantly higher than that of les s virulent strains, suggesting that capsular sialylation is also geneticall y regulated, C5a-ase is not critical for all RDP type III-3 strains to be i nvasive because the higher capsular sialic acid content of III-3 strains li mits complement activation. The identification of these and additional gene tic differences between GBS strains has important implications for our unde rstanding of the pathogenesis of these important human infections. (C) 2000 Academic Press.