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Block G -- Infection > Dr. Teltscher -- Endovascular Infections > Flashcards

Dr. Teltscher -- Endovascular Infections Flashcards

1
Q

3 methods of endovascular infection

A
  • Direct infection of blood and its components
  • Infection of endovascular device
  • Direct infection of vasculature and structures
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2
Q

4 parasites potentially involved in endovascular infection

A
  • Plasmodium
  • Babesia
  • Trypanosoma
  • Leishmania
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3
Q

3 direct infections of vasculature and structures

A
  • Suppurative thrombophlebitis
  • Endarteritis
  • Endocarditis
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4
Q

Define acute infective endocarditis

A

Abrupt toxin couse lasting days to weeks

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5
Q

Define subacute infective endocarditis

A

Indolent protracted course featuring systemic symptoms often lasting longer than weeks

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6
Q

Sex most commonly affected by endovascular infection

A

Men

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7
Q

Why is incidence of endovascular infection increasing? (4)

A

Shifting age distribution:

  • Change in nature of underlying heart diseases: rheumatic –> degenerative
  • Aging population = aged w/ heart disease survive longer
    • Benefiting from prosthetic valve replacement surgeries
  • “Healthcare associated” IE due to increased uses of endovascular technologies –> biofilm formation
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8
Q

4 predisposing factors for infective endocarditis

A
  • Native valve (the one’s with which you are born)
  • Prosthetic valve
  • Endovascular device utilization
  • IVDU
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9
Q

4 problems with native valves that can predispose to IE

A
  • Rheumatic heart disease
  • Congenital heart disease (some, but not all)
  • Degenerative heart disease
  • Mitral valve prolapse
    • Uncontrolled bacteremia and/or history of endocarditis
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10
Q

Describe the pathogenesis of IE

A
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11
Q

Distribution of sites affected by iE

A
  • Mitral alone = 28 - 45%
  • Aortic alone = 5 - 36%
  • Tricuspid = 0 - 6%
  • Pulmonic very rare
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12
Q

When does “transient bacteremia” occur?

A

When heavily colonized mucosal surfaces are traumatized

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13
Q

Typical findings of low grade and transient bacteremia

A
  • ≤ 10 CFUs/ml
  • Blood stream sterilized within 30 minutes
    • Function of “serum susceptibility” of the organism
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14
Q

Risk of transient bacteremia

A

Sufficient to infect a NBTE valvular lesion

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15
Q

3 types of virulence factors associated with pathogens involved in IE

A
  • Dextran
  • Adhesion to markers of damaged endothelium
  • Bacteria-platelet aggregates in circulating blood
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16
Q

What is Dextran

A

Complex extracellular polysaccharide (glycocalyx)

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17
Q

Dextran function

A

Promotes adherence to platelet-fibrin matrix (NBTE)

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18
Q

2 pathogens that have dextran as a virulence factor

A

S. mutans (dental caries)

Prominent among certain *Streptococcus *spp

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19
Q

Marker of damaged endothelium to which bacteria can adhere

A

Fibronectin

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20
Q

Pathogen with adhesion to fibronectin as virulence factor

A

*S. aureus *(binding and uptake into “normal” endothelium –> triggered apoptosis)

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21
Q

Bacteria with bacter-platelet-aggregates in circulating blood as virulence factor

A
  • Staphylococcus *spp.
  • Streptococcus *spp.
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22
Q

Effect of bacteria-platelet-aggregates in circulating blood

A

Decreased rate of removal of organism

Increased adherence and aggregation on vegetations

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23
Q

2 ways sub-inhibitory (prophylactic) antibiotics may prevent IE

A
  • Decreasing expression of adhesion virulent factors
  • Direct cell killing
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24
Q

Describe the environment within the vegetation

A
  • Minimal phagocyte infiltration
  • Protection from circulating immune factors
  • Major proliferation (billions CFUs/g of tissue)
  • Deeper dormant/inert/planktonic bacterial forms (may rep up to 90% of bacterial burden)
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25
Q

3 pathogens involved in community acquired IE on native valve

A
  • S. aureus
  • *Streptococcus *spp.
  • Lesser extent *Enterococcus *spp.
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26
Q

2 pathogens involved in nosocomial IE on a native valve

A
  • S. aureus
  • Lesser extent *Enterococcus *spp.
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27
Q

Pathogen associated with IVDU IE on native valve

A

S. aureus (lesser extent other bacteria)

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28
Q

6 pathogens involved in early post surgical (<2 months) IE on prosthetic valve

A
  • Coagulase negative *Staphylococcus *spp. > S. aureus
  • Important rate of others:
    • Diphtheroids
    • Gram negative bacilli
    • Candida spp.
    • Fungi
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29
Q

4 pathogens involved in intermediate post-surgical (2 - 12 months) IE on prosthetic valve

A
  • Coagulase negative *Staphylococcus *spp. > S. aureus
  • Lesser extent *Enterococcus *spp. > *Streptococcus *spp
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30
Q

Pathogens involved in late post-surgical (> 12 months) IE on prosthetic valve

A

Similar to native valve, but increased rate of CoNS/other

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31
Q

6 organisms that produce culture negative endocarditis

A
  • HACEK
    • Gram negative organisms w/ unusual growth characteristics that are not truly “culture negative” using modern techniques
  • Coxiella burnetti
  • *Bartonella *sp.
  • *Mycoplasma *spp. / *Chlamydophila *spp.
  • Trophyrema whipplei
  • Fungi (i.e. *Candida *spp., Aspergillus spp.)
32
Q

3 reasons why IE is clinically tricky

A
  • “Protean” manifestation
  • Subacute/chronic forms may have multiple B-symptoms
  • Systemic symptoms often open differential and may be misleading
33
Q

4 most common symptoms of IE

A
  • Fever
  • Chills
  • Weakness
  • Dyspnea
34
Q

Importance of cardiac auscultation in IE diagnosis

A
  • Audible murmur in 85%
  • “New murmur” or “changed murmur” = important but uncommon
35
Q

2 types of IE that do not have audible murmur

A
  • Right-sided IE
  • Mural IE
36
Q

Most important diagnostic test for IE

A

Blood cultures

37
Q

Recommended blood culture technique in IE

A
  • 3 sets, only 2 bottles per stick in first 24 hours
  • At least 10 mL of blood in each bottle
  • May need prolonged incubation
38
Q

2 electrocradiogram techniques for IE diagnosis

A

TTE

TEE

39
Q

Describe the use of TTE in IE

A
  • Utility in all suspected patients
  • May be technically inadequate in up to 20% of individuals
  • Variable sensitivity
    • Negative cannot rule out IE
    • Best or right-sided IE
  • False postive very rare
40
Q

Describe the use of TEE in IE

A
  • Invasive
  • More sensitive than TTE (65% vs. 95%)
    • Consider in suspected cases w/ negative TTE
  • Very useful for prosthetic valves
  • Negative does not R/O IE
    • May repeat in 7 - 10 days
41
Q

Modified Duke Criteria: Pathologic criteria for definite IE

A
  • Microorganisms: demonstrated by culture or histology in a vegetation OR in a vegetation that has embolized OR in an intracardiac abscess OR
  • Pathologic lesions: vegetation or intracardiac abscess present, confirmed by histology showing active endocarditis
42
Q

Modified Duke Criteria: Clinical criteria for definite IE

A
  • 2 major OR
  • 1 major and 3 minor OR
  • 5 minor
43
Q

Modified Duke Criteria: possible IE

A
  • 1 major and 1 minor OR
  • 3 minor
44
Q

Modified Duke Criteria: Rule out IE (4)

A
  • Firm alternative diagnosis OR
  • Resolution of manifestation of IE with ABX for 4 days or less OR
  • No pathologic evidence of IE at surgery or autopsy, after ABX therapy for 4 days or less
  • Does not meet criteria for possible IE
45
Q

2 major criteria for IE

A
  • Blood culture positive for IE
    • Consistent with IE from 2 separate cultures
    • Microorganisms consistent with IE from persistently positive blood cultures
    • Single postivive blood culture for *Coxiella burnetii *or antiphase I IgG Ab titer >1:800
  • Evidence of endocardial involvement
    • Echocardiogram positive for IE
    • New valvular regurgitation
46
Q

Define “persistently positive blood cultlures”

A
  • At least 2 positive cultures drawn 12 h apart
  • All of 3, or a majority of more than 4 separate cultures with first and last samples at least 1 hour apart
47
Q

5 minor criteria for IE

A
  • Predisposition (heart condition or injection drug use)
  • Fever
  • Vascular phenomenon
  • Immunologic phenomenon
  • Microbiological evidence
48
Q

6 vascular phenomena that are included in minor criteria for IE

A
  • Major arterial embolu
  • Septic pulmonary infarcts
  • Mycotic aneurysm
  • Intracranial hemorrhage
  • Conjunctivital hemorrhages
  • Janeway lesions
49
Q

4 immunologic phenomena that are included in minor criteria for IE

A
  • GN
  • Osler nodes
  • Roth spots
  • Positive RF
50
Q

Define minor microbiological evidence for IE

A

Positive blood culture, but does not meet any major criterion as noted above, or serological evidence of active infection with organism consistent with IE

51
Q

5 pathogens found in blood culture typical for IE in major criteria

A
  • Viridans streptococci
  • S. bovis
  • HACEK group
  • S. aureus
  • Community-acquired enterococci, without primary focus
52
Q

8 Acute IE pathologic heart changes

A
  • Vegetation is larger, softer, more friable
  • Associated with more suppuration, more necrosis
  • Less healing
  • Valve perforation
  • Rupture of chordae tendonae, interventricular septum, papillary muscles
  • Perivalvular abscess
  • Fistula into percardium, myocardium
  • Myocarditis, MI, pericarditis
53
Q

4 organs involved in embolic phenomena due to IE

A
  • Kidney
  • Spleen
  • Coronaries
  • Brain
54
Q

3 immune phenomena due to pathological changes of IE

A
  • Immune complex deposition
  • Complement activation
  • Autoimmune process activated by increased circulating antibodies
55
Q

3 pathologic changes of kidney architecture during IE

A

ALL biopsies have abnormal architecture

  • Abscess
  • Infarction
  • GN
56
Q

Vascular pathologic change due to IE

A

Mycotic aneurysm

57
Q

Pathogen for which mycotic aneurysm is most common

A

viridans Streptococcus

58
Q

3 mechanism of mycotic aneurysm

A
  • Direct invasion of arterial wall, abscess and/or rupture
  • (Septic) emboli occluding vasa vasorum
  • IC deposition and injury to the vascular wall

NOTE: Tend to occur at bifurcation points

59
Q

Most common neurologic event in IE

A

Cerebral emboli (20%)

60
Q

Leading CNS related cause of death in IE

A

Hemorrhagic transformation of ischemic event from cerebral emboli

61
Q

Most common parts involved in cerebral emboli

A

MCA

Branches

62
Q

3 CNS pathologic changes due to IE

A
  • Cerebral emboli
  • Purulent meningitis
  • Microabscesses
63
Q

Pathogen associated with purulent meningitis due to IE

A

S. pneumoniae

64
Q

Pathogen associated with micorabscesses in CNS due to IE

A

S. aureus

65
Q

4 pathologic changes of spleen due to IE

A
  • Enlargement
  • Infarction (usually clinically silent)
  • Abscess
    • Surgical indication or percutaneous drainage
  • Spontaneous rupture
66
Q

2 reasons for spleen enlargement in IE

A
  • Immune stimulation
  • Follicle engorgement
67
Q

Type of IE that lung changes are typically associated with

A

Right-sided

68
Q

4 pathologic lung changes associated with IE

A
  • PE (septic or “bland”) + infarction
  • Acute pneumonia
  • Pleural effusion
  • Empyema
69
Q

3 pathologic skin changes due to IE

A
  • Petechiae (20 - 40%)
  • Osler nodes (immune mediated)
  • Janeway lesions (vascular event)
70
Q

Cause of Osler nodes

A
  • IC depostiion in blood vessels
  • Arteriollar intimal proliferation with extension to venules and capillaries, may be accompanied by thrombosis or necrosis
71
Q

Describe Osler nodes

A

Tender lesions at pulp of fingers

72
Q

Cause of Janeway lesions

A

Septic emboli

73
Q

Describe Janeway lesions

A
  • May feature subcutaneous abscesses
  • Non-tender
  • Palms and soles
74
Q

3 pathologic eye changes due to IE

A
  • Roth spots
  • Conjunctival petechiae/hemorrhage
  • Flame hemorrhages
75
Q

Describe Roth spots

A

Lymphocytes, edema and hemorrhage in nerve fibre layer of the retina

Block G -- Infection (23 decks)

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