ABSTRACT

INTRODUCTION Q fever is caused by Coxiella burnetii, an obligate intracellular bacterium phylogenetically related to Legionellae species and Francisella tularensis (1). Q fever has a wide spectrum of clinical manifestations (2). Naïve patients usually contract Q fever via aerosol (few bacteria being infective) and develop primary infection. Very few primary infections are diagnosed because more than half of patients will not show any symptoms associated with seroconversion and only 2% will develop significant disease leading to specific blood samplings and/or hospitalization. Among diagnosed and severe cases, most are middle-aged males (between 50 and 60 years). Almost always, acute Q fever resolves without specific antibiotic treatment. However, C. burnetii sometimes persists in seemingly cured patients (3). In special hosts, the primary infection (symptomatic or not) may evolve to a chronic infection (4). The latency between acute and chronic infection may last from months to years. Patients with valvular damage or evolutive cancer such as lymphomas and pregnant women are at high risk of evolution to chronic infection (5). The main clinical manifestation of chronic Q fever is the endocarditis (6). Among blood culture-negative infective endocarditis, 48% are associated with C. burnetii (7). Q fever endocarditis is characterized by fibrosis, calcification, slight inflammation and vascularization, and small or absent vegetations (8). Patients have a spontaneous evolution to death and exhibit high level of antibodies specific for C. burnetii (1). The combination of doxycycline and chloroquine has changed the prognosis of the disease: fewer than 5% of patients experience relapses after 18 months of therapy (9). Circulating concentrations of doxycycline and decreased titers of anti-C. burnetii antibodies are correlated (10). Besides the two major clinical presentations of Q fever, two new evolutive forms have been recently reported. The hyperinflammatory syndrome is associated with hepatitis and autoantibodies in middle-aged male patients; corticosteroids improve patient cure (1). Persistent asthenia lasting for months or years has been reported in some patients with acute Q fever (11). Finally, Q fever is deemed a category B biological terrorist agent (12).