Coxiella burnetii, the causal agent of Q fever, is found worldwide (the “Q” stands for “query” because the cause of the fever was unknown for many years). It has several features that distinguish it from other rickettsia. For example: 1) It grows in cytoplasmic vacuoles and seems to be stimulated by the low pH of a phagolysosome, being resistant to the host degradative enzymes within that structure; 2) it is extremely resistant to heat and drying and can persist outside its host for long periods; and 3) it causes disease in livestock, such as cattle and in other mammals, but is not transmitted to humans by arthropods. Although the organism has been reported to be recovered from ticks, human infection usually occurs following inhalation of infected dust in, for example, barnyards and slaughterhouses (a transmission route made possible because of the ability of C. burnetii to withstand drying). [Note: C. burnetii has also been known to enter the body via other mucous membranes, abrasions, and the gastrointestinal tract through consumption of milk from infected animals.]

A. Clinical significance

C. burnetii reproduces in the respiratory tract and then (in the absence of treatment) is disseminated to other organs. Clinical illness takes several forms. Classic Q fever is an interstitial pneumonitis (not unlike some viral or mycoplasmal illnesses) that may be complicated by hepatitis, myocarditis, or encephalitis. C. burnetii should also be considered as a potential causative agent in culture-negative endocarditis. Infections are usually self-limiting but, in rare instances (especially endocarditis), can become chronic.

B. Laboratory identification

Serologic assays are the principal means of specific diagnosis, and serologic surveys indicate that inapparent infections are common.

 C. Treatment and prevention

 Doxycycline is the drug of choice for treatment. A vaccine has been reported to be of limited use in occupationally exposed individuals, but it is not readily available in the United States.

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