CMR FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Maurin, M.
Right arrow Articles by Raoult, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Maurin, M.
Right arrow Articles by Raoult, D.

Clinical Microbiology Reviews, October 1999, p. 518-553, Vol. 12, No. 4
0893-8512/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Q Fever

M. Maurin and D. Raoult*

Unité des Rickettsies, CNRS UPRES A 6020, Université de la Méditerranée, Faculté de Médecine, 13385 Marseilles Cedex 5, France

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.

* Corresponding author. Mailing address: Unité des Rickettsies, CNRS UPRES A 6020, Université de la Méditerranée, Faculté de Médecine, 27 Blvd. Jean Moulin, 13385 Marseilles Cedex 5, France. Phone: (33) 4 91 32 43 75. Fax: (33) 4 91 32 03 90. E-mail: Didier.Raoult{at}medecine.univ-mrs.fr.

Clinical Microbiology Reviews, October 1999, p. 518-553, Vol. 12, No. 4
0893-8512/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Antimicrob. Agents Chemother. Clin. Vaccine Immunol.
J. Clin. Microbiol. ALL ASM JOURNALS

Copyright © 1999 by the American Society for Microbiology. All rights reserved.