INTRACELLULAR SURVIVAL AND REPLICATION OF ERYSIPELOTHRIX-RHUSIOPATHIAE WITHIN MURINE MACROPHAGES - FAILURE OF INDUCTION OF THE OXIDATIVE BURST OF MACROPHAGES

We investigated the ability of a virulent wild-type parent strain and acapsular avirulent transposon mutants to enter and survive intracellu larly within murine peritoneal macrophages. In the presence of normal or immune serum, the parent and mutant strains were both ingested; how ever, the number of ingested bacteria was three- to fourfold greater i n the case of the mutant strains than in the case of the parent strain , The parent strain, but not the mutant strains, survived and replicat ed intracellularly when ingested in the presence of normal serum, wher eas both the parent and the mutant strains were readily killed when in gested in the presence of immune serum, To further investigate the mec hanism by which the parent strain can survive and replicate within mac rophages, we studied the oxidative burst response of macrophages to th ese strains by measuring chemiluminescence and intracellular reduction of Nitro Blue Tetrazolium dye, Challenge exposure of macrophages with either the parent strain preopsonized with immune serum or the mutant strains preopsonized with normal or immune serum induced a strong oxi dative burst, whereas the level was very low when the parent strain wa s preopsonized with normal serum, Phagocytosis of either the parent st rain, in the presence of immune serum, or the mutant strains, in the p resence of normal or immune serum, by macrophages reduced large amount s of intracellular Nitro Blue Tetrazolium, whereas minimal amounts wer e reduced by the parent strain in the presence of normal serum, These results suggest that virulent E. rhusiopathiae can survive and subsequ ently replicate within murine macrophages when ingested in the presenc e of normal serum and that the reduced production of reactive oxidativ e metabolites by macrophages may, in part, be responsible for this occ urrence.