Literature DB >> 1151519

Experimental bacterial endocarditis. IV. Structure and evolution of very early lesions.

D T Durack.   

Abstract

The vegetations of experimental sterile and bacterial endocarditis in rabbits were studied using light, immunofluorescent and electron microscopy. At an early stage, both lesions were composed chiefly of masses of platelets supported in a scaffolding of fibrin strands. In previous studies, this structure has often been described merely as "fibrin". After i.v. injection of Thorotrast, sterile vegetations showed remarkable accumulations of mononuclear phagocytes containing this substance, on surfaces projecting into the bloodstream. Sections fixed 30 min. after i.v. injection of streptococci also showed these phagocytes, which contained large numbers of bacteria. The possibility that BE is initiated by phagocytosis of circulating bacteria has been raised. Smaller numbers of circulating streptococci reached the vegetation by direct adhesion to exposed surfaces. In contrast, a majority of Proteus and Staphylococcus albus adhered directly to vegetations, without phagocytosis. Subsequently, these first settlers multiplied rapidly to form rounded colonies surrounded by capsules of fibrin, which apparently provided protection from phagocytosis. The vegetations grew by accretion of layers of fibrin and platelets, with colonies sandwiched between them. This suggested that a cycle of thrombosis and reseeding by circulating bacteria was a factor in their growth. Colonies showed morphological changes consistent with ageing after two days. Healing occurred by endothelialisation and organisation, and was greatly accelerated by penicillin treatment.

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Year:  1975        PMID: 1151519     DOI: 10.1002/path.1711150204

Source DB:  PubMed          Journal:  J Pathol        ISSN: 0022-3417            Impact factor:   7.996


  93 in total

1.  Invasion and killing of human endothelial cells by viridans group streptococci.

Authors:  Murray W Stinson; Susan Alder; Sarmishtha Kumar
Journal:  Infect Immun       Date:  2003-05       Impact factor: 3.441

2.  Staphylococcus aureus, Platelets, and the Heart.

Authors: 
Journal:  Curr Infect Dis Rep       Date:  2000-08       Impact factor: 3.725

3.  The Streptococcus gordonii platelet binding protein GspB undergoes glycosylation independently of export.

Authors:  Barbara A Bensing; Bradford W Gibson; Paul M Sullam
Journal:  J Bacteriol       Date:  2004-02       Impact factor: 3.490

Review 4.  Pharmacokinetic and pharmacodynamic requirements for antibiotic therapy of experimental endocarditis.

Authors:  A C Cremieux; C Carbon
Journal:  Antimicrob Agents Chemother       Date:  1992-10       Impact factor: 5.191

5.  Bacterial remnants in an aortic valve after treatment for staphylococcal endocarditis.

Authors:  E J Young; F Gyorkey
Journal:  Tex Heart Inst J       Date:  1986-12

6.  Four proteins encoded in the gspB-secY2A2 operon of Streptococcus gordonii mediate the intracellular glycosylation of the platelet-binding protein GspB.

Authors:  Daisuke Takamatsu; Barbara A Bensing; Paul M Sullam
Journal:  J Bacteriol       Date:  2004-11       Impact factor: 3.490

7.  Platelet microbicidal protein alone and in combination with antibiotics reduces Staphylococcus aureus adherence to platelets in vitro.

Authors:  M R Yeaman; P M Sullam; P F Dazin; A S Bayer
Journal:  Infect Immun       Date:  1994-08       Impact factor: 3.441

8.  In vitro resistance to platelet microbicidal protein correlates with endocarditis source among bacteremic staphylococcal and streptococcal isolates.

Authors:  T Wu; M R Yeaman; A S Bayer
Journal:  Antimicrob Agents Chemother       Date:  1994-04       Impact factor: 5.191

9.  Protective role of complement in experimental Escherichia coli endocarditis.

Authors:  D T Durack; P B Beeson
Journal:  Infect Immun       Date:  1977-04       Impact factor: 3.441

10.  Staphylococcus aureus induces platelet aggregation via a fibrinogen-dependent mechanism which is independent of principal platelet glycoprotein IIb/IIIa fibrinogen-binding domains.

Authors:  A S Bayer; P M Sullam; M Ramos; C Li; A L Cheung; M R Yeaman
Journal:  Infect Immun       Date:  1995-09       Impact factor: 3.441

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