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Cardiovascular System > Infectious Heart Disease > Flashcards

Infectious Heart Disease Flashcards

1
Q

List the common etiological agents infective endocarditis:

A

Most are part of the normal microbiota

  • Gram (+) bacteria:
    • Staphylococcus aureus – anterior nares
    • Coagulase-negative staphylococci (e.g. S. epidermidis) – skin
    • viridans streptococci (e.g. S. sanguis, S. mutans, S. mitis) – oral cavity
    • enterococci (E. faecalis, E. faecium) – GI tract
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2
Q

How do the etiological agents gain access to the endocardium?

A

Access to endocardium provided by transient bacteremia

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3
Q

How are IE pathogens successful?

A
  • able to survive antimicrobial components of serum
  • able to adhere avidly to endocardium
    • viridans streptococci
      • dextran (exopolysaccharide)
      • adhesins (surface proteins; FimA, GspB, PblA, PblB) that mediate attachment to platelets and fibrin
    • S. aureus
      • fibrinogen-binding adhesins (ClfA, coagulase)
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4
Q

How is vegetation beneficial to IE pathogens?

A

Life in a vegetation:

  • heterogeneous matrix of deposited bacteria, platelets, fibrin, other matrix ligands
  • protection from immune cells
  • bacteria can achieve high densities
  • limitations on nutrient exchange, high cell density – bacteria are not growing rapidly
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5
Q

How do vegetations impact antibiotic therapy?

A

Implications for antibiotic therapy:

  • Bactericidal activity
  • parental administration for sustained activity
  • long-term treatment required
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6
Q

What does the cell wall determine for bacteria?

A

Cell Wall (Peptidoglycan) defines shape

  1. spheres (cocci)
    • single cells
    • pairs (diplococci)
    • chains (streptococci)
    • tetrads (micrococci)
    • grapelike clusters (stapylcocci)
  2. rods (bacilli)
    • coccobacilli ⇒ long rods
  3. spirals
    • comma-shaped (Vibrio) ⇒ 4-20 coils (Spirochetes)
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7
Q

Cell wall:

Gram (+) vs. Gram (-) bacteria

A
  • Gram Positive: Thick Peptidoglycan
  • Gram Negative: Thin Peptidoglycan
    • Crosslinked to the Outer Membrane
      • Outer Membrane:Permeability barrier
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8
Q

What is the laboratory delineation of IE pathogens?

A
  1. **Blood culture **
  2. Gram-stain
    • Positive vs. Negative
  3. Shape
    • Cocci vs. Rods vs. Other
  4. Organization
    • Chains vs. Clusters
  5. Genus
    • Streptococcus vs. Staphylococcus
  6. Other tests
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9
Q

List the cell wall antibacterial agents:

A
  • cefazolin, ceftriaxone, penicillin, nafcillin
  • vancomcyin
  • daptomycin
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10
Q

List the protein synthesis inhibitors:

A

gentamicin

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11
Q

List the RNA synthesis inhibitor:

A

rifampin

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12
Q

Describe the mechanism for β-lactam antibiotics:

A

block peptidoglycan crosslinking by inhibting PBPs

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13
Q

How do β-lactam antibiotics differ?

A

Four basic types of β-lactam

  • modification at “R” groups alters properties of the antibiotic
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14
Q

How do bacteria resist β-lactam antibiotics?

A
  • Mutations in PBPs that prevent binding of β-lactam antibiotics (modification of antibiotic target)
    • Most common mechanism of β-lactam resistance found in Gram-positive bacteria:
      • Streptococcus
      • methicillin-resistant Staphylococcus aureus (MRSA)
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15
Q

How does Vancomycin differ from the β-lactam antibiotics?

A
  • Glycopepetide antibiotic
  • Mechanism: binds to D-Ala-D-Ala
    • Blocks PBPs from transglycosylation/transpeptidation
  • Not effective against G (-) due to outer membrane (permeability barrier)
  • Used for β-lactam resistant infections (e.g. MRSA) or in patients w/ β -lactam hypersensitivity
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16
Q

What is the mechanism of resistance for Vancomycin? Where are the genes for this found?

A
  • Mechanism of resistance: Modification of antibiotic target
  • Bacteria acquire genes encoding machinery to produce altered peptidoglycan structure that lacks D-Ala-D-Ala groups
    • contain D-Ala-D-Lac
  • Vancomycin is unable to bind efficiently to these modified precursors
  • Genes encoding vancomycin resistance are usually found on plasmids or transposons
17
Q

Describe the mechanism for Daptomycin.

What is its spectrum?

A
  • **Lipopeptide **
  • Bactericidal, narrow spectrum (Gram+ bacteria)
  • Mechanism of action:
    • thought to bind to and disrupt the cytoplasmic membrane
    • possibly via loss of membrane potential
    • leading to death
18
Q

Describe the mechanism of Rifampin.

How is it useful?

A
  • Bactericidal, narrow spectrum (G+ bacteria)
  • Mechanism of action:
    • binds to and inhibits RNA polymerase to prevent gene expression (inhibits transcription of DNA into RNA)
    • Resistant mutants arise due to point mutations in the target of the drug
      • RpoB subunit of RNA polymerase
  • Not generally used as monotherapy – use in combinations for synergy
19
Q
  • What do the aminoglycosides target?
  • What are adverse side effects?
  • How are they resisted?
A
  • Mechanism of action: bind irreversibly to 30S ribosomal subunit and cause misreading and premature release of ribosome from mRNA
    • incorporation of incorrect amino acid into growing protein
  • Not good for monotherapy:
    • do not penetrate many Gram-positives well
    • usually used in combination with a cell-wall-active agent to enhance penetration
  • Adverse effects: Ototoxic and nephrotoxic
  • Mechanism of resistance: Enzymatic modification of the antibiotic to prevent aminoglycoside binding to the ribosome
20
Q

Define endocardidtis

A

inflammatory disease of the endocardium

21
Q

What is Libman-Sacks endocarditis?

A

sterile endocarditis

  • related to systemic lupus erythematosus
22
Q

Difference between acute IE and subacute IE:

A
  • Acute IE:
    • invasive, caused by pathogenic organisms that give rise to a toxic course of disease
    • characterized by a more severe and sudden onset than subacute IE
  • Subacute IE:
    • more indolent course of disease caused by less pathogenic bacteria
23
Q

What are predisposing factors for IE?

A
  • valvular heart disease (rheumatic heart disease, congenital heart disease)
  • prosthetic devices (valves, pacemakers)
  • intravenous drug use
24
Q

What simultaneous events occur that result in IE?

A
  1. Alteration of valvular surface to produce a site suitable for bacterial adherence and colonization
    • trauma
    • turbulence
    • result of congenital heart defect
  2. Valvular alterations result in deposition of:
    • platelets, fibronectin, fibrin, other matrix ligands
    • Non-bacterial thrombotic endocarditis -NBTE
  3. Transient bacteremia enables bacteria to reach the site and adhere, resulting in colonization and persistence
    • resulting mass ⇒ “vegetation”
25
Q

Rank the incidence of IE in heart valves (most common to least common):

A

Mitral > aortic > tricuspid > pulmonary

  • mitral and aortic are the most common (left-sided)
  • triscupid valve is most often affected in IV drug abusers
26
Q

What processes contribute to the clinical manifestations of IE?

A

Contributing factors:

  1. infectious process on the valve and its complications
  2. embolization to other organs
  3. persistent bacteremia, often with metastatic foci of infection
  4. immunopathologic factors
  • As a result, the clinical presentation of IE is highly variable and diagnosis can be delayed
27
Q

What are some complications that can arise from IE?

A
  • congestive heart failure (CHF)
  • conduction defects (heart block)
  • major embolic episodes (myocardial infarction, stroke)
  • systemic abscesses
  • renal failure
  • mycotic aneurysm (infection of artery wall)
28
Q

A definitive clinical diagnosis of IE is made based on the presence of:

A

Modified Duke Criteria:

  • 2 major criteria

or

  • 1 major criterion and 3 minor criteria

or

  • 5 minor criteria
29
Q

What are the major microbiologic criteria for IE?

A
  • Two blood cultures positive for organisms typically found in patients with IE in the absence of an alternative primary focus
    • staphylococci, streptococci, enterococci, HACEK
  • Blood cultures persistently positive from cultures drawn more than 12 hours apart
  • 3+ separate blood cultures drawn at least 1 hour apart
  • _Positive serology for Coxiella burnetti _
30
Q

What are the major echocardiographic criteria for IE?

A
  • Echocardiogram positive for IE
    • documented by an oscillating intracardiac mass on a valve or on supporting structures in the path of regurgitant jets
    • on implanted material in the absence of an alternative anatomical explanation
  • Myocardial abscess
  • Development of partial dehiscence of a prosthetic valve
  • New-onset valvular regurgitation
31
Q

What are the minor criteria for IE?

A
  • Predisposing heart condition or intravenous drug use
  • Fever of 38°C (100.4°F) or higher
  • Vascular phenomena, including major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, or Janeway lesions
  • Immunological phenomenon such as glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor
  • Positive blood culture results not meeting major criteria or serologic evidence of active infection with an organism consistent with IE
    • Brucella, Legionella
32
Q

What types of echocardiography can be used to aid in IE diagnosis?

A
  1. Transthoracic echo (TTE)
    • ~60% sensitive for detecting vegetations, primarily for right-sided IE
  2. Transesophageal echo (TEE)
    • ~95% sensitive for detecting vegetations and perivalvular abscesses
    • preferred test for evaluation of prosthetic valves
    • Indicated in patients with suspected IE
33
Q

What are the most common G- bacteria that can cause IE?

A

HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

  • normal flora of the oropharynx
  • generally fastidious Gram-negative rods that require special culture media and prolonged periods of culture for isolation
34
Q

What bacteria are associated with acute IE?

A
  • Staphylococcus aureus
  • Coagulase-negative staphylococci
35
Q

What bacteria are associated with subacute IE?

A
  • Viridians streptococci
  • Enterococci
  • HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
36
Q

What are the most common fungi associated with IE?

A

Candida

37
Q

When would surgery be necessary as treatment for IE?

A
  • Surgical therapy to debride or replace affected valves:
    • severe valvular failure occurs
    • perivalvular abscess needs drainage

Cardiovascular System (35 decks)

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