Infections of the Cardiovascular System Flashcards
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
describe the types of IE
list the IE risk factors
describe risk factors for bacteremia and IE
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
describe the sequence of endocarditis pathogenesis
describe the hemorrhagic signs due to microbemoblization
describe the symptoms of infective endocarditis
describe clinical and laboratory diagnosis of IE
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
-
acute form:
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
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
summarize the prevalent causative agents of IE
describe the G+ve cocci lab algorithm
____ (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
____ (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
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
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
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
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
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
- superantigen binds to complex of MHC II and TCRs and leads to:
describe the function of clumping factor A
describe the function of fibronectin-binding adhesins
describe the function of neutrophil extracellular traps (NETs)
