Observations on the Pathogenesis of the Myeloid Leucemia of Fowls. ∗

Abstract

In a preceding communication 1 a new transmissible strain of leucemia has been briefly described. In the subsequent passages of this strain several of the inoculated birds died of intercurrent diseases chiefly of an acute or subacute inflammatory process of the upper respiratory tract. Birds dying of such infections but not inoculated with leucemic material did not show the pathological changes characteristic for the leucemias. The early death of several birds permitted a study of the pathogenesis of myeloid leucemia. A conspicuous result is obtained when the sequence of events in the development of the organ and blood changes is reconstructed from the following table which includes all the autopsies of 2 recent passages.

An extensive hyperplasia of the bone marrow unaccompanied by a rise in the number of the circulating white blood corpuscles appears to be the first marked pathological change which follows the inoculation of leucemic blood (Stage I). The hyperplasia of the bone marrow consists of an enormous extravascular proliferation of myelocytes and their precursors replacing the fatty tissue and narrowing the blood sinuses. Following this alteration of the bone marrow there is a rise in the number of white corpuscles in the peripheral circulation due to an invasion of cells similar to those found in the bone marrow, but extramedullary blood formation is absent (Stage II). There is a tendency for a further increase of the immature granulocytic elements in the blood stream, a concentration of the latter in the smaller blood vessels (leucostasis) and the development of extramedullary granulocytopoeitic foci (Stage III). The organs most commonly involved are the liver and the spleen. In the liver, the myeloid tissue begins to proliferate in the periportal connective tissue about the adventitia of the vessels extending by extra-vascular growth.