Ten cattle were infected with Theileria parva, the cause of East Coast fever (ECF), and serially killed to investigate the origin of parasitized lymphoblasts (PL), routes of their metastasis and lymph node changes. Histological examination of 13 selected lymph nodes from each call revealed non-specific changes including germinal centre development and regression, paracortical hyperplasia and plasmacytosis. Changes characteristic of T. parva infection included: large numbers of PL in the paracortical zone, sinuses, medullary cords and stroma; and terminal necrosis. These changes appeared first and were most marked in the parotid node draining the inoculation site and were least obvious in the mesenteric node. Ultrastructurally, lymphoblasts containing schizonts of T. parva were remarkably similar to phytohaemagglutinin-stimulated bovine lymphocytes. Although no early stages of T. parva were identified in phagocytic cells, possible pre-schizont forms were found in lymphoid cells of the parotid node of calves killed 7 and 9 days after inoculation, indicating that the parasite may actively invade lymphocytes. Electron microscopy of lymph nodes in early ECF revealed proliferation of non-parasitized lymphoblasts in the paracortical zone, marked plasmacytosis (two plasma cells were in mitosis) and little evidence of reticulum cell hyperplasia. Later in the disease, schizont-containing lymphoblasts, often in mitosis and occasionally degenerating, were present in the paracortical zone, in all the sinuses, within the trabeculae and in the medullary cords. Free schizonts were numeruous. As intracellular schizonts matured, they became more electron-dense, and eventually formed merozoites. It was concluded that parasitized lymphoblasts drain from infected local lymph nodes by efferent lymphatics to the tracheal lymph duct, whence they enter the blood. Their route of exit from the blood to the general body nodes was not determined.