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A 65-year-old man was transferred to our institution for evaluation of fever. His symptoms included subjective fever, cough productive of creamy white sputum, and nasal congestion of 3 months' duration. He denied dyspnea, hemoptysis, weight loss, or night sweats. Approximately 10 days before admission, he had been seen by his primary care physician for worsening of symptoms and was treated empirically with an undefined antibiotic. Subsequently, palpitations and severe fatigue developed, and the patient was admitted to a local hospital, where he was noted to be febrile and hypoxic with pulse oximetry readings in the high 80% range. Acute coronary syndrome was excluded, and ceftriaxone and moxifloxacin were initiated empirically. Computed tomography (CT) of the chest without intravenous contrast was performed. Compared with chest CT performed 4 years earlier, no new pulmonary infiltrate was evident; however, both the superior and the lateral aspect of the right hilum were more prominent than in the previous study and were suspicious for adenopathy. The patient was transferred to our institution approximately 2 days later for further evaluation.
On admission, the patient's main symptoms were fever, fatigue, palpitations, mild chest discomfort, cough, and nasal congestion. Findings on the rest of the systems review were unremarkable. The patient had a history of asthma, chronic sinusitis, seasonal allergic rhinitis, aspirin intolerance, nasal polyposis with multiple prior polypectomies, and benign prostatic hypertrophy. His medical regimen consisted of omeprazole, atorvastatin, doxazosin, irbesartan-hydrochlorothiazide, montelukast, and fluticasone-salmeterol. His family history was notable for a sibling's death due to lung cancer at age 28 years.
On physical examination, the patient had a temperature of 37.9 °C, heart rate of 95 beats/min (regular), blood pressure of 149/74 mm Hg, respiratory rate of 18 breaths/min, and pulse oximetry of 94% while breathing 3 L of oxygen via nasal cannula. He appeared comfortable and had palpable anterior cervical chain and submandibular lymph nodes, jugular venous distension 3 cm above the clavicle, faint inspiratory crackles at both lung bases, and a grade 2/6 systolic murmur best heard at the apex. Findings on the rest of the physical examination were normal. Laboratory results are listed in the Table.
Q fever is a zoonosis caused by the organism C burnetii, an obligate intracellular gram-negative bacterium. The designation Q fever (from Query) was coined in 1935 after an outbreak of febrile illness in an abattoir in Queensland, Australia. Although previously classified as a rickettsial organism, C burnetii has been placed into the subdivision of the Proteobacteria, which are closer to Legionella and Francisella than to Rickettsia. The most commonly identified sources of human infection are farm animals such as cattle, goats, and sheep.
Clinical signs of Q fever are often mild or absent. Symptomatic illness can be divided into acute and chronic forms. Of patients with acute Q fever, 40% to 60% have hepatitis; 20%, pneumonia plus hepatitis; 14% to 17%, pneumonia; and 17%, fever alone. Hepatitis develops more often in younger people, and pneumonia more often in older people, usually immunocompromised patients. Fibrin-ring granulomas, which have been associated with Q fever, may rarely be seen in the liver and bone marrow and may appear “doughnut-like” because of a lipid vacuole surrounded by a fibrinoid ring.8 Chest radiography can show normal findings or pleural-based opacities, effusions, atelectasis, and, rarely, hilar adenopathy. Results of laboratory studies are usually normal except for mild elevations in the peripheral white blood cell count (30% of patients); thrombocytopenia is noted in 25% of patients. The erythrocyte sedimentation rate is usually moderately elevated. Liver enzymes are elevated in almost three-fourths of patients. Q fever is principally diagnosed by serologic methods. The presence of phase I IgM and/or IgG antibodies indicates recent infection, whereas a phase I IgG antibody titer greater than 1:800 indicates chronic infection.
Chronic Q fever may develop within a year or as long as 20 years after the initial infection. It occurs primarily in patients with previous valvular heart disease, immunocompromised patients, and pregnant women. Mortality rates can be as high as 30% to 60%. Q fever endocarditis is identified on the basis of the modified Duke criteria, and a single positive blood culture for C burnetii or a C burnetii anti-phase I IgG titer of greater than 1:800 is considered a major criterion for diagnosis.
The treatment of choice for acute Q fever is doxycycline, 100 mg twice daily, for 15 to 21 days. Fluoroquinolones are also efficacious and may be used. In pregnant women, trimethoprim-sulfamethoxazole can be used as long as the neonate is monitored for potential hyperbili-rubinemia. However, given the potential toxic effects of treatment, most therapies are purely to control infection, with curative therapy initiated after the patient has been delivered of her newborn.
Once acute Q fever has been diagnosed, transthoracic echocardiography should be performed to look for valvulopathy; if present, treatment should be initiated for infective endocarditis.9 If valve lesions are not present, then repeated serologic testing should be performed at 3- and 6-month follow-up. If phase I IgG is elevated, which implies chronic Q fever infection, both transesophageal echocardiography and serum polymerase chain reaction screening for C burnetii should be performed; the latter has been reported to have up to a 100% specificity in some studies of cases of untreated Q fever endocarditis.10,11
Treatment of patients with chronic Q fever should include a combination of doxycycline and hydroxychloroquine for at least 18 months; alternative treatment regimens include doxycycline plus either a fluoroquinolone or rifampin for at least 3 to 4 years. Surgery is needed in some cases. Postexposure prophylaxis could be considered after exposure to birthing products from cattle, sheep, and goats or exposure to unpasteurized milk or milk products from these animals. Prophylaxis should be initiated within 8 to 12 days after exposure and should be continued for 1 week.
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Correct answers: 1. e, 2. e, 3. d, 4. a, 5. c