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Lymph node hemophagocytosis in rickettsial diseases: a pathogenetic role for CD8 T lymphocytes in human monocytic ehrlichiosis (HME)?

DOI: 10.1186/1471-2334-6-121

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To study histopathologic responses in the lymphatic system for correlates of immune injury, lymph nodes from patients with HME (n = 6) and RMSF (n = 5) were examined. H&E-stained lymph node tissues were examined for five histopathologic features, including hemophagocytosis, cellularity, necrosis, and vascular congestion and edema. The relative proportions of CD68 macrophages, CD8 and CD4 T lymphocytes, and CD20 B lymphocytes were evaluated by immunohistochemical staining.Hemophagocytosis was similar in HME and RMSF, and was greater than in control cases (p = .015). Cellularity in HME was not different from controls, whereas RMSF lymph nodes were markedly less cellular (p < 0.002). E. chaffeensis-infected mononuclear phagocytes were infrequent compared to R. rickettsii-infected endothelial cells. More CD8 cells in lymph nodes were observed with HME (p < .001), but no quantitative differences in CD4 lymphocytes, macrophages, or B lymphocytes were identified.Hemophagocytosis, CD8 T cell expansion, and the paucity of infected cells in HME, suggest that E. chaffeensis infection leads to macrophage activation and immune-mediated injury.The tick-borne obligate intracellular bacteria Ehrlichia chaffeensis and Rickettsia rickettsii are the causes of human monocytic ehrlichiosis (HME) and Rocky Mountain spotted fever (RMSF) diseases, respectively [1]. E. chaffeensis is transmitted by the Lone Star tick, Amblyomma americanum, and human infection typically presents with fever, myalgias, pancytopenia, and mild to moderate elevation of serum transaminases [2]. This clinical presentation is easily confused with that of RMSF, which typically presents with fever, rash, and headache. R. rickettsii is known to infect endothelial cells, leading to direct rickettsia-mediated vascular injury accompanied by a vigorous but protective Th1 immune response [3]. E. chaffeensis is known to infect cells in the monocyte/macrophage lineage, but the pathogenesis of HME is less clear [4]. Lymphohist


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