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Results for “ENDOCARDITIS, INFECTIOUS”

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At least 307 records · Page 17Linked to original sources

[The evolution of the clinical course of infectious endocarditis].

As many as 188 records of IE patients were studied as were 67 autopsies of deceased persons. Significant changes in the clinical course of IE were disclosed over the past 10-15 years versus previous 15: more prominent role of staphylococcal and gram-negative flora in the etiology of the illness, with microbial associations-caused IE cases having become more common. Diagnostic value of hemoculture did not appear to show much promise. The following items were found to be important risk factors for IE: prior viral and bacterial infection, invasive interventions, and chronic somatic diseases. There prevailed those IE forms having appeared on the intact heart valves in elderly persons and those at a mature age. In the course of the illness there tended to be more toxic and allergic manifestations, thromboembolic complications, and extensive vascular pathology.

Adolescent↗

Infectious endocarditis in pacemaker endocardial leads: report of three cases.

Three cases of endocarditis affecting endocardial leads of permanent pacemakers are presented with a review of the literature. Vegetations were identified using transesophageal echocardiography. Infection of pacemaker leads is far less common than infection at the site of the pulse generator with greater morbidity and mortality and generally requiring surgical removal of both electrodes and power source. The most frequent infective agents are stahylococcus varieties.

Adult↗

[Role of staphylococcus aureus hemolytic toxin-alpha in pathogenesis of infectious endocarditis: studies in vitro].

AIM: To study effects of alpha-toxin (AT) Staphylococcus aureus on human platelets and endothelial cells. MATERIALS AND METHODS: Concentrations of intracellular calcium in human platelets and endothelial cells were estimated by fluorescence, phosphoinositide metabolism in the endothelial cells was studied using 3H-myoinositole. RESULTS: AT induced a dose-dependent increase of intracellular calcium in blood and vascular cells, stimulates dose-dependent formation of inositol phosphates in endothelial cells. CONCLUSION: AT action on the platelets and endothelial cells results in a significant receptor-independent rise in concentration of intracellular calcium, activation of phosphoinositide metabolism, death of cells. These data support the hypothesis that the platelet and endothelial cell damage is mostly due to the passive Ca2+ influxvia pores formed by AT in cellular membrane.

Bacterial Toxins↗