Can an etiologic agent be identified in adults who are hospitalized for community-acquired pneumonia: results of a one-year study.

INTRODUCTION: Determining the cause of community-acquired pneumonia (CAP) remains problematic. In this observational study, we systematically applied currently approved diagnostic techniques in patients hospitalized for CAP in order to determine the proportion in which an etiological agent could be identified. METHODS: All patients admitted with findings consistent with CAP were included. Sputum and blood cultures, urine tests for pneumococcal and Legionella antigens, nasopharyngeal swab for viral PCR, and serum procalcitonin were obtained in nearly every case. Admission-related electronic medical records were reviewed in entirety. RESULTS: By final clinical diagnosis, 44 patients (17.0%) were uninfected. A causative bacterium was identified in only 60 (23.2%) cases. PCR identified a respiratory virus in 42 (16.2%), 12 with documented bacterial coinfection. In 119 (45.9%), no cause for CAP was found; 69 (26.6%) of these had a syndrome indistinguishable from bacterial pneumonia. Procalcitonin was elevated in patients with bacterial infection and low in uninfected patients or those with viral infection, but with substantial overlap. CONCLUSIONS: Only 23.2% of 259 patients admitted with a CAP syndrome had documented bacterial infection; another 26.6% had no identified bacterial etiology, but findings closely resembled those of bacterial infection. Nevertheless, all 259 received antibacterial therapy. Careful attention to the clinical picture may identify uninfected patients or those with viral infection, perhaps with reassurance by a non-elevated procalcitonin. Determining an etiologic diagnosis remains elusive. Better discriminators of bacterial infection are sorely needed.

Device-related infective endocarditis, with special consideration of implanted intravascular and cardiac devices in a predominantly male population.

BACKGROUND: The relationship between invasive medical devices and infective endocarditis (IE) has not been comprehensively assessed. We describe our experience of patients with IE, with particular attention to the role of pre-existing intravascular catheters and implanted cardiac devices in the pathogenesis. METHODS: We performed a retrospective review of hospital records over a 10-y period (1997-2007), and included patients with 'definite' or 'possible' IE as per the modified Duke criteria. The complete electronic medical record was reviewed for the presence of intravascular devices prior to the onset of IE, including intravascular catheters and implanted cardiac devices (defibrillators and pacemakers). RESULTS: We identified 155 patients with IE. Infection involved a native valve in 124 (80%) patients and a prosthetic valve in 15 (9.7%). In the remaining 16 (10.3%) patients, infection was attributed to an implanted cardiac device. The most commonly identified source of infection was a central venous catheter, accounting for 17.4% of patients, followed by an implanted cardiac device in 10.3% of patients. Staphylococcus aureus was the most commonly isolated organism in catheter-associated IE and cardiac device-associated IE (31.9% and 62.5%, respectively). Thirty-five (22.5%) patients died within 90 days. Mortality was 31.9% in patients with IE caused by methicillin-resistant S. aureus (MRSA). CONCLUSIONS: Intravascular catheters and cardiac implantable devices are common sources of infection leading to IE, and the intracardiac devices themselves often become infected, with MRSA as the predominant pathogen.

Severe pulmonary involvement in a case attributed to domestically acquired Seoul hantavirus in the United States.

Hantavirus is known to cause 2 distinct clinical syndromes: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome. Seoul virus is an Old World hantavirus known to cause HFRS. We report a case attributed to domestically acquired Seoul hantavirus with prominent pulmonary involvement and a fatal outcome.