Dr. Teltscher -- Endovascular Infections Flashcards Preview

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Flashcards in Dr. Teltscher -- Endovascular Infections Deck (75)
1

3 methods of endovascular infection

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

2

4 parasites potentially involved in endovascular infection

  • Plasmodium
  • Babesia
  • Trypanosoma
  • Leishmania

3

3 direct infections of vasculature and structures

  • Suppurative thrombophlebitis
  • Endarteritis
  • Endocarditis

4

Define acute infective endocarditis

Abrupt toxin couse lasting days to weeks

5

Define subacute infective endocarditis

Indolent protracted course featuring systemic symptoms often lasting longer than weeks

6

Sex most commonly affected by endovascular infection

Men

7

Why is incidence of endovascular infection increasing? (4)

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

8

4 predisposing factors for infective endocarditis

  • Native valve (the one's with which you are born)
  • Prosthetic valve
  • Endovascular device utilization
  • IVDU

9

4 problems with native valves that can predispose to IE

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

10

Describe the pathogenesis of IE

11

Distribution of sites affected by iE

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

12

When does "transient bacteremia" occur?

When heavily colonized mucosal surfaces are traumatized

13

Typical findings of low grade and transient bacteremia

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

14

Risk of transient bacteremia

Sufficient to infect a NBTE valvular lesion

15

3 types of virulence factors associated with pathogens involved in IE

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

16

What is Dextran

Complex extracellular polysaccharide (glycocalyx)

17

Dextran function

Promotes adherence to platelet-fibrin matrix (NBTE)

18

2 pathogens that have dextran as a virulence factor

S. mutans (dental caries)

Prominent among certain Streptococcus spp

19

Marker of damaged endothelium to which bacteria can adhere

Fibronectin

20

Pathogen with adhesion to fibronectin as virulence factor

S. aureus (binding and uptake into "normal" endothelium --> triggered apoptosis)

21

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

Staphylococcus spp.

Streptococcus spp.

22

Effect of bacteria-platelet-aggregates in circulating blood

Decreased rate of removal of organism

Increased adherence and aggregation on vegetations

23

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

  • Decreasing expression of adhesion virulent factors
  • Direct cell killing

24

Describe the environment within the vegetation

  • 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)

25

3 pathogens involved in community acquired IE on native valve

  • S. aureus
  • Streptococcus spp.
  • Lesser extent Enterococcus spp.

26

2 pathogens involved in nosocomial IE on a native valve

  • S. aureus
  • Lesser extent Enterococcus spp.

27

Pathogen associated with IVDU IE on native valve

S. aureus (lesser extent other bacteria)

28

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

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

29

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

  • Coagulase negative Staphylococcus spp. > S. aureus
  • Lesser extent Enterococcus spp. > Streptococcus spp

30

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

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

31

6 organisms that produce culture negative endocarditis

  • 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

3 reasons why IE is clinically tricky

  • "Protean" manifestation
  • Subacute/chronic forms may have multiple B-symptoms
  • Systemic symptoms often open differential and may be misleading

33

4 most common symptoms of IE

  • Fever
  • Chills
  • Weakness
  • Dyspnea

34

Importance of cardiac auscultation in IE diagnosis

  • Audible murmur in 85%
  • "New murmur" or "changed murmur" = important but uncommon

35

2 types of IE that do not have audible murmur

  • Right-sided IE
  • Mural IE

36

Most important diagnostic test for IE

Blood cultures

37

Recommended blood culture technique in IE

  • 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

2 electrocradiogram techniques for IE diagnosis

TTE

TEE

39

Describe the use of TTE in IE

  • 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

Describe the use of TEE in IE

  • 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

Modified Duke Criteria: Pathologic criteria for definite IE

  • 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

Modified Duke Criteria: Clinical criteria for definite IE

  • 2 major OR
  • 1 major and 3 minor OR
  • 5 minor

43

Modified Duke Criteria: possible IE

  • 1 major and 1 minor OR
  •  3 minor

44

Modified Duke Criteria: Rule out IE (4)

  • 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

2 major criteria for IE

  • 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

Define "persistently positive blood cultlures"

  • 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

5 minor criteria for IE

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

48

6 vascular phenomena that are included in minor criteria for IE

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

49

4 immunologic phenomena that are included in minor criteria for IE

  • GN
  • Osler nodes
  • Roth spots
  • Positive RF

50

Define minor microbiological evidence for IE

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

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

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

52

8 Acute IE pathologic heart changes

  • 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

4 organs involved in embolic phenomena due to IE

  • Kidney
  • Spleen
  • Coronaries
  • Brain

54

3 immune phenomena due to pathological changes of IE

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

55

3 pathologic changes of kidney architecture during IE

ALL biopsies have abnormal architecture

  • Abscess
  • Infarction
  • GN

56

Vascular pathologic change due to IE

Mycotic aneurysm

57

Pathogen for which mycotic aneurysm is most common

viridans Streptococcus

58

3 mechanism of mycotic aneurysm

  • 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

Most common neurologic event in IE

Cerebral emboli (20%)

60

Leading CNS related cause of death in IE

Hemorrhagic transformation of ischemic event from cerebral emboli

61

Most common parts involved in cerebral emboli

MCA

Branches

62

3 CNS pathologic changes due to IE

  • Cerebral emboli
  • Purulent meningitis
  • Microabscesses

63

Pathogen associated with purulent meningitis due to IE

S. pneumoniae

64

Pathogen associated with micorabscesses in CNS due to IE

S. aureus

65

4 pathologic changes of spleen due to IE

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

66

2 reasons for spleen enlargement in IE

  • Immune stimulation
  • Follicle engorgement

67

Type of IE that lung changes are typically associated with

Right-sided

68

4 pathologic lung changes associated with IE

  • PE (septic or "bland") + infarction
  • Acute pneumonia
  • Pleural effusion
  • Empyema

69

3 pathologic skin changes due to IE

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

70

Cause of Osler nodes

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

71

Describe Osler nodes

Tender lesions at pulp of fingers

72

Cause of Janeway lesions

Septic emboli

73

Describe Janeway lesions

  • May feature subcutaneous abscesses
  • Non-tender
  • Palms and soles

74

3 pathologic eye changes due to IE

  • Roth spots
  • Conjunctival petechiae/hemorrhage
  • Flame hemorrhages

75

Describe Roth spots

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