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44 Cards in this Set

  • Front
  • Back
cardiac damage is most often associated with what?
mitral valve stenosis
most cases of endocarditis infect what type of tissue?
damaged tissue
define acute rheumatic fever
-delayed nonsupporative disease (no white cells)
-Occurs after an antecedant Group A Strep infection (and the infection must be in the upper respritory tract)
-Characterized by proliferative inflammatory lesions in the connective tissue of joints, heart, skin and central nervous tissue
how long after an upper respritory tract infection by a group A strep will we start to antibodies and mitral valve damage from rheumatic fever?
2-3 weeks
what is the average time between attack and initial Gp A strep infection?
18 days
what are the ages that acute rheumatic fever are prevalent in?
yrs 5-15yr
Streptococcus pyogenes
gram + cocci in chains
(with Beta Hemolysis)

catalase - (this is how we seperate staph from strep)

Ferment sugars -> lactic acid -> low pH
describe the differences between the different hemolyses, alpha, beta, gamma
beta - total clearing (always pathogenic)
alpha - some clearing
gamma - no clearing
List some of the structural virulence factors of Group A strep
- capsule (hyaluronic acid)
- peptidoglycan layer
- group A carbohydrate
- fibrils (consist of M-proteins)
- T-antigen, ect.
what is the primary virulence factor for group A strep?
What are some soluble virulence factors for group A strep
- Streptolysin O
- Streptodornase
- Streptokinase
- Hyaluronidase
- Chemotoxins
- Erythrogenic toxin (some strains will cause scarlet fever)
-super antigens (may cause streptococcal toxic shock- even though before we only really spoke about staph based toxic shock, this does have the capability of doing that as well)
- SpyCEP - envelops that inactivates IL-8
describe the pathogenesis of Acute rheumatic fever
- molecular mimicry (the presence of epitopes in human tissue that are immunologically similar to Grp A strep antigens

M protein = Human tropomyosin and myosin

Grp A Carb. = Heart valve glycoprotein
is there a genetic component to acute rheumatic fever?
yes, only 2-3 % of the population have a ability to acquire acute rheumatic fever
Rhwumatic heart valves have been shown to contain what?
infiltrates of t-cells
If you get rheumatic fever does it reoccur?
yes, there is a high probability of it
What is the treatment of acute rheumatic fever?
Long term antibiotics (long term as in years, like 5 years) this is due to the affinity for re occurrence
What is the criteria for the clinical diagnosis of acute rheumatic fever?
1.) lab evidence of recent strep infection (usually through ASO titers)

2.) presence of 2 mojor or 1major and 1 minor jones criteria
whate are the major jones criteria?
-erythema marginatum
-subcutaneous nodules
sydenham's chorea
what are the minor jones criteria?
-previous rheumatic fever
-prolonged p-r interval on the ECG
-elevated erythrocyte sed-rate
-c-reactive protein or leucocytosis
the most common major jones criteria is what?
polyarthritis (80%)
carditis (40-50%)
what is the laboratory screening techniques for ARF?
steptozyme test, if positive do ASO (>500units = +)
treatment of acute rhematic fever
salicylates (4-8wks)
-prednizone reserved for pts with severe carditis
-heart failure - usually requires bed rest and valve replacement
what is our strategy for the prevention of acute rheumatic fever?
- prevent the primary attack, prompt recognition and treatment of strep throat DOC= PCN
- secondary attack, continuous long term prophylaxos with PCN (>5yrs)
What is PANDAS?
pediatric autoimmune neurologic disorders associated with strep.

they are probably a manifestation of sydenham's chorea (tics, tourette's and OCD and it usually improves with steroid therapy
What is Infective Endocarditis (IE)?
- An infection of the native or prosthetic valve or endocardium
- it occurs most often in patients with recognized heart disease
- hearts of such Pts undergo an edematous, cellular distortion resulting in non-bacterial thrombocytic endocarditis (NBTE) lesions (these lesions then become something that the bacteria can bind to to crease an IE lesion)
can heart cath cause damage to the valves?
yes, in about 2%
what is seen more, right or left sided endocarditis?
Right sided endocarditis, this is due to IV drug usage and invasive procedures done in the hospital
Acute Infective endocarditis?
comes on rapidly, there is high fevers, and they are brought on by staph a.
Subacute infective endocarditis?
comes on slowly, maybe you have a fever at night, often caused by alpha hemolytic strep, and they may have already had valve damage (Strep. viridans)
IV drug use infective endocarditis?
dirty unclean injections into the blood stream can inject bacteria into the blood stream, the endocarditis will be seen on the right side (Staph. aureus)
Prosthetic valve endocarditis (PVE)
there is an early onset and a late onset both caused by some damage from the prosthetic that the bacteria can then attach to (Staph. epidermidis = early)(Strep. viridans = late onset)
What are the damage causing agents in valve disorders?
-heart disease
What are some of the sources of bacteria for infective endocarditis?
dental (Strep. viridans)
IV introduction (tricuspid)
Pulmonary (Mitral Valve)
What side, right or left vegitations has lower bacterial density?
the right side, this is because there is more neutrophil access (note that both sides usually have the majority of bacteria in the metabolically inactive state, therefore resistant to antibiotics)
What valve is the most common for infective endocarditis?
Mitral valve endocarditis
What is the Venturi effect?
Cardiac abnormalities → high pressure area through narrowing to low pressure reservoir → platelet-fibrin aggregate on low pressure side
High velocity jet streams → injury on wall of L atrium, R ventricle, or chordae mitral valve leaflet → platelet-fibrin thrombi → nidus of infection
Explain traumatized valves and the role of nonbacterial thrombotic vegetations.
endothelial changes leads to the tissue being denuded of collagen, platelets then aggrigate and fibrin deposits. This allows bacteria to colonize and vegetations to form this can then stimulate thrombi (vegetations may enlarge and become a sanctuary for organisms).
what are some of the clinical signs of acute infective endocarditis (AIE)?
-abrupt onset of fever, rigots, prostration, and leucocytosis
-skin may show evidence of embolitic pustules or hemorrage
- Occassionally there will be janeway lesions
-heart murmer
What are janeway lesions?
Janeway lesions (nontender, macular lesions most commonly involving the palms and soles). Janeway lesions occur more frequently in endocarditis caused by Staphylococcus aureus. Janeway lesions are caused by septic emboli. Subcutaneous abscesses are found on histologic examination.
Subacute infective endocarditis (SIE), what are some clinical signs?
- presents as an ill defined wasting disease over a long period of time.
-patirnt not feeling well- often anorexia and weight loss
-heart murmer, splenomegaly and petechiae
-splinter hemorrhages are common
- ocasionally, osler nodes and Roth's spots are present
- slight leukocytosis and anemia
What is an Osler node?
Osler’s nodes (painful, palpable, erythematous lesions most often involving the pads of the fingers and toes). Caused by immune complexes (they want you to know that for Step 2).
What are Roth's spots?
Spots in the eye, that are due to immune complexes
How do you detect organisms for AIE?

how about for SIE?
AIE: Blood draws, draw three cultures during a 1-2 hour period (95%)

SIE: draw 3 bood cultures per day for 2 days (harder to get the organism)
How are SIE and AIE treated?
- It depends on the organism, but the Antibiotics should be bactericidal, moniter treatment with blood cultures and serum bactericidal levels (should be>1.8)
- If damage is severe, and the infection can not be cleared then we will do valve replacement.