Rôle of Coagulating Principle of Staphylococcus Aureus in Relation to Invasiveness of this Microorganism. ∗

Previous studies by one of us had shown that the localizing property of Staphylococcus aureus was referable to its ability to induce a powerfully injurious reaction in tissues inoculated with it. The severe injury to the capillaries, by increasing their permeability, doubtless allowed plasma proteins, including fibrinogen, to pass out into the inflamed area and be deposited there as coagulated plasma. The intense damage on the part of the pathogenic organisms to the draining lymphatics induced their early occlusion by the formation of fibrinous thrombi. The infected area became thus “walled-off” as early as one hour following the inoculation of the staphylococcus organism. 1 Trypan blue injected into such an area failed at this stage to diffuse to the tributary lymphatic vessels. Similar results were obtained with the Berkefeld filtrate of this microorganism. 2 , 3 These results were in marked contrast to the delayed fixation of the dye found in the case of hemolytic streptococcus infection. In skin areas of rabbits inoculated with the latter organism, the lymphatic channels maintained their patency for almost 2 days before the inflammatory reaction became sufficiently intense to induce lymphatic blockage. 1 The conclusion was drawn that the Staphylococcus aureus is primarily a non-invading organism owing to its intense local effects which cause it to be circumscribed promptly by the formation of a mechanical barrier in the form of a fibrinous meshwork as well as thrombosed lymphatics in tissues distended with edema. The generalized systemic effects caused by the hemolytic streptococcus was referred to the relatively mild local effects produced by this organism which thus allowed its relatively free dissemination into the regional lymphatic vessels.

A number of authors including Much, Gratia, Gross, and Gengou, have shown that the Staphylococcus aureus organism and the filtrate of its culture are capable of causing oxalated blood to clot in the test tube.