The most conspicuous clinical finding during the course of this virus disease is a fulminating panleucopenia. The earliest significant decrease noted is usually in the number of the lymphocytes. From the study of lymph nodes and bone marrow during the incubation period and throughout the illness, it appears that failure of leucopoiesis is the cause of leucopenia. Inclusion bodies in the primitive blood cells of the marrow suggest a direct action of the virus on these cells. When recovery occurs a marked myelogenous leucemoid response is noted.
Available data indicate the presence of a mild anemia due to a failure in erythropoiesis, less marked than the leucopenia probably because of the longer life of the adult circulating erythrocytes. The erythrocytes appear to have an increased fragility and the serum has a slight increase in icterus, suggesting an increased mean erythrocyte age. During recovery erythropoiesis does not begin until after the myeloid marrow response has begun to subside, due possibly to previous mechanical crowding of the marrow by the more rapidly growing myeloblasts and myelocytes.