Background Infection is a common complication of ventricular-assist devices (VADs) and is associated with re-hospitalization, thromboembolic events, VAD malfunction, delay in heart transplantation, and a high mortality rate. The objectives of this study were to investigate the frequency of fungal VAD infections and assess various risk factors and their effects on mortality as compared to bacterial VAD infections. Methods We conducted a retrospective chart review of patients with infected VADs at a single tertiary care center. The frequency, risk factors and outcomes of fungal vs. bacterial VAD infections were compared. Results Of the 300 patients who received a VAD, 108 (36%) developed VAD infection, including 85 bacterial and 23 fungal infections. Most common bacterial causes of infection were Staphylococcus aureus, coagulase-negative staphylococci, enterococci and Pseudomonas aeuruginosa. Most common fungal etiologic agent was Candida albicans. Only the use of TPN was associated with the development of a fungal VAD infection in multivariate analysis (OR 6.95, 95% CI 1.71–28.16, p=0.007). Patients who suffered from fungal VAD infection were less likely to be cured (17.4% vs. 56.3%, p=0.001) and had greater mortality (91% vs. 61%, p=0.006), as compared with those who experienced bacterial VAD infections. Conclusions Fungi were responsible for approximately one-fifth of VAD infections and were associated with a mortality rate of 91%. Restriction of TPN use is essential in decreasing the rate of fungal VAD infection. Trials are needed for investigating the use of echinocandins or lipid formulations of amphotericin B for prevention and/or treatment of fungal VAD infections.

Previous studies have demonstrated that Nocardia brasiliensis is susceptible to amoxicillin-clavulanic acid and that its I8-lactamases are inhibited in vitro by, clavulanic acid. A cardiac transplant patient with disseminated infection caused by N. brasiliensis was treated with this drug combination with good response, but relapsed while still on therapy. The relapse isolate was found to be identical to the initial isolate by using genomic DNA restriction fragment patterns obtained by pulsed field gel electrophoresis, but it was resistant to amoxicillin-clavulanic acid. On isoelectric focusing, the ,I-lactamase from the relapse isolate exhibited a shift in the isoelectric point (pl) of its major band from 5.10 to 5.04 compared with the enzyme from the pretreatment isolate. As determined by using values of the amount of ,-lactamase inhibitor necessary to give 50 5% inhibition of P-lactamase-mediated hydrolysis of 50 FM nitrocefin, the I8-lactamase of the relapse isolate was also 200-fold more resistant than the enzyme from the pretreatment isolate to clavulanic acid and was more resistant to sulbactam, tazobactam, cloxacillin, and imipenem. The I-lactamase of the relapse isolate exhibited a 10-fold decrease in hydrolytic activity for cephaloridine and other hydrolyzable cephalosporins compared with that for nitrocefin. Acquired resistance to amoxicillin-clavulanic acid in this isolate of N. brasiliensis appears to have resulted from a mutational change affecting the inhibitor and active site(s) in the I8-lactamase.

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A syndrome characterized by rapidly progressive ischemic necrosis involving large areas of the skin and muscle, and by peripheral gangrene associated with extensive vascular calcifications was observed in a patient with end-stage renal failure on chronic hemodialysis. In an effort to control the disease, parathyroidectomy was performed which resulted in rapid improvement of tissue perfusion. However, the patient eventually died from sepsis within 2 months after admission. This case presents the typical features of the syndrome of systemic calciphylaxis. The literature is reviewed searching for similar cases of this poorly recognized, but life-threatening, clinical syndrome. The pathogenesis, clinical manifestations, and therapy of this unusual and rapidly progressive, but potentially reversible, condition are reviewed with emphasis on its prompt recognition and appropriate management.