The potent heat-labile bactericidal property of fresh mammalian defibrinated blood or serum in vitro has been known since the studies of Nuttall (1) and Buchner (2) over 70 years ago. By 1928, it had been shown that serum components very like those of complement were necessary for this action (3). Although a number of investigators in the fields of bacteriology and immunology have interested themselves in this bactericidal power of fresh serum, little notice has been taken of it in clinical medicine, probably, as noted elsewhere (4), because it has been believed to be of doubtful effect in vivo.

Interest has been revived in the bactericidal ac-tivity of serum by the work of Pillemer, Wardlaw and associates (5, 6). They described a normally occurring serum protein of large molecular weight which they named properdin. They attributed the bactericidal property of serum, in part at least, to the presence of properdin, which acted with the four components of complement in the presence of magnesium to kill the bacteria. The findings of Wardlaw and Pillemer (6) confirmed those of Mackie and Finkelstein (7) that the bacterial strains sensitive to the effect of serum are principally from species of gram-nega-tive bacilli and that the degree of sensitivity is a characteristic of the strain rather than of the genus. However, whereas Wardlaw and Pillemer have described the action of the properdin system as being nonspecific and unrelated to antibody, Mackie and Finkelstein presented data showing that the absorption of a serum in the cold by a sensitive strain resulted in the removal of the killing effect only for that strain, leaving the effect