Role of Blocking Antibody in Disseminated Gonococcal Infection

Open Access
Publisher Website
Google Scholar
Abstract
Gonococci (GC) isolated from patients with disseminated infection (DGI) are uniformly resistant to killing by normal human serum (NHS), but are killed in large numbers by normal rabbit serum (NRS). Since resistance to human serum is necessary for DGI, we examined the mechanism of resistance by GC to NHS. Our bactericidal assay exposes 10-fold dilutions of 108 plate-grown GC/ml to undiluted serum and measures the number of GC the serum can kill. Killing is expressed as the reduction in GC compared with paired, heat-decomplemented controls. NRS sterilized >105 GC/ml of six DGI strains. When NRS was mixed (1:1) with nonbactericidal NHS, killing was reduced to <103 GC/ml. This potent inhibitor of rabbit serum could be adsorbed to preincubated and washed GC. The heat (65°C) lability of the inhibitor suggested blocking antibody. Human cord serum containing maternal IgG, but no IgM or IgA, blocked rabbit serum as effectively as normal adult or matched maternal serum. IgG fractions added to rabbit serum reduced killing of DGI strains, but IgM and IgA did not. Absorption of NHS with resistant strains increased killing of the same and other resistant strains and removed the ability to block killing by rabbit serum. Absorption with sensitive strains decreased killing. Thus, resistant strains adsorb blocking antibody and sensitive strains adsorb killing antibody. We conclude that NHS contains an IgG blocking antibody that competes with natural bactericidal antibody in man and rabbits. We believe that natural IgG binds to certain gonococci possessing the appropriate receptor and enables them to disseminate in the blood by protecting them from killing by antibody and complement.