Given that the lungs are a major organ for O. tsutsugamushi infection in humans and in different animal models, and that elevated ratios of ANG2/ANG1 transcripts are pathological hallmarks in lethal infection models [17, 35], we hypothesize that dysregulated pulmonary inflammation and Tie2/Ang2-mediated endothelial dysfunction contribute to disease pathogenesis at late stages of O. tsutsugamushi infection. Here, TEK is linked to endothelial dysfunction.