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INFECTIVE ENDOCARDITIS

Vegetations (arrows) due to viridans streptococcal endocarditis involving the mitral valve.

Infective endocarditis (IE) is an infection of the endocardial surface of the heart.

The intracardiac effects of this infection include severe valvular insufficiency, which may lead to congestive heart failure and myocardial abscesses. IE also produces a wide variety of systemic signs and symptoms through several mechanisms, including both sterile and infected emboli and various immunological phenomena.

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ETIOLOGYOrganisms Causing Major Clinical Forms of Endocarditis:

Staphylococcus aureus infection is the most common cause of IE, including PVE, acute IE, and IVDA IE. Approximately 35-60.5% of staphylococcal

bacteremias are complicated by IE. More than half the cases are not

associated with underlying valvular disease.

The mortality rate of S aureus IE is 40-50%.

ETIOLOGYOrganisms Causing Major Clinical Forms of Endocarditis:

Streptococcus viridans This organism accounts for approximately 50-60%

of cases of subacute disease. Most clinical signs and symptoms are mediated

immunologically. Streptococcus intermedius group

These infections may be acute or subacute. S intermedius infection accounts for 15% of

streptococcal IE cases. S intermedius is unique among the streptococci; it

can actively invade tissue and can cause abscesses.

ETIOLOGYOrganisms Causing Major Clinical Forms of Endocarditis:

Nonenterococcal group D organisms The clinical course is subacute. Infection often reflects underlying abnormalities of the large bowel

(eg, ulcerative colitis, polyps, cancer). The organisms are sensitive to penicillin.

Group B streptococci Acute disease develops in pregnant patients and older patients with

underlying diseases (eg, cancer, diabetes, alcoholism). The mortality rate is 40%. Complications include metastatic infection, arterial thrombi, and

congestive heart failure. It often requires valve replacement for cure.

Group A, C, and G streptococci Acute disease resembles that of S aureus IE (30-70% mortality

rate), with suppurative complications. Group A organisms respond to penicillin alone. Group C and G organisms require a combination of synergistic

antibiotics (as with enterococci).

ETIOLOGYOrganisms Causing Major Clinical Forms of Endocarditis:

Coagulase-negative S aureus This causes subacute disease. It behaves similarly to S viridans infection. It accounts for approximately 30% of PVE cases and less than 5% of NVE

cases.10 Pseudomonas aeruginosa

This is usually acute, except when it involves the right side of the heart in IVDA IE.

Surgery is commonly required for cure. HACEK organisms (ie, Haemophilus aphrophilus, Actinobacillus

actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)

These organisms usually cause subacute disease. They account for approximately 5% of IE cases. They are the most common gram-negative organisms isolated from patients

with IE. Complications may include massive arterial emboli and congestive heart

failure. Cure requires ampicillin, gentamicin, and surgery.

ETIOLOGYOrganisms Causing Major Clinical Forms of Endocarditis:

Fungi These usually cause subacute disease. The most common organism of both fungal

NVE and fungal PVE is Candida albicans. Fungal IVDA IE is usually caused by Candida

parapsilosis or Candida tropicalis. Aspergillus species are observed in fungal

PVE and NIE.

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Acute endocarditis usually occurs when heart valves are colonized by virulent bacteria in the course of microbemia. The most common cause of acute endocarditis is Staphylococcus aureus; other less common causes are Streptococcus pneumoniae, Neisseria gonorrhoeae, Streptococcus pyogenes, and Enterococcus faecalis.

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Patients with subacute endocarditis usually have underlying valvular heart disease and are infected by less virulent organisms such as viridans streptococci, enterococci, nonenterococcal group D streptococci, microaerophilic streptococci, and Haemophilus species.

Bacteremia can result from various invasive procedures

Endoscopy Rate of 0-20% CoNS, streptococci, diphtheroids

Colonoscopy Rate of 0-20% Escherichia coli, Bacteroides species

Barium enema Rate of 0-20% Enterococci, aerobic and anaerobic gram-negative rods

Dental extractions Rate of 40-100% S viridans

Transurethral resection of the prostate Rate of 20-40% Coliforms, enterococci, S aureus

Transesophageal echocardiography Rate of 0-20% S viridans, anaerobic organisms, streptococci

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primary portals

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primary portals

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PATHOPHYSIOLOGYThe clinical manifestations of IE result from: 1. Local destructive effects of intracardiac

infection (distortion or perforation of valve leaflets, rupture of chordae tendineae, perforations or fistulas between major vessels and cardiac chambers, functional valvular stenosis) with congestive heart failure;

2. Embolization of fragments of the vegetation, resulting in infection or infarction including the spleen, kidney, meninges, brain, bone, pericardium, synovium;

3. The hematogenous seeding of remote sites during continuous bacteremia (hyper-gammaglobulinemia, cryoglobulins, splenomegaly);

4. Immunologic response to the infection with tissue injury due to deposition of preformed immune complexes or antibody-complement interaction with antigens deposited in tissues (glomerulonephritis, Osler’s nodes, rheumatological manifestations).

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Clinical and Laboratory Features of Infective Endocarditis Fever 80-90 % Chills and sweats 40-75 % Anorexia, weight loss, malaise 25-50 % Myalgias, arthralgias 15-30 % Back pain 7-15 % Heart murmur 80-85 % New/worsened regurgitant murmur 10-

40 %

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Clinical and Laboratory Features of Infective Endocarditis

Arterial emboli 20-50 % Splenomegaly 15-50 % Clubbing 10-20 % Neurologic manifestations 20-40 % Peripheral manifestations (Osler's

nodes, subungual hemorrhages, Janeway lesions, Roth's spots) 2-15 %

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Clinical and Laboratory Features of Infective Endocarditis

Petechiae 10-40 % Laboratory manifestations: Anemia 70-90 % Leukocytosis 20-30 % Microscopic hematuria 30-50 % Elevated erythrocyte

sedimentation rate>90 %

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Clinical and Laboratory Features of Infective Endocarditis

Rheumatoid factor 50 % Circulating immune complexes 65-

100 % Decreased serum complement 5-40

%

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Common Peripheral Manifestations of Infective Endocarditis.Splinter hemorrhages (A) are normally seen under the fingernails. They are usually linear and red for the first-two to three days and brownish thereafter.Panel B shows conjunctival petechiae.Osler's nodes (Panel C) are tender, subcutaneous nodules, often in the pulp of the digits or the thenar eminence.Janeway's lesions (Panel D) are nontender, erythematous, hemorrhagic, or pustular lesions,

often on the palms or soles.

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Noncardiac Manifestations

Janeway’s lesions. Hemorrhagic, infarcted macules and papules on the volar fingers in a patient with S. aureus endocarditis.

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Noncardiac Manifestations

Septic vasculitis associated with bacteremia. Dermal nodule with hemorrhage and necrosis on the dorsum of a finger. This type of lesion occurs with bacteremia (e.g., S. aureus) and fungemia (e.g., Candida tropicalis).

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Noncardiac Manifestations

subconjunctival hemorrhage. Submucosal hemorrhage of the lower eyelid in an elderly diabetic with enterococcal endocarditis; splinter hemorrhages in the midportion of the nail bed and Janeway lesions were also present.

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Noncardiac Manifestations

Splinter hemorrhages, embolic Subungual hemorrhages in the midportion of the nail bed (quite different in comparison to traumatic splinter hemorrhages) was noted in several fingernails in a 60-year-old female with enterococcal endocarditis, who had associated subconjunctival hemorrhage.

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Splinter haemorrhages are linear haemorrhages lying parallel to the long axis of finger or toe nails.

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Noncardiac Manifestations

Osler's nodes. Violaceous, tender nodules on the volar fingers associated with minute infective emboli or immune complex deposition.

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Noncardiac Manifestations

Septic emboli with hemorrhage and infarction due to acute Staphylococcus aureus endocarditis.

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Noncardiac Manifestations

Vasculitis

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Clubbing. Seen in patients with chronic lung disease, cyanotic heart disease, cirrhosis and infective endocarditis.

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Infective endocarditis: metastatic infections due to emboli.

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Noncardiac Manifestations

Computed tomography of the abdomen showing large embolic infarcts in the spleen and left kidney of a patient with Bartonella endocarditis.

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The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis

Positive blood culture for Infective Endocarditis Typical microorganism consistent with IE from 2 separate blood cultures, as noted below:•  viridans streptococci, Streptococcus bovis, or HACEK group, or •  community-acquired Staphylococcus aureus or enterococci, in

the absence of a primary focus or Microorganisms consistent with IE from persistently positive

blood cultures defined as:•  2 positive cultures of blood samples drawn >12 hours apart, or

•  all of 3 or a majority of 4 separate cultures of blood (with first and last sample drawn 1 hour apart)

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The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis

MAJOR CRITERIA: Evidence of endocardial involvement Positive echocardiogram- Oscillating intracardiac mass on valve or supporting

structures or in the path of regurgitant jets or in implanted material, in the absence of an alternative anatomic explanation, or

- Abscess, or- New partial dehiscence of prosthetic valve, or New valvular regurgitation (increase or change in

preexisting murmur not sufficient)

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The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis

MINOR CRITERIA : Predisposition: predisposing heart condition or

injection drug use Fever ≥38.0◦C Vascular phenomena: major arterial emboli, septic

pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions

Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth's spots, rheumatoid factor

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The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis

MINOR CRITERIA : Microbiologic evidence: positive blood culture

but not meeting major criterion as noted previously or serologic evidence of active infection with organism consistent with infective endocarditis

Echocardiogram: consistent with infective endocarditis but not meeting major criterion

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The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis

Documentation of two major criteria, of one major and three minor criteria, or of five minor criteria allows a clinical diagnosis of definite endocarditis.

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INFECTIVE ENDOCARDITIS

Vegetations (arrows) due to viridans streptococcal endocarditis involving the mitral valve.

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Characteristic sites of vegetations within the heart. In the presence of aortic insufficiency, vegetations characteristically occur on the ventricular surface of the aortic valve (A) or on the chordae tendinae or papillary muscles (B). In mitral regurgitation, the vegetations characteristically are located on the atrial surface of the mitral valve (C) or at sites of jet lesions (D) on the atrial wall.

Further Classification Acute

Affects normal heart valves

Rapidly destructive

Metastatic foci Commonly Staph. If not treated,

usually fatal within 6 weeks

Subacute Often affects

damaged heart valves

Indolent nature If not treated,

usually fatal by one year

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Antibiotic Treatment for Infective Endocarditis Caused by Common

Organisms Streptococci Penicillin-susceptible streptococci, S.

bovis Penicillin G 2-3 million units IV q4h for 4 weeks Penicillin G 2-3 million units IV q4h plus

gentamicin 1 mg/kg IM or IV q8h, both for 2 weeks Ceftriaxone 2 g/d IV as single dose for 4 weeks Vancomycind 15 mg/kg IV q12h for 4 weeks

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Antibiotic Treatment for Infective Endocarditis Caused by Common

Organisms

Relatively penicillin-resistant streptococci

- Penicillin G 3 million units IV q4h for 4-6 weeks plus gentamicin 1 mg/kg IV q8h for 2 weeks

Penicillin-resistant streptococci, pyridoxal-requiring streptococci (Abiotrophia spp.)

- Penicillin G 3-4 million units IV q4h plus gentamicinc 1 mg/kg IV q8h, both for 4-6 weeks

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Indications for Cardiac Surgical Intervention in Patients with

Endocarditis Surgery required for optimal outcome Moderate to severe congestive heart failure due to valve

dysfunction Partially dehisced unstable prosthetic valve Persistent bacteremia despite optimal antimicrobial therapy Lack of effective microbicidal therapy (e.g., fungal or Brucella

endocarditis) S. aureus prosthetic valve endocarditis with an intracardiac

complication Relapse of prosthetic valve endocarditis after optimal

antimicrobial therapy Persistent unexplained fever (≥10 days) in culture-negative

prosthetic valve endocarditis

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Indications for Cardiac Surgical Intervention in Patients with

Endocarditis Surgery to be strongly considered for improved outcomea Perivalvular extension of infection Poorly responsive S. aureus endocarditis involving the aortic

or mitral valve Large (>10-mm diameter) hypermobile vegetations with

increased risk of embolism Persistent unexplained fever (≥10 days) in culture-negative

native valve endocarditis Poorly responsive or relapsed endocarditis due to highly

antibiotic-resistant enterococci or gram-negative bacilli

Prevention Approximately 15-25% of cases of IE are a consequence

of invasive procedures that produce a significant bacteremia. Because only 50% of those who developed valvular infection following a procedure were identified as being candidates for antibiotic prophylaxis, only approximately 10% of cases of IE can be prevented by the administration of preprocedure antibiotics.

Maintaining good oral hygiene is probably more effective in the overall prevention of valvular infection because gingivitis is the most common source of spontaneous bacteremias.

The American Heart Association periodically compiles recommendations for IE prophylaxis.