Q fever bioprosthetic aortic valve endocarditis (PVE) successfully treated with doxycycline monotherapy.

Q fever is a zoonotic infection caused by Coxiella burnetii. The most common clinical manifestation of acute Q fever infection is as an atypical community-acquired pneumonia. The pulmonary findings are accompanied by extrapulmonary findings, most typically an increase in serum transaminases and splenomegaly. Because C. burnetii is difficult to culture, the diagnosis of Q fever is usually made serologically. The diagnosis of acute Q fever atypical community-acquired pneumonia is made by demonstrating a fourfold or greater increase in titer between acute and convalescent specimens or by demonstrating elevated immunoglobulin (IgM) (phase II) titers. Chronic Q fever is manifested as granulomatous hepatitis or more commonly as culture-negative endocarditis (CNE). Chronic Q fever (CNE) is a difficult diagnosis because of difficulty in culturing the organism from the blood and the vegetations with Q fever CNE are small or absent. The diagnosis of chronic Q fever CNE is based on serology. Such patients commonly have highly elevated IgM and IgG titers (phase I/II) titers. Chronic Q fever CNE may involve native or prosthetic heart valves. Q fever prosthetic valve endocarditis is rare compared with native valve Q fever endocarditis. Q fever prosthetic valve endocarditis usually requires valve replacement for cure. We present a case of chronic Q fever bioprosthetic aortic valve endocarditis that was successfully treated with doxycycline monotherapy that did not require aortic valve replacement.

Methicillin-resistant Staphylococcus aureus (MRSA) mitral valve acute bacterial endocarditis (ABE) in a patient with Job's syndrome (hyperimmunoglobulin E syndrome) successfully treated with linezolid and high-dose daptomycin.

Job's syndrome (hyperimmunoglobulin E syndrome) is a congenitally acquired primary immune deficiency. The primary host defense defect in Job's syndrome is impaired phagocytosis. Accordingly, patients with Job's syndrome have difficulties eradicating staphylococcal infections. A continuous, high-grade Staphylococcus aureus bacteremia with a cardiac valve vegetation is the hallmark of S. aureus acute bacterial endocarditis (ABE). ABE may be caused by methicillin-sensitive Staphylococcus aureus or methicillin-resistant Staphylococcus aureus (MRSA). We report a case of Job's syndrome MRSA mitral valve ABE. Presumably because of impaired phagocytic function, his MRSA ABE was complicated by extensive metastatic septic complications manifested as brain abscess, multiple epidural abscesses, and multifocal vertebral osteomyelitis. The patient did not respond to 5 days of appropriately dosed linezolid and daptomycin and remained bacteremic because abscess drainage was not an option in this case and the continuous, high-grade MRSA bacteremia continued despite appropriate therapy. High-dose daptomycin (12 mg/kg intravenously every 24 hours) was given, and his MRSA bacteremia was rapidly terminated. Because daptomycin does not cross the blood-brain barrier in therapeutic concentrations, linezolid was used to treat the brain abscess. The extensiveness of infection in this case is remarkable and is probably related to impaired phagocytic function from Job's syndrome. High-dose daptomycin therapy rapidly cleared the bacteremia and cured the endocarditis and epidural abscesses/vertebral osteomyelitis. The patient was treated with 8 weeks of high-dose daptomycin therapy with no adverse effects. If MRSA and methicillin-sensitive S. aureus bacteremias are unresponsive to usually effective antistaphylococcal agents, and surgical drainage of abscesses and removal of infected devices are not clinically possible, then a prolonged, high dose of daptomycin is a therapeutic alternative in such situations. To the best of our knowledge, this is the first case of MRSA mitral valve ABE complicated by extensive epidural abscesses and vertebral osteomyelitis in a patient with Job's syndrome.

Herpes simplex virus (HSV) pneumonia in a heart transplant: diagnosis and therapy.

Organ transplants are frequently complicated by viral infections. The period of maximum immunosuppression, 1 to 6 months posttransplantation, predisposes one to intracellular pathogens. The most common intracellular viral pathogens in transplant recipients include cytomegalovirus (CMV), herpes simplex virus (HSV), and respiratory syncytial virus (RSV). Cytomegalovirus and HSV are common viral pathogens in the early transplant period (0-1 month posttransplant). Although respiratory syncytial virus commonly presents in the late posttransplant period (> or =6 months posttransplant), HSV pneumonia may be acquired in organ transplants by endogenous reactivation caused by immunosuppression or may be introduced from colonized oropharyngeal secretions into the lower respiratory tract during intubation in patients on ventilators. In ventilated patients without severe preexisting lung disease, HSV pneumonia presents with otherwise unexplained profound/prolonged hypoxemia or "failure to wean." As other viral pneumonias, HSV pneumonia is characterized by profound hypoxemia requiring a high FIo(2), and a highly increased A-a gradient (> or =30). These findings are indicative of an oxygen diffusion defect typical of noninfectious (eg, sarcoidosis) or infectious disorders (eg, HSV, cytomegalovirus, respiratory syncytial virus, Pneumocystis (carinii) jiroveci pneumonia) primarily affecting the interstitium of the lung. We present a case of HSV pneumonia in a heart transplant recipient and include a review of the clinical presentation, diagnostic findings, and therapy of HSV pneumonia.