INFECTIVE ENDOCARDITIS

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

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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.

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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).

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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.

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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.

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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, Oslers 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 rategt90

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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
Janeways 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
  gt12 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.
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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 (gt10-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

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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.