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February 27, 2017
Infective Endocarditis Clinical Presentation-Microbiology-Pathology

Clinical Presentation-Microbiology-Pathology

Introduction

During the last five decades, significant advances have occurred in the diagnosis and treatment of patients with infective endocarditis. Imaging studies such as transthoracic and transesophageal echocardiography have facilitated an early and accurate diagnosis of this condition in most patients. The introduction and broad use of antimicrobial therapy have led to the successful treatment of this disease in the majority of patients with total eradication of the disease process. Finally, surgical intervention has become the most effective and indispensable treatment in selected patients particularly those with advanced valvular lesions resulting in significant valvular regurgitation, and those with persistent sepsis and/or affected with virulent micro-organisms. It is important, however, to stress that infective endocarditis remains a very serious condition which carries a high risk of morbidity and mortality.

Recent data suggest that the overall incidence of infective endocarditis continues to increase despite the use of preventative measures such as antibiotic prophylaxis in patients with valvular heart disease undergoing invasive procedures. This incidence is estimated at 5 to 15 per 100,000 people per year. In the mitral position, the existence of predisposing conditions such as rheumatic valve disease, or degenerative disease is a common finding. Healthcare associated factors such as intravenous therapy and long-term hemodialysis catheter are also important predisposing risk factors, particularly in developed countries. Infective endocarditis can also occur in patients with prosthetic mitral valve with an actuarial cumulative incidence of 3.2 to 5.7 percent at five years. The risk is greatest during the first 12 months following surgery (1 to 2%) and declines overtime to a lower rate around 0.2 to 0.35 percent per year.

 

Clinical presentation

Acute endocarditis is often caused by a virulent microorganism (e.g. Staphylococcus aureus) and the clinical course is usually fulminating. Clinical manifestations of acute infective endocarditis include sepsis, heart failure and peripheral embolization. Sepsis is revealed by a high grade fever, chills and various neurologic symptoms. Renal failure due to glomerulonephritis is seen in about 10 to 20 % of acute cases. Musculoskeletal symptoms are also frequently reported. At physical examination, the diagnosis of a new cardiac murmur is in favor of the diagnosis. Janeway lesions and Roth spots are occasionally observed.

Subacute endocarditis is commonly due to less virulent microorganism (e.g. Streptococcus viridans) and is typically seen in patients with preexisting mitral valve disease. Subacute endocarditis is characterized by prolonged low-grade fever, joint pain, myalgia, and splenomegaly. The diagnosis should be strongly considered in patients with preexisting valvular disease and long-lasting fever of unknown origin. At physical examination, the modification of a preexisting cardiac murmur or the detection of a new murmur involving another valve is suggestive of the diagnosis. Osler's nodes can be observed in subacute endocarditis. Blood cultures are often negative, particularly if the patient has received broad spectrum antibiotics for symptomatic treatment of fever.

Prosthetic mitral valve endocarditis can present as acute or subacute endocarditis.

Duke criteria have been used for the diagnosis of infective endocarditis. The association of 2 major, 1 major and three minor, or 5 minor criteria is required to establish the diagnosis.

In most instances, the diagnosis is made after the observation of characteristic valvular lesions on echocardiography and the isolation of the microorganism on blood cultures.

Stephen Hales

 

Microbiology

Mitral valve endocarditis is most often due to infection by either Streptococcal or Staphylococcal bacteria. The principal organisms involved in native valve endocarditis are Streptococcus viridians or bovis and Staphylococcus aureus. However, during the last two decades, Staphylococcus epidermidis has been detected with an increasing frequency in patients with native valve endocarditis and underlying degenerative disease (5-8% of cases). Staphylococcus aureus is a virulent microorganism and can cause infective endocarditis in patients with a normal mitral valve. Fungal infective endocarditis (Candida albicans, Aspergillus fumigatus ) is rare but associated with a high morbi-mortality.

The microbiology of infective endocarditis is relatively predictable in some patients with additional risk factors. Staphylococcus aureus remains the most common causative microorganism in IV drug abusers as well as in patients with insulin dependent diabetes mellitus. The infection of cardiac valves by Pseudomonas aeruginosa and other gram-negative bacilli is also diagnosed with increasing frequency among IV drug abusers during the last decade. Nosocomial infective endocarditis is typically caused by gram-positive cocci. Staphylococcus aureus is often identified as the infectious agent in health care-associated endocarditis related to long-term indwelling catheters.

Early prosthetic valve endocarditis, defined as endocarditis occurring the first 6 months following surgery, is most often due to Staphylococcus epidermidis, Staphylococcus aureus, and Enterococcus faecalis . The microbiology profile of late prosthetic endocarditis is similar to that of native mitral endocarditis with the addition of gram-negative bacilli, particularly the HACEK group (Heamophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella), and fungi (candida species).

 

Pathology

Primary native mitral endocarditis

In patients with native mitral endocarditis, the infectious process can cause several types of lesions including vegetations, chordae rupture, leaflet abscess/ perforation, and mitral annular abscess.

Vegetations are often localized on the atrial side of mitral leaflets, particularly the anterior leaflet. They may be mobile or adherent with a sessile or pedicled base of insertion and vary in size and rate of growth. Highly virulent microorganisms such as methicillin resistant staphylococcus aureus (MRSA) and fungal infections may produce large vegetations with extensive valvular destruction and are at high risk for systemic embolization. Occasionally, these large vegetations may cause mitral valve obstruction with congestive heart failure. Vegetations may remain adherent to the mitral valve leaflets and become organized and calcified overtime without significant hemodynamic disturbances.

If the infectious process extends to the free margin of the mitral leaflets, or starts directly at the subvalvular apparatus, chordae rupture with leaflet prolapse is a common finding. These lesions are typically localized at the middle scallop of the anterior (A2) or the posterior leaflet (P2), or the postero-medial commissural area.

The valvular abscess consists of necrotic and inflammatory tissue underneath the endocardial surface of the leaflets. It frequently involves the anterior leaflet and may produce a true aneurysm of the body of the leaflet. Leaflet perforation is the final stage in the evolution of an abscess, although extension into the annulus and/or intervalvular fibrous body may also occur. In the latter scenario, partial anterior leaflet detachment with severe valvular regurgitation is commonly observed.

Mitral annular abscess is the most serious valvular lesion and can occur either following the rapid extension of infection from the body of the leaflet or primarily in the presence of preexisting calcified annulus. In the absence of appropriate surgical treatment, this condition may further be complicated by false aneurysm of the left ventricle or the atrio-ventricular groove with potentially a fatal outcome.

Secondary native mitral endocarditis

Aortic valve endocarditis may cause concomitant mitral valve endocarditis because of the proximity of these two anatomic structures. In the first scenario, an aortic annular abscess can extend by contiguity to the aorto-mitral curtain and then to the mitral annulus. Subsequently the infection can further spread to the anterior leaflet of the mitral valve, which may result in its partial/complete detachment from the annulus.

In the second scenario, the diastolic jet of aortic insufficiency can cause a lesion on the anterior mitral leaflet which can be a vegetation, leaflet abscess, and/or leaflet perforation. This so-called "kissing lesion" is observed in 10-15 % of cases of double valve endocarditis (See echocardiography page).

Prosthetic mitral valve endocarditis

Four types of lesions are typically seen in prosthetic valve endocarditis: vegetations, perforation of bioprosthetic cusp, valve dehiscence with paravalvular leak, and paravalvular abscess. Early bioprosthetic endocarditis usually involves the sewing ring and leads to an annular abscess and paravalvular leak. In contrast, late bioprosthetic endocarditis starts typically at the leaflets potentially leading to valve obstruction or regurgitation secondary to a large vegetation or leaflet perforation, respectively. Even in these late cases, a major concern remains the extension of infection to the sewing ring with subsequent annular abscess and valve dehiscence. Mechanical prosthetic endocarditis usually involves the sewing ring with similar complications as mentioned above. Early diagnosis and treatment is the key in the management of patients with prosthetic valve endocarditis.




REFERENCES

Hasbun R, Vikram HR, Barakat LA, et al. Complicated left-sided native valve endocarditis in adults: Risk classification for mortality. JAMA 2003;289:1933-1940

Murdoch DR, Corey GR, Hoen B, et al: Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: The international collaboration on endocarditis prospective cohort study. Arch Intern Med 2009;169:463-473

Lopez J, Revilla A, Vilacosta I, et al. Age-dependent profile of left-sided infective endocarditis: A 3-center experience. Circulation 2010;121:892-897

de Sa DD, Tleyjeh IM, Anavekar NS, et al. Epidemiological trends of infective endocarditis: A population-based study in Olmsted County, Minnesota. Mayo Clin Proc 2010;85:422-426

Wang A, Athan E, Pappas PA, et al. Contemporary clinical profile and outcome of prosthetic valve endocarditis. JAMA 2007;1354-61

Rutledge R, Kim J, Applebaum RE. Actuarial analysis of the risk of prosthetic valve endocarditis in 1,598 patients with mechanical and bioprosthetic valves. Arch Surg 1985; 120:469

Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med 1994;96(3):200-209

Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis 2000; 30:633-638


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