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Chapter 18 : Persistence of Infective Endocarditis

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Abstract:

Infective endocarditis describes a family of persistent microbial infections of the heart valves. This chapter explores their ability to behave as endogenous pathogens and is instructive as we try to understand persistence of the larger constellation of endocarditis-associated pathogens. Infective endocarditis generally occurs in individuals with previously diseased or damaged heart valves, most frequently after bacteremia containing viridans streptococci or . Many of the most common microorganisms associated with infective endocarditis are considered to be of low virulence, often causing no known disease in their native niches. Patients with infective endocarditis show elevated anti-phospholipid antibodies associated with endothelial-cell activation, thrombin generation, and impairment of fibrinolysis. Adhesion to platelets and preformed platelet-fibrin clots would appear intuitively to be associated with the ability of microbes to infect platelet vegetations and cause infective endocarditis. Dextran synthesis by viridans streptococci has been suggested to be a virulence factor in infective endocarditis, promoting adhesion and persistence. The ability of microbes to induce platelet aggregation in vitro may be associated with the pathogenicity of those strains in infective endocarditis. The host distinguishes the commensals from exogenous pathogens. When commensals breach the mucosa and infect the heart valves in infective endocarditis, the host immune repertoire against these endogenous pathogens is programmed for systemic tolerance.

Citation: Herzberg M. 2000. Persistence of Infective Endocarditis, p 357-374. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch18

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FIGURE 1

Tripartite model of infective endocarditis. The persistence of endocarditis reflects the balance between the host's ability to repair an injured valve and promote or support a bland nonbacterial thrombotic vegetation and the virulence of the infecting microbe.

Citation: Herzberg M. 2000. Persistence of Infective Endocarditis, p 357-374. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch18
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Image of FIGURE 2
FIGURE 2

Mechanisms of microbial persistence in infective endocarditis.

Citation: Herzberg M. 2000. Persistence of Infective Endocarditis, p 357-374. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch18
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