Many pathogenic strains of bacteria producing acute infection in man are characterized by capsules or surface factors which resist phagocytosis.' Differences in antigenic structure of these surface components have allowed separation of individual pathogenic strains and study of the role of specific antibody in resistance to, or recovery from, infections caused by these microbial species. To date, no satisfactory serologic procedures have been available for differentiating individual strains of pathogenic staphylococci, and the role of humoral immunity in resistance to staphylococcal infection or the course of straphylococcal disease has remained uncertain. In 1959, Cohn and Morse showed that certain pathogenic staphylococci resist phagocytosis.2 In the majority of their studies the Smith staphylococcus was used as a prototype strain. Koenig has recently confirmed and extended these observations in an experimental mouse infection using two variants of the Smith strain.' These findings suggested that pathogenicity among staphylococci might relate to possession of specific surface or capsular factors analogous to those characterizing other pyogenic cocci. Subsequent studies showed that phagocytosis resisting components could be extracted from the Smith strain,' that specific antibody was required for rapid ingestion of the diffuse variant of the Smith staphylococcus,2' ' that the phagocytosis promoting antibody was present in human sera,"6' and that antibody was not removed by absorption with other microorganisms or certain strains of staphylococci.5 Because of this suggestive specificity, experiments were undertaken to determine whether systems containing appropriate sera and living leukocytes would permit "typing" of pathogenic staphylococci in the same way the bacteriocidal test is used to detect type-specific antibody directed against Group A streptococci.7'