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Flashcards in Infectious Heart Disease Deck (37):

List the common etiological agents infective endocarditis:

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


How do the etiological agents gain access to the endocardium? 

Access to endocardium provided by transient bacteremia


How are IE pathogens successful?

  • 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) 


How is vegetation beneficial to IE pathogens?

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


How do vegetations impact antibiotic therapy?

Implications for antibiotic therapy:

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


What does the cell wall determine for bacteria?

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)


Cell wall:

Gram (+) vs. Gram (-) bacteria

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


What is the laboratory delineation of IE pathogens?

  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


List the cell wall antibacterial agents:

  • cefazolin, ceftriaxone, penicillin, nafcillin
  • vancomcyin
  • daptomycin


List the protein synthesis inhibitors:



List the RNA synthesis inhibitor:



Describe the mechanism for β-lactam antibiotics:

block peptidoglycan crosslinking by inhibting PBPs


How do β-lactam antibiotics differ?

Four basic types of β-lactam

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


How do bacteria resist β-lactam antibiotics?

  • 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)


How does Vancomycin differ from the β-lactam antibiotics?

  • 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 


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

  • 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


Describe the mechanism for Daptomycin

What is its spectrum?

  • 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


Describe the mechanism of Rifampin

How is it useful?

  • 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


  • What do the aminoglycosides target? 
  • What are adverse side effects
  • How are they resisted?

  • 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


Define endocardidtis

inflammatory disease of the endocardium


What is Libman-Sacks endocarditis?

sterile endocarditis

  • related to systemic lupus erythematosus


Difference between acute IE and subacute IE:

  • 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


What are predisposing factors for IE?

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


What simultaneous events occur that result in IE?

  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


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

Mitral > aortic > tricuspid > pulmonary

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


What processes contribute to the clinical manifestations of IE?

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


What are some complications that can arise from IE?

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


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

Modified Duke Criteria:

  •  2 major criteria


  • 1 major criterion and 3 minor criteria


  • 5 minor criteria


What are the major microbiologic criteria for IE?

  • 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 


What are the major echocardiographic criteria for IE?

  • 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


What are the minor criteria for IE?

  • 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


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

  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


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

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


What bacteria are associated with acute IE?

  • Staphylococcus aureus
  • Coagulase-negative staphylococci


What bacteria are associated with subacute IE?

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


What are the most common fungi associated with IE?



When would surgery be necessary as treatment for IE?

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