Francisella tularensis Endocarditis

Francisella tularensis, the agent of tularemia, is a widely distributed and extremely virulent gram-negative coccobacillus that induces disease in both human and animal hosts. Transmission of F. tularensis usually occurs by way of an arthropod vector or by direct animal contact; however, infection may also occur through aerosol inhalation, contamination of ocular or oral mucous membranes, or ingestion of bacteria. The manifestations of tularemia are protean and are classified into 6 syndromes: ulceroglandular, glandular, oculoglandular, pharyngeal, typhoidal, and pneumonic. Rare but reported manifestations include pericarditis and meningitis [1]. It is suspected that many cases go undiagnosed because of the often confusing presentations, the lack of clear exposure history, and the rarity of culture growth. To our knowledge, we describe the first documented case of F. tularensis endocarditis in a human host. A 42-year-old man presented with a 2to 3-day history of fever, chills, nonproductive cough, and pain on the left side of his chest. His medical history was remarkable only for cocaine and alcohol abuse. He denied iv drug use. At admission, he had a temperature of 39.87C, pulse rate of 101, respiratory rate of 20, and blood pressure of 138/84 mm Hg. Physical examination demonstrated no cervical, axillary, or inguinal adenopathy. Lung examination revealed markedly decreased airflow to the left base and midlung with bronchial breath sounds and sparse crackles. A grade 2/6 systolic murmur was detected at the left lower sternal border of the fifth intercostal space. This murmur was not present during prior documented examinations. Initial laboratory studies showed a WBC count of /L, hemoglobin level of 14.0 g/mL, hematocrit of 9 12.3 3 10 41.2%, and platelet count of /L. Urine analysis showed 9 90 3 10 31 blood, 21 ketones, 31 protein, 16–18 RBCs, and 8–10 granular casts per high-power field. Further laboratory studies disclosed the following values: sodium, 125 mEq/mL; potassium, 3.1 mEq/mL; chloride, 86 mEq/mL; CO2, 30.2 mEq/mL; blood urea nitrogen, 9 mg/dL; creatinine, 1.3 mg/dL; lactate dehydrogenase, 113 U/L; and alanine aminotransferase, 42 U/ L. Serology for HIV was negative. Chest radiography showed previously described findings of bilateral emphysematous changes with bullae. A new poorly defined density without calcification or cavity was found in the left midlung. He was admitted to the general medicine service with a presumptive diagnosis of community-acquired pneumonia. After blood specimens for culture were obtained, a therapeutic regimen of cefotetan and erythromycin was initiated. He remained