Endocarditis



Endocarditis


Joseph J. Maleszewski, M.D.

Fabio R. Tavora, M.D., Ph.D.

Allen P. Burke, M.D.



Infectious Endocarditis


Terminology

Infectious (or infective) endocarditis denotes a bacterial or fungal infection of the endocardium. Although most cases involve the valve surfaces, endocarditis may occur on other areas of turbulent flow, for example, at ventricular or septal defects or at areas of instrumentation.1 It may occur on native valves (native valve endocarditis [NVE]) or prosthetic valves (prosthetic valve endocarditis [PVE]).

There is a great variation in time course of endocarditis, depending in part on virulence factors of the offending organism. The term “subacute bacterial endocarditis” is often used for smoldering infections, for example, by low-virulence bacteria such as those belonging to the HACEK (Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella sp.) group.2


Risk Factors and Pathogenesis

NVE can occur on either structurally normal valves or structurally abnormal valves, which are prone to surface disruption. Patients with normal valves often have predisposing conditions such as intravenous drug use, intravenous lines, end-stage renal disease, poor oral hygiene, compromised immune systems, or malignancy (Table 177.1). In ˜25% of patients, neither structural valve abnormalities nor predisposing conditions are evident.

The pathogenesis of infectious endocarditis begins presumably as sterile thrombi, which become secondarily infected, with the proliferation of organisms, enlargement of the thrombus, and recruitment of neutrophils and proteases, which destroy the valve. Abnormal flow around the valve, which increases the risk for infection, is caused by congenital valve abnormalities, especially bicuspid aortic valve and mitral valve prolapse (Table 177.1).









TABLE 177.1 Conditions Predisposing to Infectious Endocarditis













Structural Valve Lesions Predisposing to Infectious

Sources of Bacteremia Predisposing to Infectious Endocarditisa


Rheumatic valve disease


2%-6%


Mitral valve prolapse


4%-13%


Bicuspid aortic valve


12%-18%


Congenital heart disease


0%-4%


Hypertrophic cardiomyopathy


2%


Degenerative aortic stenosis (tricuspid)


0%-5%

Hemodialysis


2%-27%


Intravenous drug abuse


2%-27%


Intravascular procedures (peripheral and central lines, pacemakers, angiography)


0%-2%


Surgeries or procedures


2%-7%


Immunosuppression:


3%-7%


Cutaneous infection


1%-2%


Colon cancer


0%-1%


a Excluding chronic alcoholism and diabetes mellitus.


Data derived from Castonguay MC, et al. Surgical pathology of native valve endocarditis in 310 specimens from 287 patients (1985-2004). Cardiovasc Pathol. 2013;22(1):19-27; Collins JA, Zhang Y, Burke AP. Pathologic findings in native infective endocarditis. Pathol Res Pract. 2014;210(12):997-1004, Refs.3,4



Infectious Agents

Nosocomial infections are most often caused by staphylococci (47%), followed by alpha-hemolytic streptococci (14%), enterococci (5%), and other organisms (29%).5 In two recent series of primarily communityacquired endocarditis, the relative frequency of staphylococcal infection approached that of streptococcal disease (Table 177.2).3,4

Some cases of culture-negative endocarditis are caused by fastidious Gram-negative organisms of the HACEK group,6,7,8 which constitute ˜1% to 3% of cases of community-acquired endocarditis on native and prosthetic valves, and may have a relatively good prognosis. Some organisms are especially virulent; for example, bacteremia with Staphylococcus aureus imparts a 13% risk,9 whereas pneumococcus <2%.10

In children, more than 75% of endocarditis patients have preexisting congenital heart disease, often with prior surgery. Similar to adults, Streptococcus viridans and S. aureus are the predominant organisms.11








TABLE 177.2 Organisms Causing Infectious Endocarditis in Series of Surgically Excised Valves




































Organism

Percent


Streptococci (total)

39%-54%

Viridans


Enterococcus/group D


Other

32%-28%


4%-13%


7%-9%a


Staphylococcus (total)

32%-37%

Aureus


MRSA


Epidermidis

20%-35%


5%-20%


2%-8%


Other

6%-7%b


HACEK

0%-3%


Fungi

1%-3%


Culture negative

2%-11%


a Including one case of Abiotrophia spp.

b Corynebacterium, Pseudomonas, Serratia.


Data derived from Castonguay MC, et al. Surgical pathology of native valve endocarditis in 310 specimens from 287 patients (1985-2004). Cardiovasc Pathol. 2013;22(1):19-27; Collins JA, Zhang Y, Burke AP. Pathologic findings in native infective endocarditis. Pathol Res Pract. 2014;210(12):997-1004, Refs.3,4 HACEK: Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella, Kingella.









TABLE 177.3 Causes of Culture-Negative Endocarditis





































Agent

Type of Organism

Method of Identification


Coxiella burnetii

Intracellular bacteria (previously rickettsia)

Serology, PCR, immunohistochemistry


Bartonella (henselae, quintana)

Intracellular bacteria (previously rickettsia)

Serology, silver impregnation stains, PCR, culture


Tropheryma whipplei

Bacteria

Histology using PAS, immunohistochemistry, silver impregnation stains, PCR


HACEKa

Bacteria, various Gram-negative rods

Culture


Mycoplasma hominis

Bacteria Culture


Abiotrophia elegans

Bacteria, related to streptococci

Culture


Legionella pneumophila

Bacteria

Culture, serology, immunofluorescence


a HACEK organisms include Haemophilus parainfluenzae, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae.



Clinical Findings

The clinical symptoms arise from valvular insufficiency in the majority of patients, with concomitant infectious symptoms. Uncommonly, large vegetations can obstruct the valve orifice and cause stenosis. Such large, obstructive, vegetations are indicative of fungal infection. The classic signs of Osler nodes and Janeway lesions are increasingly uncommon, but embolic phenomena such as splinter hemorrhages, Roth spots, and glomerulonephritis are frequently observed. The Duke criteria previously classified cases into possible and probable endocarditis, although current diagnosis rests largely on cardiac imaging, evidence of embolization, signs and symptoms of infection, and blood cultures. Clinical evidence of embolism, especially to the central nervous system, is common. Less symptomatic are emboli to the nail beds (splinter hemorrhages) and infarcts to the kidneys and spleen.


Culture-Negative Endocarditis

The rate of culture-negative endocarditis is about 10% and is higher in community-acquired infections, due to antibiotic treatment prior to diagnosis.3,4 Extensive serologic testing, culture for esoteric organisms, and polymerase chain reaction testing reveal an etiology in over 75% of cases of endocarditis with initial negative culture. The most common organisms that are not detected routinely are Coxiella burnetii and Bartonella species.12 The HACEK organisms and Tropheryma whipplei (Whipple disease) may also be frequent causes of culture-negative endocarditis (Table 177.3).13 HACEK refers to the bacterial species Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella, and Kingella.


Gross Pathologic Findings

Left-sided valves are most commonly infected, with approximately equal frequency between mitral and aortic valves. Left-sided valves are more frequent even in intravenous drug users than right-sided endocarditis, although infections of the tricuspid and pulmonary valves are highly suspicious of intravenous drug abuse. Tricuspid valve endocarditis may occur in community-acquired infection, usually in intravenous drug addicts, or hospital-acquired infections from implanted devices.

The gross hallmarks of infectious endocarditis are the presence of irregular vegetations and, in later stages, perforation or destruction of the valve apparatus (Figs. 177.1, 177.2, 177.3). The finding of a true perforation is nearly pathognomonic for endocarditis, as long as the distinction between perforation and fenestration is made (Chapter 138) (Fig. 177.4). Fenestrations, in contrast to perforations, are a normal finding in older patients and are present distal to the closing edge of semilunar valves.

Only gold members can continue reading. Log In or Register to continue

Related posts:

  1. Pediatric Interstitial Lung Disease and Hermansky-Pudlak Syndrome
  2. Pulmonary Capillaritis
  3. Small Cell Carcinoma
  4. Lymphoepithelioma-Like Carcinoma

Stay updated, free articles. Join our Telegram channel
Tags:
Aug 19, 2016 | Posted by in CARDIOLOGY | Comments Off on Endocarditis

Full access? Get Clinical Tree
Get Clinical Tree app for offline access