The ability of Staphylococcus aureus to produce coagulase has customarily been taken as an in vitro reaction indicating potential virulence for this organism. Evidence for the existence oi f 2 different kinds of coagulase was first reported by Duthie( 1 ) . The soluble coagulase causes clotting of plasma (fibrinogen) in presence of an accessory factor, whereas the bound coagulase causes clumping of the organism by plasma or fibrinogen alone. It is of interest to determine if either kind of coagulase is of itself an essential virulence factor. This was done by selecting a strain of S. azmzts known to be virulent for rabbits and possessing both kinds of coagulase. Mutants lacking either kind of coagulase were then derived from this strain and checked for virulence in rabbits. A simultaneous loss of virulence could possibly indicate a direct relationship with the particular missing coagulase, whereas if the mutant retained its virulence in the absence of a coagulase then this factor could not be essential for virulence. The parent strain, S. aweus 182, used in these experiments, was chosen because i t polssessed several possible virulence factors, including the soluble and bound coagulases, alpha and delta hemolysins, leucocidin activity, hyaluronidase and fibrinolysin. It was sensitive to penicillin, streptomycin, and other antibiotics and was of the phage type 42 B/52/80/81. This strain was originally isolated from the human nasopharynx and was virulent for rabbits.Materials and methods. To isolate coagulase negative mutants, 6 hour old cultures of S. uureus strain 182 grown in trypticase soy broth were washed with saline and subjected to 1JV irradiation sufficient to reduce the population to 1 % survival. The irradiated suspensions were then diluted and spread on trypticase soy agar containing 1.5% human plasma. On this medium coagulase positive

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The presence of fresh serum has been shown to be required for rapid phagocytosis and intracellular killing of virulent staphylococci by human blood leukocytes (1, 2). When human serum is subjected to heating, it no longer promotes killing but still causes demonstrable phagocytosis, though slower in rate and reduced in amount. The phagocytosis-promoting ability of human serum is apparently dependent upon the presence of antibody against the staphylococcal surface antigen or antigens and is removed by adsorption with ribitol teichoic acid isolated from the staphylococcal cell wall (3). The present report deals with the results of our study on the heat-labile serum factor responsible for rapid phagocytosis and intracellular killing of staphylococci. MATERIALS AND METHODS. Human serum and leukocytes. Fresh samples of adult human blood were obtained from healthy subjects by venipuncture. Leukocytes were prepared by dextran sedimentation and were washed and resuspended in Hanks' solution.