Epidemic hemorrhagic fever was discovered and studied independently by Russians and Japanese in the Amur R. basin before and during World War n. It is an infectious disease caused by a filterable agent to which the usual laboratory animals are not susceptible. This infection is probably mite borne. Characteristically, there is a bimodal incidence with one wave in spring and another higher peak in the fall. The disease appeared in typical fashion in UN Forces in Korea in 1951. Clinically, severe cases show acute fever, purpura, shock, and acute renal failure. A leukemoid blood picture is common. Most of the fatalities (88%) occur within the first 2 weeks. Death is usually due to shock in the early stages with uremia a factor later. Basic morphological changes consist of (a) marked engorgement, increased permeability, and rupture of capillaries; (b) focal necrosis suggestion infarction in kidney, pituitary, adrenal, pancreas, and liver; and (c) a cellular reaction by tissue phagocytes, lymphocytes, and immature granulocytes. The swollen kidney with hemorrhagic pyramids, pale cortex, and peripelvic hemorrhage is most characteristic. Marked medullary congestion, findings similar to lower nephrons nephrosis, and central necrosis of structures in the pyramid are common. The enlarged boggy pituitary and hemorrhagic right atrium are striking. Extensive necrosis of the anterior lobe and focal myocarditis are often seen. Neither these findings nor focal adrenal hemorrhage, which is not uncommon, fully explain the severe shock seen.