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To the Editor: Coxiella burnetii, a strict intracellular bacterium, is the etiologic agent of Q fever, a worldwide zoonosis. Humans are infected by inhaling contaminated aerosols from amniotic fluid or placenta or handling contaminated wool (1). The bacterium is highly infectious by the aerosol route. Two forms of the disease are typical: acute and chronic. Acute Q fever is the primary infection and in specific hosts may become chronic (1,2). The major clinical manifestations of acute Q fever are pneumonia and hepatitis. Less common clinical manifestations are aseptic meningitis and/or encephalitis, pancreatitis, lymphadenopathy that mimics lymphoma, erythrema nodosum, bone marrow necrosis, hemolytic anemia, and splenic rupture (2). The main clinical manifestation of the chronic form is culture-negative endocarditis, but infection of vascular grafts or aneurysms, hepatitis, osteomyelitis, and prolonged fever have also been described (1,2). Fluoroquinolones, co-trimoxazole, and doxycycline are active against C. burnetii in vitro, and ceftriaxone has been shown to have a bacteriostatic effect and could be effective in the phagolysosome of C. burnetii–infected cells (3). However, the treatment of choice for Q fever is doxycycline.
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Suputtamongkol et al. (2003) studied this question.
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