Impaired chemotaxigenesis by type III group B streptococci in neonatal sera: relationship to diminished concentration of specific anticapsular antibody and abnormalities of serum complement.

A chemotaxigenesis (CTG) assay employing adult or neonatal sera, type III group B streptococci (GBS) and polymorphonuclear leukocytes (PMNs) was designed to evaluate the role of PMN mobilization in the pathogenesis of type III GBS infection in neonates. Generation of C5a in healthy adult sera with moderate-high (3-40 micrograms/ml) or low (less than or equal to 2 micrograms/ml) levels of specific anticapsular antibody was confirmed by PMN aggregometry and by the neutralization of CTG by goat anti-human C5. CTG was significantly (P less than 0.001) greater in high as compared to low specific antibody-containing adult sera; stepwise increases in CTG occurred when specific IgG was added to untreated, but not heat-inactivated, hypogammaglobulinemic serum. Immunospecificity of CTG was shown by a failure of type III GBS to generate C5a in heterologous (type Ia) high antibody sera. Mean CTG values in three high and 16 low antibody-containing sera from healthy term neonates were 24% and 62% of high (P less than 0.001) and low (P less than 0.01) antibody adult sera, respectively. The addition of both complement and specific IgG to low antibody-containing neonatal sera was required to enhance their CTG activity to high antibody adult values. CTG by type III GBS in neonatal sera-neonatal PMN mixtures was only 25% (high antibody sera) and 14% (low antibody sera) of values for paired maternal sera mixtures reacted with adult PMNs (P less than 0.001). These studies demonstrate that CTG by type III GBS in neonatal sera is markedly diminished and that low concentrations of specific anticapsular antibody and abnormalities of complement function contribute to impaired PMN mobilization in human neonates.