Under certain conditions, which are stated and discussed, columns of agglutinated red cells develop in small systemic vessels. The intravascular agglutination is reversible, but in some instances the de-agglutination fails to occur and primary infarction results. A primary infarct in the nasal lining may become infected to cause coryza, sniffles or distemper. In other instances de-agglutination is complete after a few sees. In still other instances the de-agglutination is so incomplete that small clusters of erythro-cytes circulate away into the veins as fragile emboli. The more stable of these fragile emboli sometimes reach the arterial side in a mammal by passing through the pulmonary capillaries. Some of them may pass antidromically through some of the many arteriovenous anastomoses in the very young kangaroo. The emboli are too fragile in the tadpole and frog to cause infarction, but they can occlude post-reticular endarteries and also small arterial anastomoses of complex arterial networks in a mammal and cause petechial infarcts, which coalesce, in some instances, forming relatively massive ones. The fragile emboli are washed and hammered to pieces by the blood whenever they lodge in either a prereticular or a relatively prereticular endartery. Most of the infarcts in the body are probably caused by these fragile emboli.