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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravegetation host inflammatory cell function may play a role in the more salutary clinical outcomes in human right- vs. left-sided endocarditis. To study this in vivo, 90 rabbits with tricuspid Pseudomonas aeruginosa endocarditis received either no therapy (controls), nitrogen mustard (HN2) to induce combined granulocytopenia + monocytopenia, etoposide (VP-16-213) to induce selective monocytopenia, or dexamethasone. Intravegetation inflammatory cell influxes were scored on a semiquantitative histopathologic scale. In VP-16-213 and dexamethasone recipients and tricuspid endocarditis controls, gradual decreases in mean intravegetation bacterial densities were observed over a 13-day infection period; in contrast, HN2 treatment was associated with a significant increase in intravegetation bacterial densities by day 13 of infection (p less than 0.001 vs. other tricuspid endocarditis groups). Histopathologically, vegetations from untreated controls and dexamethasone recipients showed granulocyte influxes during infection, while HN2 treatment resulted in predominantly granulocyte depletion within infected tricuspid vegetations; VP-16-213 caused mononuclear cell depletion at this site. This study supports the concept that the granulocyte plays a critical role in modulating spontaneous endocardial clearances of bacteria in experimental tricuspid endocarditis.
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PMID:Pathogenic effects of monocytopenia, granulocytopenia and dexamethasone on the course of experimental Pseudomonas aeruginosa endocarditis in rabbits. 250 46

The role of blood monocytes in the attachment of streptococci to endocardial vegetations was investigated in an experimental Streptococcus sanguis endocarditis by depletion of blood monocytes with the cytostatic drug VP 16-213 alone and combined with anticoagulant treatment with warfarin sodium. The numbers of streptococci in the vegetations of control, monocytopenic, and monocytopenic/anticoagulated rabbits were comparable. In the vegetations streptococci were found mainly in areas free of phagocytic cells. It is concluded that streptococci do not have to be phagocytosed by monocytes in the circulation before being deposited on the surface of endocardial vegetations. Even the vegetations of intensively anticoagulated/monocytopenic rabbits showed colonies of streptococci embedded in polymerized fibrin and cellular material, this matrix possibly being held together by streptococcal dextran.
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PMID:Effects of monocytopenia and anticoagulation in experimental Streptococcus sanguis endocarditis. 737 72

In the pathogenesis of bacterial endocarditis (BE), the clotting system plays a cardinal role in the formation and maintenance of the endocardial vegetations. The extrinsic pathway is involved in the activation of the coagulation pathway with tissue factor (TF) as the key protein. Staphylococcus aureus is a frequently isolated bacterium from patients with BE. We therefore investigated whether S. aureus can induce TF activity (TFA) on fibrin-adherent monocytes, used as an in vitro model of BE. We also assessed in vivo in rabbits with catheter induced vegetations, the effect of S. aureus infection on vegetational TFA. In vitro experiments showed that adherent S. aureus induced TFA on fibrin-adherent monocytes which was optimal at a bacterium/monocyte ratio of 1 to 1. Monocyte damage occurred when this ratio exceeded 4 to 1 (visually) or 6 to 1 (propidium iodide influx) Consequently, TFA decreased. In vivo S. aureus led to very high bacterial numbers in the vegetations and a significant increase of their weight. However, TFA of infected vegetations was the same as of sterile ones. This may be due to the high bacteria to monocyte ratio as well as bacterium-induced monocyte damage. Teicoplanin treatment of infected rabbits reduced bacterial numbers in the blood and in the vegetations. Two-day treatment resulted in an increase of vegetational TFA, but after four-day treatment vegetational TFA dropped, most probably due to a suboptimal bacterium/monocyte ratio. S. aureus endocarditis in etoposide (Vepesid)-treated rabbits, leading to a selective monocytopenia, caused a rapid death of the animals. In these rabbits no vegetations were found at all. We conclude that, like Streptococcus sanguis and Staphylococcus epidermidis, S. aureus is able to induce TFA in fibrin-adherent blood monocytes. In addition, monocytes have a protective effect during the course of S. aureus endocarditis.
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PMID:Role of monocytes in experimental Staphylococcus aureus endocarditis. 1089 97