ABSTRACT
OBJECTIVES: This study reports a high-volume tertiary care center experience with the microbiology of cardiac implantable electronic devices (CIED) infections with assessment of temporal trends and profiles of late versus early infections. BACKGROUND: The rates of CIED infections have been increasing. With changing demographics, patient and device characteristics, prophylactic measures, and the wide use of broad-spectrum antibiotics, there is need for updated contemporary data on the microbiology of CIED infections. METHODS: The study included 816 consecutive patients with confirmed CIED infections who underwent transvenous lead extraction at our institution between the years 2000 and 2011. Blood cultures were obtained in addition of pocket swabs, pocket capsule, and leads. RESULTS: Staphylococcal species remained the most common pathogens in CIED infections (68.4%), especially coagulase-negative species (37.6%). Methicillin-resistant staphylococci were the pathogens in 33.8% of all CIED infections and accounted for 49.4% of all staphylococcal infections. Gram-negative pathogens were identified in 8.9% of cases, whereas 13.2% were with negative cultures. CIED infections related to streptococci (2.5%), enterococci (4.2%), anaerobes (1.6%), fungi (0.9%), and mycobacteria species (0.2%) were less common. Of pocket infections, 49.5% occurred more than 1 year after pocket manipulation, and 53.6% of these were related to coagulase-negative staphylococci. In contrast, most endovascular infections were related to Staphylococcus aureus. The proportions of culture negative infections have increased (p < 0.0001). CONCLUSIONS: The study provides contemporary data on the microbiology of CIED infections. The rates of methicillin resistance seem to be greater than those reported from the preceding decade.
ABSTRACT
Transgenic mice, containing a chimeric gene in which the cDNA for phosphoenolpyruvate carboxykinase (GTP) (PEPCK-C) (EC 4.1.1.32) was linked to the alpha-skeletal actin gene promoter, express PEPCK-C in skeletal muscle (1-3 units/g). Breeding two founder lines together produced mice with an activity of PEPCK-C of 9 units/g of muscle (PEPCK-C(mus) mice). These mice were seven times more active in their cages than controls. On a mouse treadmill, PEPCK-C(mus) mice ran up to 6 km at a speed of 20 m/min, whereas controls stopped at 0.2 km. PEPCK-C(mus) mice had an enhanced exercise capacity, with a VO(2max) of 156 +/- 8.0 ml/kg/min, a maximal respiratory exchange ratio of 0.91 +/- 0.03, and a blood lactate concentration of 3.7 +/- 1.0 mm after running for 32 min at a 25 degrees grade; the values for control animals were 112 +/- 21 ml/kg/min, 0.99 +/- 0.08, and 8.1 +/- 5.0 mm respectively. The PEPCK-C(mus) mice ate 60% more than controls but had half the body weight and 10% the body fat as determined by magnetic resonance imaging. In addition, the number of mitochondria and the content of triglyceride in the skeletal muscle of PEPCK-C(mus) mice were greatly increased as compared with controls. PEPCK-C(mus) mice had an extended life span relative to control animals; mice up to an age of 2.5 years ran twice as fast as 6-12-month-old control animals. We conclude that overexpression of PEPCK-C repatterns energy metabolism and leads to greater longevity.
