Ebright: Infective Endocarditis Flashcards

1
Q

Infective Endocarditis

DEFINITION

A

Infection of the endocardial surface of the
heart

Implies the physical presence of
microorganisms in the lesion

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2
Q

Organism location (6)

A
• Heart valves (most common)
• Septal defects
• Mural endocardium
• Arterio-venous shunts
• Arterio-arterial shunts (patent ductus arteriosus –
persistent communication between left pulmonary
artery and the descending aorta)
• Coarctation of aorta
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3
Q

Epidemiology

A
  • Approximately 1 case per 1000 hospital admissions
  • More than 50% of cases are older than 50 years
  • Males more commonly affected (ratio 1.7:1)
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4
Q

Epidemiology - Valve Involved

A

Left
• mitral 28-45%
• aortic 5-36%

  • mitral/aortic combined 0-35%
  • tricuspid 0-6%
  • pulmonic <1%
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5
Q

Epidemiology - Association with Underlying
Valvular Disease

Rheumatic heart disease:
Congential heart disease:

IE essentially does not occur with:

A

Rheumatic heart disease (25%)
•mitral most common

Congential heart disease
•patent ductus arteriosus, ventricular septal defect,
coarctation of the aorta, tetralogy of Fallot
•congenitally bicuspid aortic valve (20% of cases >age 60 poor prognosis)

*IE essentially does not occur with secundum atrial
defects (low-pressure shunt; little turbulence)

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6
Q

Epidemiology - Association with Underlying Valvular
Disease

“Degenerative” cardiac lesions

Other conditions

A

“Degenerative” cardiac lesions (30-40% cases without underlying valve disease)
• Ex: calcified mitral annulus, post myocardial infarction, thrombus

  • syphilitic heart disease
  • arterioatrial fistulas
  • hemodialysis shunts/fistulas
  • intracardiac pacemaker wires
  • intracardiac prostheses
  • intravenous drug abuse
  • mitral valve prolapse with mitral regurgitation
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7
Q

Pathogenesis
What results in deposition of platelets
and fibrin?

A
Turbulent flow results in deposition of platelets
and fibrin (nonbacterial thrombotic endocarditis).
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8
Q

Pathogenesis
Non-bacterial thrombotic endocarditis (NBTE)

What is a prerequisite for bacterial colonization?
Found in:
What are pathogenic mechanisms?
Found most frequently on which side of cardiac valve?
Along what line?

A

• Alteration of valve surface is prerequisite for bacterial colonization
• Found in many conditions causing acute/chronic illness
• Hypercoagulability and/or endothelial damage are
pathogenic mechanisms
• Found most frequently on low-pressure side of cardiac valve
• Along the line of closure

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9
Q

Pathogenesis

Hemodynamic factors

A

Lesions with high degrees of turbulence readily create conditions that lead to bacterial colonization

*low flow states (secundum atrial defects) rarely associated with IE

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10
Q

Pathogenesis
Transient bacteremia:

Where does it occur?
How long does it usually take to clear the bloodstream?
What can the bacteria in the bloodstream then do?

A
  • Occurs when mucosal surface heavily colonized with bacteria is traumatized
  • Bloodstream is usually clear 15-30 minutes after the procedure
  • Bacteria in bloodstream can then colonize NBTE lesions
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11
Q

Pathogenesis
Microorganism - NBTE Interaction

How do organisms differ?
What do bacteria do once they bind?
What does vegetation create?

A
  • Organisms differ in their propensity to cause (Infective Endocarditis) IE
  • Once bacteria bind they proliferate, causing further platelet –fibrin deposition.
  • Vegetation creates an environment of impaired host resistance (bacteria covered by platelets/fibrin)
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12
Q

Pathogenesis

Immunopathologic Factors

A
  • Stimulation of humoral and cellular immunity
  • Rhematoid factor can be positive
  • Antinuclear antibodies can be present
  • Circulating immune complexes
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13
Q

Pathologic Changes

Vegetation located:
Complications:

A

Vegetation located along line of closure of valve leaflet

Complications
– valve ring abscess
– perforation of valve leaflet
– myocardial abscesses (20%)
– rupture of chordae tendinae, interventricular
septum, papillary muscle
– valvular stenosis (large lesions)
– myocarditis
– pericarditis
– myocardial infarction (40-60% of autopsied
cases)
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14
Q

Vegetations
Pathologic Changes
Kidney

A

• abscess
• infarction
• glomerulonephritis (focal or diffuse)
secondary to immune complex deposition

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15
Q

Pathologic Changes
Mycotic aneurysm:

Usually develop during:
Tend to occur where?
Mechanism leads to:
direct bacterial invasion:
embolic occlusion of:
immune complex deposition:
Clinically silent until:
A

• Usually develop during active disease, but can occur
months to years later
• tend to occur at bifurcation points
• mechanism leading to aneurysm
• direct bacterial invasion of arterial wall with
abscess formation
• embolic occlusion of vasovasorum
• immune complex deposition with injury to
vessel wall
• Clinically silent until rupture occurs

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16
Q

Pathologic Changes

CNS
Spleen
Lung (Rt. Sided)

A

Central nervous system
• cerebral emboli (1/3 of cases)
•also mycotic aneurysms, cerebritis, abscesses

Spleen
•infarctions common (but usually clinically silent)
•abscesses

Lung (Rt. Sided)
•embolic
•pleural effusion/empyema

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17
Q

Pathologic Changes

Skin
Eyes

A

Skin
•petechiae 20-40%
•Osler’s nodes (immune complex)
•Janeway lesions (septic emboli)

Eyes
•Roth spots

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18
Q

Clinical Manifestations

“Incubation period”
Average: Symptom onset to diagnosis

Process contributing to the clinical picture (4)

A

Clinical Manifestations
“Incubation period” 2 weeks but time from symptom onset to diagnosis averages 5 weeks (and depends on causative organism)

Process contributing to the clinical picture
– infectious process on the valve
– bland/septic emboli to any organ system
– constant bacteremia (with metastatic foci)
– circulating immune complexes

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19
Q

Clinical Manifestations

Fever:

Nonspecific Symptoms:

Heart Murmur:

A

Fever (95%)
• Usually remittent
• absent in: CHF, renal failure, older age,
terminal illness, prior antibiotic therapy

Nonspecific Symptoms
• anorexia, weight loss, fatigue, chills,
weakness, nausea, vomiting, night sweats
• often result in incorrect initial diagnosis

Heart murmur (85%)
(classically a new or changing murmur)
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20
Q

Clinical Manifestations

Peripheral manifestations (3):

A

Peripheral manifestations (50%)
•clubbing 10-20%
•splinter hemorrhages
•petechiae

21
Q

Clinical Manifestations

Osler’s nodes:
Janeway lesions:
Roth spots:

A

Osler’s nodes: small painful nodular
lesions on the pads of fingers/toes or
thenar eminence 0-25%
(immune complex deposition)

Janeway lesions: hemorrhagic, macular,
painless plaques with predilection for the
palms/soles (emboli)

Roth spots: oval, pale, retinal lesions
surrounded by hemorrhage, usually near
the optic disk

22
Q

Clinical Manifestations
Splenomegaly
Musculoskeletal
Major embolic episode

A
  • Splenomegaly 25-60%
  • Musculoskeletal complaints
  • Major embolic episode to any organ system
23
Q

Clinical Manifestations

Central Nervous System %?
Major cerebral emboli %?
Subarachnoid hemmorhage due to:
Other 3:

A

• Central Nervous System 20-40%
• Major cerebral emboli 10-31%
• subarachnoid hemorrhage due to
mycotic aneurysm

  • seizures
  • cranial nerve palsies
  • toxic encephalopathy
24
Q

Clinical Manifestations

Renal failure %

A

Clinical Manifestations

• Renal failure 25-35%

25
Q

Clinical Manifestations in
Injection Drug Users

What is the most common valve affected?
Often present with what?

A
• tricuspid valve most common
• often present with prominent
pulmonary findings (septic emboli
to lungs)
• often occurs on otherwise normal
heart valves
26
Q

Lab Abnormalities

(4)

A
• Anemia common 70-90%***
• thrombocytopenia 5-15%
• leukocytosis 20-30%
• sedimentation rate (ESR) nearly
always elevated 90-100%
27
Q

URINALYSIS

Proteinuria:%
Microscopic hematuria:%
Red Cell Casts:%
Others (4)

A
  • proteinuria (50-65%)
  • microscopic hematuria (30-60%)
  • red cell casts (12%)
  • gross hematuria
  • pyuria
  • white cell casts
  • bactiuria
28
Q

Lab Abnormalities

Blood culture

What is the bacteremia?

What occurs in >90% of the cases?

Less likely to be positive if:

Procedure for collecting blood cultures:

A
  • most important lab test
  • bacteremia usually continuous
  • In >90% of cases the first 2 sets of blood cultures drawn will yield the organism responsible
  • less likely to be positive if patient has received antibiotics in the prior 2 weeks
  • procedure for collecting blood cultures – 3 sets within 24 hours (3 separate venipunctures)
29
Q

What is the most important lab test?

A

Blood culture

30
Q

2D Echocardiogram

A

Can visualize vegetations greater than 2 mm in size

31
Q

Transesophageal echocardiogram (TEE)

What does the negative study not include?
What are rare?
Dependent upon:
Valuable to assess:
Better than:
Are patients with vegetation at increased risk of embolization?

A
  • Negative study does not exclude IE
  • False-positive results are rare
  • Dependent upon experience of technician/reader •Valuable to assess local complications of IE (valve ring abscess)
  • Better for visualizing aortic valve than 2D Echo •Patients with vegetations are not at increased risk of embolization.
32
Q

Diagnosis

A

Combination of clinical and diagnostic criteria used to classify as definite, possible, or not IE.

33
Q

Streptococcus viridans
(Gram-positive cocci)

Typically:
80% have:
A common cause of what?
Comprised of what?
Prognosis?
Most common cause of endocarditis in pts with:
A
• typically subacute
• 80% have underlying valve disease
• a common cause of IE (dental procedures)
• many species comprise the viridans group of
Streptococci
• good prognosis
• most common cause of endocarditis in
patients with mitral valve prolapse
34
Q

Enterococci
(Gram-positive cocci)

How common?
Easy to treat?
Usually acute?
Commonness of peripheral manifestations:
Seen in what population?
A

• increasingly common cause of endocarditis
• very difficult to treat
• usually subacute
• peripheral manifestations uncommon
• seen in older men after genitourinary procedures
and young women after obstetrical procedures

35
Q

Streptococcus pneumoniae
(Gram-positive cocci)

How common?
Usually:
predilection for:
Often in what population:
Many have:
Outcome:
A
  • unusual cause
  • usually fulminant (suddenly or quickly)
  • predilection for aortic valve (70%)
  • often alcoholics
  • many have meningitis (70%)
  • poor outcome (50% mortality)
36
Q

Staphylococcus aureus
(Gram-positive cocci in clusters)

Coagulase +/-?
Causes what % of staph endocarditis?
Attacks what?
Prognosis?

A

• coagulase-positive staphylococci (S. aureus)
• causes 80-90% of cases of Staphylococcal
endocarditis
• commonly attacks “normal” heart valves (1/3 of
cases)
• prognosis poor (40% mortality)

37
Q

Staphylococcus aureus

More commonly causes what?
Metastatic infection to where is common?
In what population?

A

• more commonly causes myocardial abscess,
purulent pericarditis, and valve ring abscesses
than other causes of IE
• metastatic infection to lung, brain, spleen,
kidney common
• common causes of IE in injection drug users
but in IDU has less fulminant course with
less mortality

38
Q

Staphylococcus epidermidis
(Gram-positive cocci in clusters)

Coagulase +/-?
Common cause of what?
Can cause what in neonates?
Prognosis:

A

• coagulase-negative
• common cause of prosthetic valve endocarditis
• can cause endocarditis in neonates
• medical and/or surgical therapy usually
successful

39
Q

Gram-negative bacilli

Common?
Risks:
What is common?
Prognosis:
Commonly require what? Where? Why?
A

• uncommon but increasing
• risks: injection drug users, prosthetic valve
recipients, cirrhosis
• CHF common
• prognosis poor (70-80% mortality)
• commonly require early valve replacement,
especially left-sided disease due to Pseudomonas spp.

40
Q

“HACEK” Group
(“culture-negative endocarditis”)

Requires how long to grow?

HACEK stands for:

Acute?

Need to:

A

• Fastidious; require 2-3 weeks to grow

H Haemophilus aphrophilus
A Actinobacilus actinomycetemcomitans
C Cardiobacterium hominis
E Eikenella corrodens
K Kingella kingae (and other species)
  • subacute course
  • need to alert microbiology lab to supplement media and hold cultures longer
41
Q

Fungi

Risks (4)

A

• injection drug users
• patients after reconstructive cardiovascular
surgery
• patients after prolonged IV/antibiotic therapy
• cure virtually impossible without surgery

42
Q

Therapy

Abx:
Surgery if (5):
A

• Prolonged course of antibiotics (4-6 weeks) with bactericidal
agents directed against the specific pathogen

• Surgical intervention indication if:
– congestive heart failure unresponsive to medical therapy
– greater than 1 major systemic embolic complication
– inability to clear organism from blood stream (time varies with organism and antimicrobial used)
– prosthetic valve endocarditis, esp. early (usually)
– certain hard to cure organisms e.g. fungi, Pseudomonas species

43
Q

DEFINITION

A

Infection of endocardial surface of the heart

the endothelium

44
Q

PATHOGENESIS

A

Direct infection of “normal” endothelium by
highly virulent organisms (S. aureus)

Secondary infection of damaged endothelium
and platelet-fibrin thrombus during
subsequent bacteremic periods

45
Q

INFECTING ORGANISMS
Most common bacteria:
Less common:

A

• Most common are bacteria, such as S. aureus,
viridans streptococcus, and enterococcus
species (high binding potential)
• Less common are other organisms such as
HACEK, gram negative bacilli (pseudomonas),
pneumococcus, chlamydia, and fungi

46
Q

CLINICAL ILLNESS (3)

A
  1. Local
  2. Systemic (constitutional)
    – Bacteremia
    – Immunologic
  3. Embolic
47
Q

MICROBIOLOGIC DIAGNOSIS

A
  • Persistent, continuous bacteremia

* Blood cultures are “always” positive

48
Q

TREATMENT (3)

A
  1. Deep in vegetation, organisms are
    metabolically inactive
  2. Within the vegetation there is poor nutrient
    supply and poor blood supply
  3. Antibiotics must be bactericidal, high dose,
    and prolonged