Unusual presentations of acute Q fever include aseptic meningitis, meningoencephalitis, peripheral neuropathy, GBS, myocarditis, pericarditis, thyroiditis, bone marrow necrosis, erythema nodosum, glomerulonephritis, and orchitis. Q fever in pregnancy can lead to miscarriage and neonatal death (Raoult et al. 2002).

Although acute Q fever usually resolves spontaneously, antibiotic treatment can reduce the duration of symptoms and may diminish the risk of complications. The treatment of choice is tetracycline or doxycycline given for 7-14 days. Alternative antibiotic regimens include chloramphenicol, quinolones, rifampin, and trimethoprim. In vitro efficacy of erythromycin is poor, but there is some evidence of clinical efficacy in vivo (Raoult 2003).

Possible long-term toxicity of tetracycline use includes nervous and sensory system effects. Benign intracranial hypertension has been described in children and adults on tetracycline and doxycycline (Digre 2003; Gardner et al. 1995; Lochhead and Elston 2003); this complication has resulted in visual-field loss (Digre and Corbett 2001; Gardner et al. 1995; Lochhead and Elston 2003).

The diagnosis of Q fever should be considered in patients who have an appropriate clinical presentation and substantial animal exposure. Nonspecific laboratory findings include increased erythrocyte sedimentation rate, low platelet counts, increased liver enzymes, and multiple transient autoantibodies.

Specific diagnosis of Q fever is complicated. Growth of C. burnetii in culture is not only difficult, but also fraught with biosafety hazards because of its high infectivity and tendency to aerosolize. Most cases of C. burnetii infection are diagnosed serologically. Acute infection is accompanied by a rise in IgM antibody to phase II antigens followed by an IgG response to phase II antigen. In contrast, chronic infection is characterized by high titers of IgA and IgM to phase I and II antigens. IgM antibodies can remain increased for long periods and are not indicative of recent infection (Fournier et al. 1998).

Current methods of antibody detection include indirect immunofluorescence assay (IFA), ELISA, and the less sensitive and less specific complement-fixation assay. Indirect immunofluorescence is now considered to be the reference for serologic diagnosis. Acute infection can be diagnosed on the basis of a 4-fold rise in titer in paired serum samples. Single IFA titers of 1:50 IgM and 1:200 IgG to phase II antigen are considered diagnostic of acute infection, and a titer of 1:800 IgG to phase I antigen is considered diagnostic of chronic infection. Probes that use DNA amplification with PCR are now available to identify C. burnetii in blood, urine, and tissue samples (Parker et al. 2006).

Relatively little is known about C. burnetii infection in HIV patients. In principle, as an intracellular pathogen with long-term persistence in human hosts, C. burnetii might be expected to cause more frequent and more severe infections in the immunocompromised state. Indeed, Raoult et al. (1993) noted a 10-fold increase in the incidence of Q fever among HIV-seropositive