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Micro Exam 1 > Ebright: Infective Endocarditis > Flashcards

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

Micro Exam 1 (18 decks)

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