Infections of the Cardiovascular System Flashcards

1
Q

describe endocarditis

A

infection of endocardial surface of the heart, which may encompass one or more valves or a septal defect in congenital heart disease

  • aortic
  • mitral
    • dysfunction by rupture of chordae tindinae
  • tricuspid: intravenous drug user
  • pulmonic: rare
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2
Q

describe the types of IE

A
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3
Q

list the IE risk factors

A
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4
Q

describe risk factors for bacteremia and IE

A
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5
Q

describe the pathogenesis of endocarditis

A
  • heart valves do not have blood vessels
  • deposition of immune complexes, platelets and fibrin leads to nonbacterial thrombotic vegetation and inflammation
  • bacteria adhere to platelet-fibrin deposits and multiply
    • 80% of cases are caused by staphylococci, streptococci, and enterococci
  • inflammation and activation of neutrophils
  • damage of endocardium due to invasion by bacteria
  • mature vegetation includes bacteria
  • arterial organ embolization → interruption of blood flow due to clotting
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6
Q

describe the sequence of endocarditis pathogenesis

A
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7
Q

describe the hemorrhagic signs due to microbemoblization

A
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8
Q

describe the symptoms of infective endocarditis

A
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9
Q

describe clinical and laboratory diagnosis of IE

A
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10
Q

describe the etiology of IE (native valve)

A
  • native valve (NVE):
    • acute form:
      • affects those with intact valves
      • rapid and aggressive onset
      • Staphylococcus aureus, B-hemolytic Streptococcus
    • subacute form:
      • affects those with preexisting valve disease
      • clinical course that may extend over several months
      • risk factors: dental surgery, indwelling intravenous catheters, IV drug use
      • α-hemolytic Streptococcus, Enterococcus, HACEK group
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11
Q

describe the etiology of IE (prosthetic, PVE)

A
  • prosthetic (PVE): artificial valve, pacemaker
    • illness with low grade fever or acute toxic illness
    • early PVE: S. aureus or coagulase negative S. epidermidis, Diphtheroids, fungi
    • late PVE: S. aureus or coagulase negative, may present in subacute fashion
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12
Q

describe the etiology of IE (IVDU)

A
  • IVUD: right-sided nosocomial infective endocarditis (NVE) may present pleuropulmonary symptoms
    • Staphylococcus aureus
    • P. aeruginosa
      • is slower than S. aureus
      • has high rate of neurological involvement
    • left-sided IVDU IE has similar etiology to non-IVDU disease: SA, Enterococcus sp., Gram-rods, Candida sp., or polymicrobial
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13
Q

summarize the prevalent causative agents of IE

A
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14
Q

describe the G+ve cocci lab algorithm

A
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15
Q

____ (type of bacteria) are leading in acute nosocomial IE, prosthetic valve IE, community-acquired IE and IVDU

A

coagulase-positive S. aureus are leading in acute nosocomial IE, prosthetic valve IE, community-acquired IE and IVDU

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16
Q

____ (type of bacteria) are leading in subacute prosthetic valve IE and subacute nosocomial IE

A

coagulase-negative S. epidermidis are leading in subacute prosthetic valve IE and subacute nosocomial IE

17
Q

invasive ____ of Staphylococcus aureus facilitate spreading

explain this

A

invasive exotoxins of Staphylococcus aureus facilitate spreading

  • hemolysins and leucocidins are cell membrane-damaging proteins
  • hyaluronidase, proteases, collagenase, elastase
  • staphylokinase, fibrinolysin, lipases, nucleases
18
Q

describe the anti-phagocytic function of Staphylococcus aureus

A
  • protein A (MSCRAMM = microbial surface compounds recognizing adhesive matrix molecules) binds to Fc portion of IgG molecule, inverts IgG and prevents opsonization
  • coagulase binds to prothrombin, polymerases fibrinogen to fibrin and utilizes it to coat the bacterial cell to protect it from the phagocytosis
19
Q

describe the adhesive function of Staphylococcus aureus

A

adhere to epithelial cells of heart valve and endothelium and form vegetation

  • microbial surface compounds recognizing adhesive matrix molecules (MSCRAMMs)
    • uses polysaccharide intercellular adhesins (PIA) to attach to fibronectin and fibrinogen
    • forms biofilms
20
Q

describe the invasion and evasion of Staphylococcus aureus

A
  • clumping factor A aggregates platelets
  • cell wall adhesins bind to fibrinogen and invades neutrophils and non-phagocytic cells via fibronectin and integrin
  • survives intracellularly by producing carotenoids and catalase as “microcolonies”; form L-forms
21
Q

describe Staphylococcus aureus in the blood stream

A
  • granulated neutrophils release DNA, histones and elastase to catch S. aureus into the neutrophil extracellular traps
  • if S. aureus is lysed, then peptidoglycan along with toxins serve as superantigens:
    • superantigen binds to complex of MHC II and TCRs and leads to:
      • proliferation of T cells
      • release of cytokines (IL-6, IL-1 (fever), IL-2, IFN-g))
      • on macrophages release of TNF-a (IL-8 inflammation) → hypotension
22
Q

describe the function of clumping factor A

A
23
Q

describe the function of fibronectin-binding adhesins

A
24
Q

describe the function of neutrophil extracellular traps (NETs)

A
25
Q

describe the coagulase-negative Staphylococci

A
26
Q

describe the microbial pathogenesis of Staphylococcus epidermidis

A
27
Q

list the characteristics of Streptococcus

A
  • facultative anaerobic G+ve diplococci or chains
  • catalase-negative and oxidase-negative
28
Q

describe Abiotrophia defectiva

A
29
Q

describe the complement and phagocytosis evasion virulence factors of Streptococcus

A
  • protein M anchored in the cell wall and binds to MHC type II, blocks complement system and PMN leukocytes
30
Q

describe the spread of Streptococcus via lymph and blood

A
  • encapsulated, biofilm-forming
  • cytolysins (plasmid coded), hemolysis and leukocidins
31
Q

describe the microbial pathogenesis of Streptococcus mutans

A
32
Q

describe the biology of Enterococcus

A
33
Q

describe the microbial pathogenesis of Enterococcus faecalis

A
34
Q

describe the lab diagnosis of Streptococci and Enterococci in IE

A