Endocarditis Infecciosa

Background
Infective endocarditis (IE) is defined as an infection of the endocardial surface of the heart, which may include one or more heart valves, the mural endocardium, or a septal defect. Its intracardiac effects include severe valvular insufficiency, which may lead to intractable congestive heart failure and myocardial abscesses. IE also produces a wide variety of systemic signs andsymptoms through several mechanisms, including both sterile and infected emboli and various immunological phenomena.[1, 2, 3]
The history of IE can be divided into several eras. Lazaire Riviere first described gross autopsy findings of the disease in 1723. In 1885, William Osler presented the first comprehensive description of endocarditis in English. Lerner and Weinstein presented a thoroughdiscussion of this disease in modern times in their landmark series of articles, “Infective Endocarditis in the Antibiotic Era,” published in 1966 in the New England Journal of Medicine.[4, 5, 6]
IE currently can be described as infective endocarditis in the era of intravascular devices, as infection of intravascular lines has been determined to be the primary risk factor for Staphylococcus aureusbloodstream infections (BSIs). S aureus has become the primary pathogen of endocarditis.[7]
IE generally occurs as a consequence of nonbacterial thrombotic endocarditis, which results from turbulence or trauma to the endothelial surface of the heart. A transient bacteremia then seeds the sterile platelet/fibrin thrombus, with IE as the end result. Pathologic effects due to infection can includelocal tissue destruction and embolic phenomena. In addition, secondary autoimmune effects, such as immune complex glomerulonephritis and vasculitis, can occur. (See Pathophysiology.)
IE remains a diagnostic and therapeutic challenge. Its manifestations may be muted by the indiscriminate use of antimicrobial agents or by underlying conditions in frail and elderly individuals or immunosuppressedpersons. (See Diagnosis.)
Effective therapy has become progressively more difficult to achieve because of the proliferation of implanted biomechanical devices and the rise in the number of resistant organisms. Antibiotic prophylaxis has probably had little effect in decreasing the incidence of IE. (See Treatment and Management.)
For other discussions on IE, see Pediatric Bacterial Endocarditis,Infectious Endocarditis, Neurological Sequelae of Infective Endocarditis, and Antibiotic Prophylactic Regimens for Endocarditis.
Types of infective endocarditis
Endocarditis has evolved into several variations, keeping it near the top of the list of diseases that must not be misdiagnosed or overlooked. Endocarditis can be broken down into the following categories:
* Native valve endocarditis(NVE), acute and subacute
* Prosthetic valve endocarditis (PVE),[8] early and late
* Intravenous drug abuse (IVDA) endocarditis
Other terms commonly used to classify types of IE include pacemaker IE and nosocomial IE (NIE).
The classic clinical presentation and clinical course of IE has been characterized as either acute or subacute. Indiscriminate antibiotic usage and an increase inimmunosuppressed patients have blurred the distinction between these 2 major types; however, the classification still has clinical merit.[9]
Acute NVE frequently involves normal valves and usually has an aggressive course. It is a rapidly progressive illness in persons who are healthy or debilitated. Virulent organisms, such as S aureus and group B streptococci, are typically the causative agentsof this type of endocarditis. Underlying structural valve disease may not be present.
Subacute NVE typically affects only abnormal valves. Its course, even in untreated patients, is usually more indolent than that of the acute form and may extend over many months. Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease, typically are the...