31 research outputs found

    Mycobacterium chelonae, an ‘atypical’ cause of an LVAD driveline infection

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    We describe the first patient with a left ventricular assist device (LVAD) driveline infection caused by Mycobacterium chelonae presenting with persistent infection despite conventional antibiotics. Treatment was successful with surgical debridement, driveline exit relocation, and a 4-month period of antibiotics. In the case of a culture-negative LVAD driveline infection, non-tuberculous mycobacteria should be considered. This case illustrates tha

    Effects on cardiac function, remodeling and inflammation following myocardial ischemia-reperfusion injury or unreperfused myocardial infarction in hypercholesterolemic APOE*3-Leiden mice

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    Many novel therapies to treat myocardial infarction (MI), yielding promising results in animal models, nowadays failed in clinical trials for several reasons. The most used animal MI model is based on permanent ligation of the left anterior descending (LAD) coronary artery in healthy mice resulting in transmural MI, while in clinical practice reperfusion is usually accomplished by primary percutaneous coronary interventions (PCI) limiting myocardial damage and inducing myocardial ischemia-reperfusion (MI-R) injury. To evaluate a more similar murine MI model we compared MI-R injury to unreperfused MI in hypercholesterolemic apolipoprotein (APO)E*3-Leiden mice regarding effects on cardiac function, left ventricular (LV) remodeling and inflammation. Both MI-R and MI resulted in significant LV dilation and impaired cardiac function after 3 weeks. Although LV dilation, displayed by end-diastolic (EDV) and end-systolic volumes (ESV), and infarct size (IS) were restricted following MI-R compared to MI (respectively by 27.6% for EDV, 39.5% ESV, 36.0% IS), cardiac function was not preserved. LV-wall thinning was limited with non-transmural LV fibrosis in the MI-R group (66.7%). Two days after inducing myocardial ischemia, local leucocyte infiltration in the infarct area was decreased following MI-R compared to MI (36.6%), whereas systemic circulating monocytes were increased in both groups compared to sham (130.0% following MI-R and 120.0% after MI). Both MI-R and MI models against the background of a hypercholesterolemic phenotype appear validated experimental models, however reduced infarct size, restricted LV remodeling as well as a different distributed inflammatory response following MI-R resemble the contemporary clinical outcome regarding primary PCI more accurately which potentially provides better predictive value of experimental therapies in successive clinical trials.Cardiolog

    Australasian pilchard mortalities

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    A large-scale epizootic occurred in the Australasian pilchard Sardinops sagax between March and September 1995. The deaths occurred along 5000km of the Australian coastline and 500km of the New Zealand coastline. Affected fish died within a few minutes of clinical signs of respiratory distress and death was associated with hypoxaemia and hypercapnia. Significant lesions were confined to the gills and comprised acute to subacute inflammation followed by epithelial hypertrophy and hyperplasia. The lesions were initially focal but progressed to become generalized over about 4days. Only a herpesvirus was consistently present in gills of affected fish and absent from unaffected pilchards. There was no correlation with oceanographic conditions or the presence of plankton. The rate of spread of the mortality front (approximately 30km/day) in relation to the migration rate of pilchards and prevailing currents suggested that a vector might be involved. The disease may be the result of a virus introduced into Australian waters, or of a newly emerged virus
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