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==Overview==
==Overview==
Endocarditis may be classified based on the underlying pathophysiology of the process (infective vs. non-infective), the onset of the disease (acute vs. subacute or short incubation vs. long incubation), results of the cultures (culture positive vs. culture negative), the nature of the valve (native vs. prosthetic) and the valve infected ([[aortic]], [[mitral]], or [[tricuspid valve]]).
Endocarditis may be classified based on the underlying pathophysiology of the process (infective vs. non-infective), the onset of the disease (acute vs. subacute or short incubation vs. long incubation), results of the cultures (culture positive vs. culture negative), the nature of the valve (native vs. prosthetic) and the valve affected ([[aortic]], [[mitral]], or [[tricuspid valve]]).


== Infective Endocarditis ==
== Infective Endocarditis ==

Revision as of 13:48, 31 August 2015

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Endocarditis may be classified based on the underlying pathophysiology of the process (infective vs. non-infective), the onset of the disease (acute vs. subacute or short incubation vs. long incubation), results of the cultures (culture positive vs. culture negative), the nature of the valve (native vs. prosthetic) and the valve affected (aortic, mitral, or tricuspid valve).

Infective Endocarditis

Given the poor vascular supply of the heart valves, entrance of infection fighting components of the bloodstream (such as white blood cells) are reduced. So if an organism (such as bacteria) establishes a foothold in the valves, the bodies ability to fight the infection inside the valve structures is reduced.

Normally, blood flows smoothly through these valves. If they have been damaged (for instance in rheumatic fever) the trauma of non-laminar flow can increase the risk of infection. Likewise, damage to the endothelium or lining of the vascular structures improves the ability of bacteria to bind to the surface.

Non-Infective Endocarditis

Non-infective or marantic endocarditis is rare. A form of sterile endocarditis is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and the antiphospholipid syndrome. Non-infective endocarditis may also occur in patients with cancer, particularly mucinous adenocarcinoma.

Short Incubation Versus Long Incubation

Traditionally, infective endocarditis has been clinically divided into acute and subacute (because the patients tend to live longer in subacute as opposed to acute) endocarditis. This classifies both the rate of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity.

This terminology is now discouraged. The terms short incubation (meaning less than about six weeks), and long incubation (greater than about six weeks) are preferred.

Culture Positive Versus Culture Negative

Infective endocarditis may also be classified as culture-positive or culture-negative. Culture-negative endocarditis is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be 'fastidious' because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.

Native Valve Endocarditis Versus Prosthetic Valve Endocarditis

Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important. Prosthetic-valve endocarditis constitutes 10-20% of cases of endocarditis. The greatest risk is during the first 6 months after valve surgery. Staphylococcus epidermidis is the most common cause. The infection often extends into the anulus and cardiac tissues.

References

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