Listeria monocytogenes encephalitis mimicking Herpes Simplex virus encephalitis: the differential diagnostic importance of cerebrospinal fluid lactic acid levels.

Listeria monocytogenes is a common cause of bacterial meningitis in elderly patients and in those with impaired cellular immunity. The most common central nervous system infection caused by L. monocytogenes is acute bacterial meningitis; meningoencephalitis is uncommon and encephalitis is rare. Early diagnosis of L. monocytogenes meningitis is difficult because only 50% of cerebrospinal fluid (CSF) Gram stains are negative. L. monocytogenes is one of the few central nervous system pathogens associated with red blood cells in the CSF. When L. monocytogenes presents as encephalitis with red blood cells in the CSF, the clinical presentation mimics most closely herpes simplex virus (HSV)-1 encephalitis. Because the therapies for L. monocytogenes and HSV-1 are different, early diagnostic differentiation is clinically important. The CSF lactic acid is the best way to rapidly differentiate between these two entities; the CSF lactic acid level is elevated in L. monocytogenes but is not elevated in HSV-1 encephalitis. The case presented is an elderly man with chronic lymphocytic leukemia who presented with encephalitis. Advanced age and chronic lymphocytic leukemia predispose him to a wide variety of pathogens, but the rapidity and severity of his clinical presentation made L. monocytogenes and HSV-1 encephalitis the most likely diagnostic possibilities. The CSF Gram stain was negative, but the elevated CSF lactic acid levels with encephalitis and red blood cells in the CSF indicated L. monocytogenes as the most likely pathogen. We present a case of L. monocytogenes encephalitis mimicking HSV-1 encephalitis. While receiving ampicillin therapy, the patient remained unresponsive for more than 1 week and then suddenly regained consciousness and recovered without neurologic sequelae.

Quadrivalvular marantic endocarditis (ME) mimicking acute bacterial endocarditis (ABE).

Marantic endocarditis (ME) is defined by noninfectious valvular vegetations. The most common disorders associated with ME are malignancy with or without hypercoagulable state, intercardiac instrumentation, residual vegetations from previously treated infective endocarditis (IE), renal insufficiency, and burns. Another important cause of ME is systemic lupus erythematosus when accompanied by vegetations, that is, Libman-Sacks endocarditis. ME should be differentiated from IE because they may present with similar clinical features. Both ME and IE may present with fever and a heart murmur with or without embolic phenomenon. Leukocytosis and elevated erythrocyte sedimentation rate suggest the diagnosis of IE. The hallmark of IE is a cardiac vegetation and continuous high-grade bacteremia. After exclusion of the causes of culture negative endocarditis, the absence of bacteremia clearly differentiates ME from IE. We present a case of ME mimicking acute bacterial endocarditis (ABE). The differential diagnostic features of ME versus IE are discussed. To the best of our knowledge, this is the first reported case of quadrivalvular ME with massive vegetations on all cardiac valves, as well as the aorta, atria, and pulmonary artery.

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.

Pacemaker-induced Staphylococcus aureus mitral valve acute bacterial endocarditis complicated by persistent bacteremia from a coronary stent: Cure with prolonged/high-dose daptomycin without toxicity.

Continuous high-grade Staphylococcus aureus bacteremia suggests acute bacterial endocarditis (ABE), a protected focus, ie, an abscess, or a device-related infection. Daptomycin was curative of S. aureus ABE and coronary stent-related bacteremia. Prolonged high-dose daptomycin therapy (12 mg/kg per day for 41 days) is not associated with any toxicity. Persistent S. aureus bacteremia in ABE should suggest myocardial or perivalvular abscess. If intracardiac abscess can be ruled out and there is no extracardiac source of the S. aureus bacteremia, then a device-related infection should be considered.