RESUMO
Babesia is a malaria-like protozoan parasite spread by Ixodes ticks primarily from the white-footed deer mouse to humans. Typically it causes subclinical disease, but occasionally causes acute febrile disease with hepatosplenomegaly. We report a case of spontaneous splenic rupture of a 56-yr-old man with acute Babesia microti infection.
Assuntos
Babesia microti/patogenicidade , Babesiose/complicações , Parasitemia/transmissão , Ruptura Esplênica/patologia , Animais , Babesiose/parasitologia , Humanos , Masculino , Pessoa de Meia-Idade , Ruptura Espontânea , Ruptura Esplênica/etiologia , Tomografia Computadorizada por Raios XRESUMO
Monocyte chemoattractant protein-1 (MCP-1) is a pro-inflammatory chemokine believed to play a major role in atherogenesis. Injured endothelial cells express MCP-1, which attracts monocytes to the blood vessel wall and leads to the formation of atheromas. Cytomegalovirus infection may also play a role in atherogenesis and accelerates inflammation in tissues that overexpress MCP-1. To examine the relationship of cytomegalovirus infection and MCP-1, we infected MCP-1 transgenic mice with murine cytomegalovirus (MCMV) and collected serum 6 days post-infection to evaluate TH1-related cytokine levels by ELISA. Serum levels of IL-10, IL-12 and IFN-gamma were increased in MCP-1 transgenic mice on day 6 following MCMV infection, while levels of IL-1beta and TNF-alpha were undetectable. However, MCP-1 serum levels were reduced >50% in MCP-1 transgenic mice following MCMV infection compared to uninfected transgenic mice. This effect was not as dramatic when an M33 null MCMV was administered to MCP-1 transgenic mice. The mechanism by which MCMV lowers serum MCP-1 levels is unknown, but this effect may enhance the survival of the virus and thus allow CMV to contribute to the chronic inflammation of atherogenesis.
