Infective Endocarditis and Other Intravascular Infections

Freedman, Lawrence R.

doi:10.1007/978-1-4684-8208-9

Cited by 35 publications

(14 citation statements)

References 111 publications

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“…Platelet microbicidal activity is very likely to operate in humans as well, as VS and Staphylococcus aureus isolated from vegetations of endocarditis patients are generally less susceptible than oral isolates (7,8,38). Despite an apparent selective advantage, the VS isolates from IE patients are presumably still subject to the platelet defense system, since these isolates are only slightly less susceptible to purified thrombocidins in vitro (9, 41).In the rabbit model of experimental IE, a catheter inserted retrograde across the aortic valve induces platelet-fibrin vegetations (18,19,32). The rabbits are then challenged with an intravenous (i.v.)…”

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Interleukin 1α Increases the Susceptibility of Rabbits to Experimental Viridans Streptococcal Endocarditis

et al. 2006

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Major predisposing conditions for infective endocarditis (IE) are the presence of a cardiac platelet-fibrin vegetation and of circulating bacteria with relatively low susceptibility to microbicidal activity of blood platelets. The influence of proinflammatory conditions on development of IE is unknown. We studied the effects of the presence of a catheter, inserted to induce platelet-fibrin vegetations, and of the proinflammatory cytokine interleukin-1␣ in rabbit experimental IE. Leaving the catheter in place after challenge with viridans streptococci predisposed for experimental IE. IE susceptibility rapidly decreased between 0 to 6 h after catheter removal. The catheter did not predispose for IE by providing a site for bacterial adherence, as almost all explanted catheters were culture negative. To mimic the proinflammatory influence of the catheter, rabbits were injected with interleukin-1␣ at 24 h after catheter removal and at 0, 1, and 3 h before bacterial challenge. Interleukin-1␣ injected 3 h prior to challenge significantly increased IE incidence due to a platelet releasatesusceptible Streptococcus oralis strain, with rapidly increasing numbers of bacteria within the vegetations. IE due to the Streptococcus sanguis strain less susceptible to platelet releasate was not enhanced. We conclude that proinflammatory stimuli, either a catheter or interleukin-1␣, enhanced susceptibility to IE due to the platelet releasate-susceptible S. oralis. As with rabbits, temporary intravascular proinflammatory conditions may predispose for IE in humans at risk for this serious infection.Infective endocarditis (IE) denotes infection of the endocardial surface of the heart (3). The presence of sterile vegetations at the damaged surface of the endocardium (1) and bacteria and fungi circulating in the bloodstream that are able to adhere to and to colonize the vegetation (3,9,13,29,35) are prerequisites in the pathogenesis of IE. A great diversity of microorganisms cause IE, with viridans streptococci (VS) as the predominant microorganisms encountered in native valve IE (3,14,16,24,27,30,33,34).Another major determinant for the development of IE is the susceptibility of the circulating microorganisms to platelet microbicidal activity (2, 7-9) due to cationic proteins such as thrombocidin or platelet microbicidal proteins, released after thrombin stimulation (7,9,26,36,39). Neutralization of this defense mechanism enhanced susceptibility of rabbits to IE due to platelet releasate-susceptible VS (8). Platelet microbicidal activity is very likely to operate in humans as well, as VS and Staphylococcus aureus isolated from vegetations of endocarditis patients are generally less susceptible than oral isolates (7,8,38). Despite an apparent selective advantage, the VS isolates from IE patients are presumably still subject to the platelet defense system, since these isolates are only slightly less susceptible to purified thrombocidins in vitro (9, 41).In the rabbit model of experimental IE, a catheter inserted retrograde across the aort...

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confidence: 99%

“…In the rabbit model of experimental IE, a catheter inserted retrograde across the aortic valve induces platelet-fibrin vegetations (18,19,32). The rabbits are then challenged with an intravenous (i.v.)…”

mentioning

confidence: 99%

Interleukin 1α Increases the Susceptibility of Rabbits to Experimental Viridans Streptococcal Endocarditis

et al. 2006

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“…Recent investigations have led to an understanding of the initiating event in the pathogenesis of infective endocarditis, the adherence of circulating organisms to sterile fibrin-platelet thrombi in the surface of damaged valves (1). However, the factors responsible for subsequent vegetation development have not been elucidated.…”

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Tissue factor is a major stimulus for vegetation formation in enterococcal endocarditis in rabbits.

Drake¹,

Rodgers²,

Sande³

1984

J. Clin. Invest.

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Abstract. We examined the possible mechanisms of local initiation of coagulation in vegetation formation in enterococcal endocarditis by using a rabbit model. Contact activation and tissue factor expression by freshly excised aortic valves were assessed using assays developed for use with cultured cells. Bacteria alone lacked procoagulant activity and contact activation of plasma by excised valves did not occur. 4-d infected but not control valves expressed significant tissue factor activity (231±17 mU vs. 51±7 SE), which did not correlate with numbers of bacteria in vegetations. Tissue factor activity was also present in valves from rabbits infected for and 2 d, as well as those from granulocytopenic and monocytopenic animals. Our findings suggest that tissue factor, expressed by host cells in response to infection, is a major stimulus for fibrin deposition in vegetation development.

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“…This model of experimental endocarditis is a stringent test of antibiotic bactericidal activity, since the polymorphonuclear leukocytes have limited access to the bacteria embedded in the valvular vegetations (7). Because of the low therapeutic efficacy of coumermycin in endocarditis induced by one S. aureus * Corresponding author.…”

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“…Two additional methicillin-susceptible strains of S. aureus, coded strain 7 and strain 560, were used to induce endocarditis to test further the therapeutic efficacy of coumermycin. (10-and 100-fold) of this concentrate (containing 109 and 108 CFU/ml, respectively) were prepared by dilution in normal saline.…”

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Treatment of Staphylococcus aureus endocarditis in rats with coumermycin A1 and ciprofloxacin, alone or in combination

Perronne¹,

Malinverni²,

Glauser³

1987

Antimicrob Agents Chemother

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Infective Endocarditis and Other Intravascular Infections

Abstract: A Continuation Order Plan is available for this series. A continuation order will bring delivery of each new volume immediately upon publication. Volumes are billed only upon actual shipment. For further information please contact the publisher.

Cited by 35 publications

References 111 publications

Interleukin 1α Increases the Susceptibility of Rabbits to Experimental Viridans Streptococcal Endocarditis

Interleukin 1α Increases the Susceptibility of Rabbits to Experimental Viridans Streptococcal Endocarditis

Tissue factor is a major stimulus for vegetation formation in enterococcal endocarditis in rabbits.

Treatment of Staphylococcus aureus endocarditis in rats with coumermycin A1 and ciprofloxacin, alone or in combination

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