The etiologic evaluation of pericardial effusion is frequently unsuccessful when noninvasive methods are used. To determine the cause of the current episode, all patients with echographically identified pericardial effusion from May 1998 to December 2002 underwent noninvasive diagnostic testing of blood, throat, and stool samples. Patients with postpericardiotomy syndrome were excluded. To analyze the value of our tests, we tested randomly selected blood donors as negative controls. Among 204 included patients, 107 (52.4%) had a final etiologic diagnosis: the etiology of 52 was highly suspected at first examination and later confirmed (thyroid deficiency, 5 cases; systemic lupus erythematous, 7; rheumatoid arthritis, 7; scleroderma, 3; cancer, 25; and renal insufficiency, 5). A definite etiologic diagnosis was made in 11 patients from pericardial fluid analysis (cancer, 5 cases; tuberculosis, 3; Streptococcus pneumoniae, Citrobacter freundii, and Actinomyces, 1 case each). Among 141 patients considered to have idiopathic pericarditis, 44 (32.1%) gained an etiologic diagnosis by our systematic testing strategy. This included serologic evaluation of serum (Coxiella burnetii, 10 cases; Bartonella quintana, 1; Legionella pneumophila, 1; Mycoplasma pneumoniae, 4; influenza virus, 1), viral culture of throat swabs (enterovirus, 8 cases; and adenovirus, 1), high-level antinuclear antibodies (>1/400, 3 cases), and thyroid-stimulating hormone (15 abnormal results). Antibodies to Toxoplasma and cytomegalovirus, enterovirus recovered from rectal swabs, and low-level antinuclear antibodies were seen with equal frequency in patients and controls. Using our evaluation strategy, the number of pericardial effusions classified as idiopathic was less than in other series. Systematic testing for Q fever, Mycoplasma pneumoniae, thyroid abnormalities, and antinuclear antibodies, accompanied by viral throat cultures, frequently enabled us to diagnose diseases not initially suspected in patients with pericardial effusion.

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We studied 32 cases of Q fever endocarditis diagnosed in France between January 1985 and December 1989 to evaluate the efficacies of the different regimens of antibiotics used for treatment. Each patient was monitored during the treatment (range, 12 to 60 months), and clinical and biological information was computerized. Various treatments were prescribed, including doxycycline alone (9 cases) or in association with rifampin (4 cases), quinolones (16 cases), or sulfamethoxazole-trimethoprim (1 case). Two patients died before the beginning of the treatment. Nineteen patients had hemodynamic failure and subsequently underwent valve replacement. Nine valve tissue cultures were positive despite previous antibiotic treatment. In terms of their effects on mortality, the difference between doxycycline alone and doxycycline plus quinolones is statistically significant. We conclude that the addition of quinolones to doxycycline is beneficial. On the basis of clinical, serological, and valve tissue culture results, no treatment was able to cure Q fever endocarditis within 2 years, even with a combination of antibiotics. We advise a minimum duration of treatment of 3 years with therapy combining quinolones and doxycycline.

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The incidence of auto-immune disorders is unexpectedly high and could explain some manifestations of acute Q-fever e.g the resistance to therapy with antibiotics which are not yet clear. Then the association during the acute stage of auto-immune disorders with the persistence of clinical or biological findings after three weeks therapy could recommend the use of corticosteroids.

Broad-range PCR followed by sequencing offers several advantages when used to complement culture results for the diagnosis of fastidious bacteria and for patients taking antibiotics. However, its use should be restricted mainly for culture-negative cases when infection is suspected on the basis of clinical signs and symptoms or inflammatory syndrome. Future developments will include the use of real-time PCR in a closed system and pathogen-specific PCR for the molecular diagnosis of osteoarticular infections.

Sera from 40 patients (25 men, and 15 women) with clinical features compatible with the diagnosis of chronic Q fever were received. Total or partial clinical data were available. All of them had serological evidence of chronic Q fever (IgG class anti-phase I titer greater than 800). The final diagnosis was vascular infection in four cases (with two positive cultures for Coxiella burnetii), bone infection in two patients (one positive culture), chronic hepatitis in one patient, and endocarditis in 32. The last patient had an isolated fever with a chronic Q fever serologic profile. Among the 32 with endocarditis, valve replacement was performed in 59%, and valve cultures were positive in 14/18 patients. Twenty-nine of these patients had previously known valvulopathy; 23 were exposed to cattle, sheep or goats; and four had an immunocompromised situation. Ten patients died; two before any treatment, five of cardiac failure during or a few weeks after surgery, and three during the medical treatment. For antibiotic treatment, tetracycline alone was employed in seven cases. For the other patients, combined therapy including tetracycline and another drug (rifampin, fluoroquinolones, cotrimoxazole, or erythromycin) was initiated. Three patients were considered to be completely cured.