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Review
, 12 (4), 518-53

Q Fever

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Review

Q Fever

M Maurin et al. Clin Microbiol Rev.

Abstract

Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of >/=1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.

Figures

FIG. 1
FIG. 1
Phylogenetic tree showing the relationships of C. burnetii to other species belonging to the Proteobacteria. The tree was constructed by the neighbor-joining method with 16S rRNA gene sequences.
FIG. 2
FIG. 2
Doughnut granuloma (arrow) in a liver section from a patient with acute Q fever hepatitis. Hematoxylin-phloxin-saffron stain. Magnification, ×250.
FIG. 3
FIG. 3
Chest X ray of a patient with Q fever pneumonia.
FIG. 4
FIG. 4
Magnetic resonance image of Q fever meningoencephalitis.
FIG. 5
FIG. 5
Q fever endocarditis. Immunohistochemistry on cardiac valve, using immunoperoxidase staining, reveals the presence of C. burnetii (arrow). Magnification, ×100.
FIG. 6
FIG. 6
P388D1 macrophage-like cells chronically infected with C. burnetii Nine Mile strain. Cells containing large vacuoles full of bacteria are visible on the Gimenez stain (arrow). Magnfication, ×400.

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