Citations

A 62-year-old man with essential hypertension and right L4-L5 hemilaminectomy was referred to rheumatology for evaluation of severe arthralgia and myalgia for 12 months. Review of symptoms was significant for night sweats and 20 pounds unintentional weight loss. Physical examination was significant for holosystolic murmur best heard at the cardiac apex of unclear chronicity. Laboratory investigations revealed elevated inflammatory markers, white blood cell count and B-type natriuretic peptide. Transoesophageal echocardiogram showed flail posterior mitral leaflet with severe mitral regurgitation and two vegetations (2.5×1 cm and 1.6×0.3 cm). Abdominal CT showed new focal splenic infarcts, and a brain MRI revealed subacute infarcts, consistent with the embolic phenomenon. Blood cultures grew Granulicatella elegans. The patient underwent mitral valve replacement surgery followed by 6 weeks of parenteral therapy with vancomycin and gentamicin, with full recovery at a 3-month follow-up.

A 51-year-old man with a medical history of coronary artery disease and dyslipidaemia presented with acute myocardial infarction resulting in cardiogenic shock, necessitating intra-aortic balloon pump placement and extracorporeal membrane oxygenation (ECMO). His hospital course was complicated by several infectious complications including ECMO circuit Pseudomonas aeruginosa bloodstream infection and presumed infected right atrial thrombus. He subsequently underwent urgent left ventricular assist device placement and had a prolonged hospital stay. On day 100 of admission, he developed acute hypoxic respiratory distress with new pulmonary infiltrates. Sputum cultures grew Cryptococcus neoformans. Blood culture also grew C. neoformans after 96 hours of incubation and cryptococcal serum antigen was elevated at 1:20. Cerebrospinal fluid studies from a lumbar puncture were normal. He was treated with 2 weeks of combination antifungal therapy followed by life-long fluconazole suppression.

A 61-year-old man presented to the emergency department in the summer with a right seventh cranial nerve lower motor neuron palsy and worsening paraesthesias for 6 weeks. He had debilitating pain at the scalp and spine. Prior work up was unrevealing. The patient resided in the upper Midwest region of the USA and worked outdoors, optimising the landscape for white tailed deer. Repeat cerebrospinal fluid testing revealed a lymphocytic pleocytosis and positive IgM Lyme serology. Brain MRI demonstrated enhancement of multiple cranial nerves bilaterally. He was diagnosed with early Lyme neuroborreliosis and treated with 28 days of intravenous ceftriaxone. While the painful meningoradiculitis, also known as Bannwarth syndrome, is more commonly seen in Europe, facial palsy is more frequently encountered in the USA. Clinical manifestations of neuroborreliosis are important to recognise as the classic presentation varies by geography and on occasion repeat serological testing may be necessary.

A 61-year-old man with relapsing chronic lymphocytic leukaemia, status post allogeneic stem cell transplant and multiple chemotherapy regimens presented to the emergency room after suffering a grand mal seizure. His evaluation revealed a 1.5–2 cm ring-enhancing left temporal lobe brain lesion on the CT scan. This brain lesion was resected and the histopathology revealed an invasive fungal organism resembling mucormycosis. Amplification and sequencing of the 28S ribosomal RNA gene identified the organism as Rhizomucor pusillus. The patient was treated with liposomal amphotericin B 5 mg/kg every 24 hours for 4 weeks, and then was transitioned to oral posaconazole. Serial brain imaging at 1 and 3 months, while on therapy, showed significant improvement.

An 88-year-old man with history of bioprosthetic aortic valve replacement was hospitalised with fever, chills, malaise and right lower extremity cellulitis. Laboratory investigations revealed leucocytosis and blood cultures grew Helcococcus kunzii. Although transoesophageal echocardiography was negative for endocarditis, the patient was treated with 4 week of intravenous ceftriaxone. However, he was readmitted 6 weeks later with symptoms of fever, chills and hypoxia in setting of recurrent H. kunzii bacteraemia. A repeat transoesophageal echocardiogram revealed a mobile mass on bioprosthetic aortic valve, severe perivalvular insufficiency with pseudoaneurysm formation, and severe native mitral and tricuspid valve regurgitation. Cardiothoracic surgery was consulted and the patient underwent replacement of aortic valve and aortic root, and tricuspid and mitral valve repairs. Histological examination of excised bioprosthetic aortic valve revealed active endocarditis with cocci identified on silver stain. Patient was successfully treated with 4-week course of intravenous ceftriaxone and was doing well at 2-year follow-up.

BackgroundDevice infection is associated with increased mortality in patients receiving cardiovascular implantable electronic device (CIED) therapy. However, long‐term mortality associated with CIED infections has not been systematically analyzed in larger studies. This study sought to determine the long‐term mortality associated with CIED infection in a large cohort of Medicare beneficiaries.MethodsWe used a retrospective study design to analyze 3‐year mortality in 200,219 Medicare fee‐for‐service patients admitted for CIED generator implantation, replacement, or revision between January 1, 2007 and December 31, 2007. Multivariate analysis adjusting for age, sex, race, and 28 comorbidities was performed to determine the relative risk (RR) of death in the 12 quarters following CIED infection.ResultsPatients with CIED infection, compared to device recipients without infection, had increased mortality that persisted for at least 3 years after the admission quarter for all device types: pacemakers (PMs: 53.8% vs 33%; P < 0.001), implantable cardioverter defibrillator (ICD: 47.7% vs 31.6%; P < 0.001), and cardiac resynchronization therapy‐defibrillator (CRT‐D: 50.8% vs 36.5%; P < 0.001). After adjusting for patient demographics and comorbidities, significantly increased RR of death following CIED infection persisted for at least 3 years following PM infection, and for at least 2 years with single‐ and dual‐chamber ICD infection.ConclusionsCIED recipients who develop device infection have increased, device‐dependent, long‐term mortality even after successful treatment of infection. The etiology of this persistent increased risk of death associated with CIED infection is unknown and merits further investigation.