Septic discitis and septic pulmonary emboli: rare complications of Proteus mirabilis urinary tract infection.

Proteus mirabilis is a gram-negative bacterium frequently considered a pathogen of the urinary tract. Septic discitis and septic pulmonary emboli resulting from P. mirabilis urosepsis is a rare phenomenon. We report a 39-year-old woman who was admitted to our hospital with a complicated urinary tract infection resulting in bacteraemia, septic discitis, paraspinal abscesses and septic emboli. She was treated with a prolonged course of intravenous antibiotics resulting in the clinical resolution of her symptoms. Based on our PubMed search of the English literature, this is only the second reported case of septic discitis caused by P. mirabilis This paper illustrates that physicians should include septic discitis caused by P. mirabilis as a possible aetiology of low back pain in patients with active or recently treated urinary tract infection. Additionally, this article discusses the pathogenesis and other complications resulting from P. mirabilis bacteraemia.

The First Reported Case of Post-Atrioventricular Node Ablation Enterococcus Faecalis Bacteremia in a Patient With Colonic Tubular Adenomas and Chronic Steroid Use.

We present the case of a 73-year-old immunosuppressed male with a history of multiple benign, colonic adenomas who was admitted to our hospital with Enterococcus faecalis (E. faecalis) bacteremia. The patient also had a prior history of dual-chamber pacemaker placement for sick sinus syndrome. Two days before the admission, the patient had undergone radiofrequency ablation of the atrioventricular (AV) node for refractory atrial flutter without receiving any peri-procedural antibiotic prophylaxis. Despite high-grade bacteremia and a high NOVA (Number of positive blood cultures, Origin of the bacteremia, previous Valve disease, Auscultation of heart murmur) score, there was no evidence of infective endocarditis on transesophageal echocardiogram (TEE). The patient was treated successfully with appropriate intravenous antibiotics, and he recovered well. To the best of our knowledge, this is the first reported case of post-AV node ablation E. faecalis bacteremia. We conclude that the presence of colonic lesions and immunosuppression can increase the risk of peri-procedural E. faecalis bacteremia, and clinicians should consider antibiotic prophylaxis in this high-risk patient group.

Low-dose caffeine administration increases fatty acid utilization and mitochondrial turnover in C2C12 skeletal myotubes.

Caffeine has been shown to directly increase fatty acid oxidation, in part, by promoting mitochondrial biogenesis. Mitochondrial biogenesis is often coupled with mitophagy, the autophagy-lysosomal degradation of mitochondria. Increased mitochondrial biogenesis and mitophagy promote mitochondrial turnover, which can enhance aerobic metabolism. In addition, recent studies have revealed that cellular lipid droplets can be directly utilized in an autophagy-dependent manner, a process known as lipophagy. Although caffeine has been shown to promote autophagy and mitochondrial biogenesis in skeletal muscles, it remains unclear whether caffeine can increase lipophagy and mitochondrial turnover in skeletal muscle as well. The purpose of this study was to determine the possible contribution of lipophagy to caffeine-dependent lipid utilization. Furthermore, we sought to determine whether caffeine could increase mitochondrial turnover, which may also contribute to elevated fatty acid oxidation. Treating fully differentiated C2C12 skeletal myotubes with 0.5 mM oleic acid (OA) for 24 hr promoted an approximate 2.5-fold increase in cellular lipid storage. Treating skeletal myotubes with 0.5 mM OA plus 0.5 mM caffeine for an additional 24 hr effectively returned cellular lipid stores to control levels, and this was associated with an increase in markers of autophagosomes and autophagic flux, as well as elevated autophagosome density in TEM images. The addition of autophagy inhibitors 3-methyladenine (10 mM) or bafilomycin A1 (10 µM) reduced caffeine-dependent lipid utilization by approximately 30%. However, fluorescence and transmission electron microscopy analysis revealed no direct evidence of lipophagy in skeletal myotubes, and there was also no lipophagy-dependent increase in fatty acid oxidation. Finally, caffeine treatment promoted an 80% increase in mitochondrial turnover, which coincided with a 35% increase in mitochondrial fragmentation. Our results suggest that caffeine administration causes an autophagy-dependent decrease in lipid content by increasing mitochondrial turnover in mammalian skeletal myotubes.