Extramedullar hematopoiesis in acute murine toxoplasmosis

Acute murine toxoplasmosis induced by the virulent RH strain of the obligate intracellular parasite Toxoplasma gondii , leads to various pathological changes in the whole organism and ultimately lethal outcome. As significant changes occur within the hematopoietic system, the aim of the study was to assess the role of extramedullary hematopoiesis in the host defense reaction. Acute infection was obtained in CBA mice by intraperitoneal injection of 2 × 10 2 tachyzoites. Changes in the number of granulocyte-macrophage (CFU-GM) and erythroid (BFU-E and CFU-E) progenitor cells, were evaluated in the liver and spleen. Specimens of the spleen and the liver were histopathologically examined by light and electron microscopy. The results obtained demonstrated significant changes in the number of different splenic hematopoietic cells from the 3rd hour of toxoplasmic infection onward, together with histologically confirmed myeloid, erythroid and megakaryocytic hyperplasia in the spleen. Analysis of the liver specimens revealed significant extramedullary hematopoiesis within hepatic lobules. The changes observed during acute toxoplasmosis confirmed the presence of greatly stimulated hematopoiesis, which is not confined to the spleen, an active hematopoietic organ in mice, but also present in the liver which is normally postnatally devoid of hematopoiesis. The liver hematopoietic involvement suggests that the host defense system during a massive severe infection such as toxoplasmosis activates all hematopoietic mechanisms available, including those that are normally operative only during fetal life.