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Micro Term 4 > Infections of the Cardiovascular System > Flashcards

Flashcards in Infections of the Cardiovascular System Deck (34):
1

describe endocarditis

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

2

describe the types of IE 

3

list the IE risk factors 

4

describe risk factors for bacteremia and IE

5

describe the pathogenesis of endocarditis

  • 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

6

describe the sequence of endocarditis pathogenesis

7

describe the hemorrhagic signs due to microbemoblization

8

describe the symptoms of infective endocarditis

9

describe clinical and laboratory diagnosis of IE

10

describe the etiology of IE (native valve)

  • 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

11

describe the etiology of IE (prosthetic, PVE)

  • 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

12

describe the etiology of IE (IVDU)

  • 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

13

summarize the prevalent causative agents of IE

14

describe the G+ve cocci lab algorithm 

15

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

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

16

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

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

17

invasive ____ of Staphylococcus aureus facilitate spreading

explain this

invasive exotoxins of Staphylococcus aureus facilitate spreading

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

18

describe the anti-phagocytic function of Staphylococcus aureus

  • 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

describe the adhesive function of Staphylococcus aureus

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

describe the invasion and evasion of Staphylococcus aureus

  • 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

describe Staphylococcus aureus in the blood stream

  • 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

describe the function of clumping factor A 

23

describe the function of fibronectin-binding adhesins

24

describe the function of neutrophil extracellular traps (NETs)

25

describe the coagulase-negative Staphylococci

26

describe the microbial pathogenesis of Staphylococcus epidermidis

27

list the characteristics of Streptococcus

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

28

describe Abiotrophia defectiva

29

describe the complement and phagocytosis evasion virulence factors of Streptococcus

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

30

describe the spread of Streptococcus via lymph and blood

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

31

describe the microbial pathogenesis of Streptococcus mutans

32

describe the biology of Enterococcus

33

describe the microbial pathogenesis of Enterococcus faecalis

34

describe the lab diagnosis of Streptococci and Enterococci in IE