How sweet is the pacemaker?

Pacemaker infections can be difficult to diagnose, especially when they present with non-specific symptoms and signs a long time after insertion of the device. Unidentified or partially treated low-grade chronic sepsis can result in multisystem disease processes with significant mortality and morbidity. Therefore, a high index of suspicion is required to identify the pacemaker as the source of sepsis and treat it effectively. This report describes a case of chronic pacemaker wire infection, which eventually presented with Sweet's syndrome, a rare manifestation of infective endocarditis.

An unusual but reversible cause of ventricular fibrillation.

A 61-year-old woman was admitted with general malaise, chest pain and breathlessness. During her inpatient stay she sustained a ventricular fibrillation (VF) arrest which was successfully terminated with direct current cardioversion. Cardiac investigations revealed poor left ventricular systolic function but unequivocally normal coronary arteries. During the course of her admission a macular rash developed and following investigations including a renal biopsy, a new diagnosis of systemic lupus erythematosus (SLE) and related myocarditis was reached. First presentation of lupus with myocarditis and VF is uncommon, however reaching the correct diagnosis is important as due to the reversible nature of the condition and improvement in left ventricular systolic function with medical therapy, an implantable cardioverter defibrillator (ICD) might not be appropriate. Our case report demonstrates the importance of screening for reversible conditions when considering ICD therapy for secondary prevention of malignant arrhythmias.

Amodiaquine and artemether-lumefantrine select distinct alleles of the Plasmodium falciparum mdr1 gene in Tanzanian children treated for uncomplicated malaria.

The artemisinin-based combination therapies artemether-lumefantrine (AL) and amodiaquine (AQ) plus artesunate have been adopted for treatment of Plasmodium falciparum malaria in many African countries. Molecular markers of parasite resistance suitable for surveillance have not been established for any of the component drugs in either of these combinations. We assessed P. falciparum mdr1 (Pfmdr1) alleles present in 300 Tanzanian children presenting with uncomplicated falciparum malaria, who were enrolled in a clinical trial of antimalarial therapy. Pfmdr1 genotype analysis was also performed with isolates from 182 children who failed AQ monotherapy and 54 children who failed AL treatment. Pfmdr1 alleles 86Y, 184Y, and 1246Y were more common among treatment failures in the AQ group than among pretreatment infections. The converse was found in the AL-treated group. Children presenting with the 86Y/184Y/1246Y Pfmdr1 haplotype and treated with AQ were significantly more likely to retain this haplotype if they were parasite positive during posttreatment follow-up than were children treated with AL (odds ratio, 33.25; 95% confidence interval, 4.17 to 1441; P, <0.001). We conclude that AL and AQ exert opposite within-host selective effects on the Pfmdr1 gene of P. falciparum.