In ordinary cases of pyæmia the occurrence of internal _phlebitis_ or _arteritis_ with the inevitable thrombosis is an important step in causation. Any inflammation of the inner coat of the vessel leads promptly to the formation of a coagulation of the contained blood, and blocking of the lumen. Beginning on the diseased or abraded surface, the clot forms backward along the line from which the blood normally comes (proximal in the arteries; distal, in the veins), until it reaches the next considerable colateral branch. The clot is firmly adherent to the intima except at the free end, which is conical and projects into the blood current. If small portions are detached from the thrombus and washed on in the blood stream they become arrested when they reach a vessel too small to admit them, it may be a smaller artery, or it may be a capillary, and always in the line of the circulation,—from the systemic circulation to the lungs, or from the lungs to the system at large. This is =embolism=. Wherever arrested, the contact of the leucocytes and hæmatoblasts with the inner coat of the vessel, leads to metabolic changes and firm adhesion, and the pus microbes in the clot determine suppuration and abscess. Eberth and Schimmelbusch have shown that the hæmatoblasts, even more than the other blood elements, when acted on by the pus microbes become viscous and stick not only to each other, but to any floating body, and to the inner serous coat of the vessel, particularly when the latter has been abraded or injured. This clumping together of the hæmatoblasts forms white clots which block the smaller vessels, but in the viscous condition they further the coagulation of the fibrine, and again when they come in contact with the intima, instead of passing through, or moving on, they remain adherent and start the formation of thrombi. This is above all common in given tissues, and the medulla of bone has in this respect a bad preëminence, so that acute suppurative osteomyelitis, is a familiar lesion and is liable to become chronic, and determine distant abscesses and general infection long after. The thrombus thus formed is an infective coagulum, tending to constant encrease, as the clot is a favorable culture-field for the microbes, and the tendency is to coagulate more and more of the adjacent blood. It tends further to disintegration, as the action of the microbes and their toxins on the leucocytes, transforms these into pus cells, inducing softening of the mass, and the washing on of individual infective pus cells and minute portions of the clot to form infective centres and abscesses at distant parts. If the pathogenesis of the invading microbe is weak and the resistance of the leucocytes potent, such clots may remain circumscribed or may even be absorbed, but in the opposite conditions with potent and numerous microbes and abundant and effective toxins, the disposition is not only to a continuance of infection, but to an acute febrile pyæmia.