Endothelial cell changes are associated with pulmonary edema and respiratory distress in mice infected with the WA1 human Babesia parasite

A C3H/HeN mouse model was established to study the pathogenesis of the huma n babesial parasites, WA1 and Babesia microti. To evaluate the course of pa rasitemia and the associated lesions, mice were inoculated intraperitoneall y with either WA1-infected, B, microti-infected, or uninfected hamster red blood cells. WA1-infected mice developed dyspnea and moderate parasitemias, after which death occurred. Babesia microti-infected mice experienced low parasitemias with no apparent morbidity or mortality. WA1-infected mice wer e thrombocytopenic but not anemic. Hemograms for B. microti-infected mice w ere similar to controls. Postmortem examination of WA1-infected mice reveal ed prominent lesions in the lungs, including pulmonary edema and intravascu lar margination of leukocytes. No pulmonary changes were detected in B. mic roti-infected mice. Blood gas measurements of WA1-infected mice showed redu ced oxygen saturation and pH, and increased carbonic acid compared to contr ols, indicating hypoxia and respiratory acidosis. Ultrastructure studies of WA1-infected lungs showed hypertrophied endothelial cells containing trans cellular channels associated with protein-rich intra-alveolar fluid. Endoth elial cell activation was demonstrated by an upregulation of intercellular adhesion molecule-1 in the lungs of WA1-infected mice. The results suggest that recruitment of inflammatory cells to the lungs in WA1-infected mice in duces endothelial cell alterations, leading to pulmonary edema and acute re spiratory failure.