Despite its apparently strict granulocytotropism, thrombocytopenia is a consistent hallmark of infection with the agent of human granulocytic ehrlichiosis (HGE), regardless of host species. Laboratory mice are valuable models of HGE agent infection kinetics and immunity, but initial studies of HGE infection in mouse models have failed to demonstrate thrombocytopenia. More thorough analysis of platelet kinetics, however, reveals a consistent and rapid, marked decrease (50% decline by day 2-4 after infection) in circulating platelet number in both C3H/HeN and C57BL/6J mice during infection with the HGE agent. The roles of splenic consumption and immune-mediated destruction were evaluated as potential mechanisms of the thrombocytopenia. Both splenectomized mice and mice with severe combined immunodeficiency (lacking B and T lymphocytes) became similarly thrombocytopenic in response to infection with the HGE agent. This study validates the appropriateness of the mouse as a model of HGE, including its usefulness for the investigation of thrombocytopenia.
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health