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x. ID > 3/22 Ch 14 Endocarditis > Flashcards

3/22 Ch 14 Endocarditis Flashcards

∆ = difference

1
Q

∆ between transient, intermittent and continuous bacteremia?

A

transient - occurs during normal daily activities (brushing teeth, bowel movements) or with manipulation of infected tissues

intermittent - occurs with infection and obstruction (e.g., pyelonephritis, cholecystitis), undrained abscesses

continuous “high grade”- occurs with endovascular infection: endocarditis, infected arterial aneurysm, infected grafts and shunts

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2
Q

Why get at least 2 sets of blood samples to determine if the patient has bacteremia?

A

for reasons of both sensitivity (higher volume of blood results in higher yield) and specificity (multiple positive cultures makes it more likely that a positive is a “true-positive”).

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3
Q

Normal skin flora (contaminants) in blood culture?

A

Coagulase-negative staphylococci (unless a FB is in place)
Bacillus spp.
Propionibacterium acnes
± viridans streptococci

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4
Q

When should you suspect contamination in a blood culture?

A
  • clinical course is not suggestive of bacteremia
  • a primary infection with the same organism(s) is absent
  • predisposing factors absent (prosthetic devices, IDU, neutropenia)
  • no leukocytosis or left shift in CBC
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5
Q

T/F True pathogens are often contaminants of blood.

A

False! True pathogens are rarely contaminants

Examples include
Gram-negative bacilli
Anaerobes
S. aureus
S. pyogenes (group A strep)
S. pneumoniae
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6
Q

pathogenesis of endocarditis?

A

Endothelial damage results from turbulent flow, by trauma (e.g., catheters, particulate matter), or by chronic inflammation.

Localized thrombosis occurs, serving as a nidus for infection during transient bacteremia.

Platelet-fibrin layers form an effective barrier between embedded bacteria and circulating neutrophils (vegetation – an infected platelet-fibrin thrombus)

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7
Q

What is infective endocarditis?

A

a localized microbial infection of cardiac valves or mural endocardium

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8
Q

What are two types of infective endocarditis?

A 
Acute endocarditis (ABE)
Subacute endocarditis (SBE)
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9
Q

factors predisposing infective endocarditis?

A 
Injecting drug use
Mitral valve prolapse, especially if mitral regurgitation or thickened leaflets
Degenerative valve disease
Rheumatic heart disease
Poor dental hygiene
Long-term hemodialysis
Previous endocarditis
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10
Q

Acute infectious endocarditis - definition?

A

Acute onset (within a week), rapidly progressive symptoms; occurs on normal or abnormal valves (often aortic + mitral)

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11
Q

etiology of acute infectious endocarditis?

A

virulent organisms
S. aureus most common
ß-hemolytic streptococci
Pneumococcus

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12
Q

presentation of acute infectious endocarditis?

A

High fever (vs. SBE)
Rigors (shaking chills) (vs. SBE)
Rapid development of CHF

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13
Q

Subacute infectious endocarditis - definition?

A

symptoms usually present for weeks-months before diagnosis; occurs on abnormal valves

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14
Q

etiology of Subacute infectious endocarditis?

A

“low grade” pathogens
Viridans streptococci most common
Coagulase-negative staphylococci - common; often associated with medical interventions

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15
Q

clinical presentation of Subacute infectious endocarditis?

A 
Fever
Anorexia, weight loss, malaise, night sweats
Myalgias (40-50%)
Splenomegaly
Renal (hematuria, insufficiency)
production of major emboli
Stroke - results in
- Amaurosis fugax
- Abd pain, ileus, bleeding
- Coronary emboli
- splenic infarcts, splenic abscess
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16
Q

What is the classic presentation of endocarditis?

MUST KNOW EVERY SINGLE ONE

A

1) Fever (can be absent in patients with chronic diseases, antibiotics treatment, infections with less virulent organisms, elderly)
2) Roth Spots (white spots on retina surrounded by hemorrhage)
3) Osler nodes (tender, raised lesions on the finger/toe pads)
4) Murmur - reflects rapid valve destruction

5) Janeway Lesions (small, non-tender erythematous lesions on palm or sole)
6) Anemia
7) Nail-bed “splinter” hemorrhages
8) Emboli

“from jane”

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17
Q

Nonbacterial thrombotic endocarditis (“marantic endocarditis”) - definition?

A

sterile vegetations, seen in connective tissue diseases, malignancy

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18
Q

Nonbacterial thrombotic endocarditis (“marantic endocarditis”) pathogens?

A

NONE! actually seen in connective tissue diseases, malignancy

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19
Q

Culture-negative Endocarditis - definition?

A

endocarditis without etiology with negative cultures

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20
Q

Culture-negative Endocarditis - etiology?

A

1) recent antibiotic treatment
2) inadequate microbiological techniques
3) Fastidious organisms (many, but * are listed in FA)
- *Bartonella species (cat-scratch bacillus, trench fever)
- *Q fever (Coxiella burnetii)
- Nutritionally variant streptococci
- HACEK organisms
- Chlamydia species
- Legionella species
- Brucella species
- Fungi

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21
Q

What are HACEK organisms?

A 
Haemophilus
Actinobacillus
Cardiobacterium hominis
Eikenella
Kingella
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22
Q

What must you do if you suspect Culture-negative Endocarditis?

A

special media
serologic testing
prolonged incubation of culture

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23
Q

IVDU endocarditis definition?

A

endocarditis in IV drug users; usually in people with no congenital heart disease

24
Q

What valve is normally affected in IVDU endocarditis?

A

tricuspid

25
Q

IVDU endocarditis pathogens?

A

S. aureus
Gram-negatives (esp. Pseudomonas)
polymicrobial
Candida albicans

26
Q

clinical presentation of IVDU endocarditis?

A

High fever, cough, chills, malaise

Pleuritic chest pain from septic pulmonary emboli is a hallmark R-sided infected endocarditis

27
Q

prosthetic valve endocarditis - definition of early vs late? What is it usually associated with?

A

Early PVE – occurs within 2mo of surgery; usually acquired in the hospital

Late PVE – occurs >12 mo after surgery; usually “community-acquired”

Often associated with invasion of peri-vavular tissue, resulting in valvular

  • abscesses
  • obstruction
  • dysfunction
  • dehiscence (wound rupture)
28
Q

What bugs are usually involved in prosthetic valve endocarditis?

A

Early PVE
S. aureus
coagulase-negative staphylococci

Late PVE
Streptococci

29
Q

cardiac complications of endocarditis?

A

Valve damage causing CHF

  • Extension of infection beyond the valve annulus (myocardial abscess)
  • Extension into septum, causing heart block

Purulent pericarditis

30
Q

neurologic complications of endocarditis?

A

embolic stroke in a patient with fever and underlying valvular disease

mycotic aneurysm leading to rupture and hemorrhage; early diagnosis by MRI scan or CT scan

31
Q

most common site of endocarditis complications? how is it diagnosed?

A

Spleen the most common site (splenic abscess a common complication); diagnosed by CT scan

32
Q

which pathogens have been implicated in the mortality of infective endocarditis?

A

Viridans streptococci: 4 – 16%
Enterococci: 15 – 25%
S. aureus: 25 – 47%
50% for gram-negatives, fungi

33
Q

Factors Affecting Mortality in infective endocarditis?

A

1) Causative organism
2) Complications or coexisting conditions (e.g., CHF, neurologic events, renal failure)
3) Perivalvular extension
4) Appropriate surgical intervention
5) valve affected - much lower mortality rate from right-sided IE

34
Q

how do you lower the risk of infective endocarditis?

A

prophylactic antibiotics given for patients at high risk (underlying valve disease), and when they undergo procedures that are likely to lead to bacteremia.

35
Q

how is infective endocarditis diagnosed?

A

clinical picture, labs, ECHO, and clinical acumen

36
Q

typical labs of infective endocarditis?

A

anemia, leukocytosis, abnormal urinalysis, elevated ESR and CRP

37
Q

what is the hallmark of infective endocarditis?

A

“sustained bacteremia” - 3 separate venipunctures taken over several hours for SubacuteBE or over several minutes for Acute BE and inoculated in aerobic + anaerobic media

38
Q

How method would you use to view vegetations?

A 
Transthoracic ECHO (TTE)
Transesophageal ECHO (TEE)
39
Q

Pros/Cons of Transthoracic ECHO (TTE)?

A

Pros: rapid, non-invasive, cheap, high specificity (98%)

Cons: body habitus may preclude good study, sensitivity (60-70%)

40
Q

Pros/Cons of Transesophageal ECHO (TTE)?

A

Pros: high sensitivity for vegetations (75-95%) without compromising specificity, especially useful for prosthetic valves, more likely than TTE to detect myocardial abscess

Cons: $$$, invasive

41
Q

What criteria is used to ultimately determine if one has infective endocarditis?

A

Duke Criteria – don’t have to memorize; just know that it exists

Specificity said to be 99%
Negative predictive value 92%

42
Q

What are basic principles guiding treatment of infective endocarditis?

A

Always obtain blood cultures first!

For SBE - delay treatment while awaiting culture results

For ABE - start treatment as soon as blood cultures have been obtained

followed by antibiotics (prolonged course of parenteral agents, high doses, and in-patient treatment until the patient has has responded)

43
Q

When do you stop treating a patient with infective endocarditis?

A

until the patient has clearly responded (afebrile, repeat BCs negative) and the risk of complications has diminished
specific pathogens and treatments

44
Q

Viridans streptococci treatment?

A

Penicillin G or ceftriaxone, 4 weeks

45
Q

Streptococci with MIC

A

Penicillin for 4 weeks + gentamicin, 2 weeks

46
Q

Enterococci, fastidious or resistant streptococci

A

Penicillin + gentamicin, 2-6 weeks

47
Q

MSSA

A

Nafcillin, 4 weeks

48
Q

MRSA

A

Vancomycin, 4 weeks

49
Q

HACEK organisms

A

Ceftriaxone, 4 weeks

50
Q

Prosthetic valves treatment for “sensitive” strep

A

gentamicin, 2 wks

51
Q

Prosthetic valves treatment for “resistant” strep

A

gentamicin, 4-6 wks

52
Q

Prosthetic valves treatment for MSSA, MRSA and coagulase-negative staphylococci (organisms that make biofilms)

A

gentamicin + rifampin

53
Q

When is valve replacement surgery best done?

A

for both native and prosthetic valve endocarditis; best before severe CHF or spread of infection to peri-valvular tissue

54
Q

Indications for valve replacement surgery?

A

1) persistent bacteremia despite appropriate therapy
2) perivalvular invasive disease (development of heart block)
3) moderate to severe CHF
4) recurrent major emboli (or one with a large vegetation)
5) large vegetations
6) specific organisms: Pseudomonas, fungi, highly resistant enterococci.

55
Q

If you see these organisms, you should consider doing a valve replacement surgery

A

Pseudomonas
fungi
highly resistant enterococci

56
Q

Risk of subsequent infective endocarditis with prosthetic valve?

A

Risk of infecting the new prosthetic valve is very low; can get superior outcomes with combined medical/surgical approach in the setting of poor prognostic factors, eg staphylococcal infection

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