patients in France. Later studies have yielded conflicting results (Madariaga et al. 2004; Montes et al. 1995; Raoult et al. 1993).

Long-Term Adverse Health Outcomes of Q Fever

C. burnetii persists in circulating monoctyes and bone marrow of healthy people who had a diagnosis of Q fever and recovered from the acute illness.

Complications of Acute Q Fever

About 2% of patients with acute Q fever manifest neurologic involvement. Long-term neurologic deficits have been described in that population: motor weakness, blurred vision, residual paresthesia, sensory loss, peripheral neuropathy, and behavioral changes (Bernit et al. 2002; Drancourt et al. 1991; Ferrante and Dolan 1993; Raoult et al. 2005). There are case reports of other rare neurologic deficits. Although the neurologic deficits can be long-term, onset occurs during the acute syndrome. Thus, the association between acute Q fever with neurologic involvement and long-term neurologic deficits is self-evident.

Chronic Sequelae of Coxiella burnetii Infection

The scientific literature contains evidence of five chronic syndromes associated with C. burnetii infection: post-Q fever chronic fatigue syndrome, culture-negative endocarditis, vascular infection, chronic hepatitis, and osteomyelitis. In general, older age and immunosuppression appear to be risk factors for the development of chronic Q fever (Fenollar et al. 2001). There also appear to be risk factors specific to particular syndromes. Although infection with C. burnetii may be chronic, chronic Q fever itself is rarely reported and usually occurs among those with pre-existing abnormalities of cardiac valves or endovascular grafts.

The largest case series to date reviewed 74,202 suspect cases referred to the French National Reference Center for Rickettsial Diseases during a 14-year period (1985-1998) (Raoult et al. 2000). Serum samples were initially screened with the IFA assay for reactive IgM and IgA antibodies to C. burnetii. Samples that tested positive underwent a second IFA assay to determine antibody titers; a phase II IgG titer of at least 200:1 and a phase II IgM titer of at least 50:1 indicated recent Q fever. With that method, investigators identified 7,543 probable cases. To confirm them, the reference center collected, tested, and cultured additional serum, blood, or tissue samples from the patients. C. burnetii was detected with the IFA assay in the samples of 1,383 cases whose serum had IgG titers of at least 800:1. Clinical data on the confirmed cases indicated that 1,070 of the patients suffered acute Q fever and 313 chronic Q fever. Raoult and colleagues reported the clinical and epidemiologic characteristics of these cases (Raoult et al. 2000). The committee drew on their findings (Table 5.4) and others to reach conclusions about the strength of association between C. burnetii infection and the five long-term adverse health outcomes noted above.



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