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131 Cards in this Set
- Front
- Back
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What is Endocarditis?
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Inflammatory disease of the endocardium (most commonly the heart valves)
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What is unique about Libman-Sacks Endocarditis?
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- Sterile endocarditis (no infection)
- Related to systemic lupus erythematosus |
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What are the types of Infective Endocarditis (IE)?
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- Acute
- Subacute |
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What is unique about Acute Infective Endocarditis (IE)?
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- Invasive
- Pathogenic organism gives rise to toxic course of disease - More severe and sudden onset |
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What is unique about Subacute Infective Endocarditis (IE)?
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- Indolent (lazy) course of disease
- Less pathogenic bacteria |
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What are the important factors that may predispose someone to getting Infective Endocarditis (IE)?
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- Valvular heart disease (rheumatic or congenital)
- Mitral valve prolapse w/ regurgitation or thickened leaflets - Mitral regurgitation, aortic stenosis, aortic regurgitation, ventricular septal defect - Prosthetic devices (valves, pacemakers) - IV drug use |
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What are the most common etiological agents of Infective Endocarditis (IE)? Where are they located?
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Most commonly members of normal microbiota:
- S. aureus - anterior nares - Coagulase-neg. Staphylococci (S. epidermidis) - skin - Viridans Streptococci (S. sanguis, S. mutans, S. mitis) - oral cavity - Enterococci (E. faecalis, E. faecium) - GI tract |
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Which microbiota commonly cause infectious endocarditis and are found in anterior nares?
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Staphylococcus aureus
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Which microbiota commonly cause infectious endocarditis and are found on the skin?
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Coagulase-negative Staphylococci (eg, S. epidermidis)
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Which microbiota commonly cause infectious endocarditis and are found in the oral cavity?
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Viridans Streptococci
- S. sanguis - S. mutans - S. mitis |
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Which microbiota commonly cause infectious endocarditis and are found in the GI tract?
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Enterococci
- E. faecalis - E. faecium |
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What are the properties of successful Infective Endocarditis pathogens?
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- Survive in serum despite anti-microbial components
- Adhere avidly to endocardium |
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What are some molecules that pathogens adhere to in the endocardium, leading to Infective Endocarditis?
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- Dextran (exopolysaccharide)
- Adhesins (surface proteins: FimA, GspB, PblA, PblB) - Fibrinogen-binding adhesions (ClfA, coagulase) |
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What are some mechanisms of adherence to the endocardium by pathogens causing Infective Endocarditis? Which pathogens use these mechanisms?
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- Dextran (exopolysaccharide) - used by viridans streptococci
- Adhesins (surface proteins: FimA, GspB, PblA, PblB) - mediates attachment to platelets and fibrin - used by viridans streptococci - Fibrinogen-binding adhesins (ClfA-clumping factor A, coagulase) - used by S. aureus |
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What is necessary for the pathogenesis of Infective Endocarditis?
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Simultaneous occurrence of several independent events:
- Altered valve surface (trauma, turbulence, congenital heart defect) → bacterial adherence → colonization - Valve alteration → deposition of platelets, fibronectin, fibrin, other matrix ligands (= non-bacterial thrombotic endocarditis, NBTE) - Transient bacteremia → bacteria adheres to valve → colonization → vegetation |
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What molecule is important for attachment of S. aureus to NBME (non-bacterial thrombotic endocarditis)?
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Fibrinogen-binding adhesins (clumping factor A (clfA) and coagulase)
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What can cause an alteration of the valvular surface? What is this necessary for?
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- Trauma, turbulence, or congenital heart defects
- Generates a suitable site for bacterial adherence and colonization - Results in deposition of platelets, fibronectin, fibrin, and other matrix ligands |
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What is necessary for bacteria to reach the site of the endocardium to form a colony / vegetation?
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- Transient bacteremia (common and occurs regularly whenever mucosal surfaces colonized w/ bacteria are traumatized, eg, dental procedure)
- Could also be secondary to dissemination from infection at another site |
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What enlarges a vegetation?
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- Further deposition of platelets and fibrin
- Bacterial growth |
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What are some common procedural causes of bacteremias?
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- Dental procedures (eg, extraction, surgery, chewing candy, tooth brushing, oral irrigation)
- Upper airway procedures (eg, bronchoscopy, tonsillectomy, nasotracheal intubation, GI endoscopy, sigmoidoscopy/colonoscopy) - Urologic procedures (urethral dilation or catheterization, cystoscopy) - OB/GYN procedures (normal vaginal delivery) |
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What is the likelihood of bacterial adherence to the heart valves?
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Mitral > Aortic > Tricuspid > Pulmonary
*Tricuspid most common in IV drug users |
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Bacteria commonly associated with Infective Endocarditis adhere more avidly to what?
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Valves (as opposed to organisms not often associated w/ Infective Endocarditis)
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What do bacteria that cause Infective Endocarditis need to be resistant to?
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Serum components because they rely on a transient bacteremia to get to valves
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What are the consequences of growth in vegetations?
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- Protection from immune cells (infiltration impaired by matrix)
- High densities of bacteria (deep bacteria have reduced metabolism) - Release of bacteria from vegetations → persistent bacteremia (potential for hematogenous seeding of extra-cardiac foci) - Host response (pro-inflammatory cytokines) - Tissue destruction by microbe (valvular damage) - Embolic phenomena (d/t fragmentation of vegetation) |
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What are the components of a vegetation?
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Heterogenous matrix of deposited bacteria, platelets, fibrin, and other matrix ligands
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How are bacteria in a vegetation protected from immune cells?
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Matrix surrounding vegetation limits infiltration by immune cells
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How are bacteria in a vegetation protected from antibiotics?
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Bacteria deep within the matrix exhibit reduced metabolic activity because of limited nutrient exchange (reduces activity of antibiotics)
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What can cause a persistent bacteremia in Infective Endocarditis? What can this also cause?
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- Release of bacteria from vegetations can lead to persistent bacteremia
- Potentially may cause hematogenous seeding of extra-cardiac foci |
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How does the growth of vegetations dictate the type of antibiotic therapy that should be used?
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- Bactericidal activity (because of slowed bacterial metabolism, bacteriostatic is not sufficient)
- Parenteral administration (for sustained activity) and frequent dosing (prevent relapse) - Long-term treatment required (4-6 weeks) - Need high antibiotic concentration in vegetation |
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What processes contribute to the clinical picture of Infective Endocarditis?
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- Infectious process on the valve
- Embolization to other organs - Persistent bacteremia (w/ metastatic foci of infection) - Immunopathologic factors - Ultimately, a highly variable presentation, which can delay diagnosis |
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What are the most common symptoms and signs of Infective Endocarditis?
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- Fever (80-95%)
- Malaise, chills/sweats (40-75%) - Heart murmur (80-85%, new or worse in 10-40%) - Embolic phenomena (cerebral, splenic, lung, skin eye) (5-50%) - Roth spots (retinal lesions) - Mucocutaneous lesions (petechiae, Osler nodes, Janeway lesions, splinter hemorrhages) - Rheumatoid Factor in cases >6 weeks - Anemia (70-90%) - Leukocytosis (20-30%) - Microscopic hematuria (30-50%) - Glomerulonephritis (d/t circulating immune complexes) |
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How common are heart murmurs in Infective Endocarditis? How often is it new or worse than before?
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- 80-85% have heart murmur
- 10-40$ have new or worse heart murmur |
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Where do emboli from Infective Endocarditis commonly affect?
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- Cerebrum
- Spleen - Lungs - Skin - Eyes |
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What is the term for retinal lesions in Infective Endocarditis? Description?
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Roth spots
- Oval, pale retinal lesions - Surrounded by hemorrhage - Consist of lymphocytes surrounded by edema and hemorrhage - In nerve fiber layer of retina |
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Where do you find Roth Spots?
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*Nerve fiber layer of retina
- Oval, pale retinal lesions - Surrounded by hemorrhage - Consist of lymphocytes surrounded by edema and hemorrhage |
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What are the mucocutaneous lesions seen in Infective Endocarditis?
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- Petechiae (conjunctival)
- Osler nodes (small, painful nodules on pads of fingers and toes) - Janeway lesions (hemorrhagic, painless macules on palms and soles) - Splinter hemorrhages |
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What is the term for small, painful nodules on pads of fingers and toes?
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Osler Nodes - mucocutaneous lesions
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What is the term for hemorrhagic, painless macules on palms and soles?
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Janeway lesions
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What antibody do you see in cases of Infective Endocarditis that last longer than 6 weeks?
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Rheumatoid Factor: anti-IgG IgM antibody
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What can circulating immune complexes cause in Infective Endocarditis?
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Glomerulonephritis
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What are the complications of Infective Endocarditis?
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- Congestive heart failure (CHF)
- Conduction defects (heart block) - Major embolic episodes (MI, stroke) - Systemic abscesses - Renal failure - Mycotic Aneurysm (infection of artery wall) |
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How do you diagnose Infective Endocarditis?
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Modified Duke Criteria:
- Need 2 major OR 1 major + 3 minor OR 5 minor criteria Major microbiologic criteria: - Typical organism from 2 separate blood cultures - Organism from persistently positive blood cultures - Positive serology for C. burnetti Major Echo criteria: - New valvular regurgitation - Positive echocardiagram for endocardial involvement Minor criteria: - Predisposing heart condition or IV drug use - Fever (>100.4 degrees F) - Vascular phenomena (excluding petechiae, splinter hemorrhages) - Immulonogical phenomenon (glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor) - Positive blood culture not consistent w/ Infective Endocarditis (eg, Brucella, Legionella) |
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What are the major microbiological criteria for the Modified Duke Criteria to diagnose Infective Endocarditis?
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- Pos. blood culture for organism typical of IE in absence of alternative primary focus
- Blood cultures positive from culture more than 12 hours apart - 3+ separate blood cultures drawn >1 hour apart - Positive serology for Coxiella burnetti |
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What are the major Echocardiographic criteria for the Modified Duke Criteria to diagnose Infective Endocarditis?
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- Oscillating intracardiac mass on valve or on supporting structure, in path of regurgitant jets, or on implanted material in absence of another explanation
- Myocardial abscess - Development of partial dehiscence (opening) of prosthetic valve - New-onset valvular regurgitation |
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What are the minor criteria for the Modified Duke Criteria to diagnose Infective Endocarditis?
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- Predisposing heart condition or IV drug use
- Fever (>100.4 degrees F) - Vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, or Janeway lesions) - Immulonogical phenomenon (glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor) - Positive blood culture not consistent w/ Infective Endocarditis (eg, Brucella, Legionella) |
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What views can you use for an Echo to diagnose Infective Endocarditis? Which is better?
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- Transthoracic Echo (TTE): only 60% sensitive for detecting vegetations, primarily for right-sided IE
- Transesophageal Echo (TEE): 95% sensitive for detecting vegetations and perivalvular abscesses; preferred test for evaluating prosthetic valves |
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Which test is indicated in patients with suspected Infective Endocarditis?
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Transesophageal Echo (TEE) - 95% sensitive for detecting vegetations and perivalvular abscesses
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What is the preferred test for evaluating prosthetic valves?
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Transesophageal Echo (TEE) - 95% sensitive for detecting vegetations and perivalvular abscesses
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What shape are the most common pathogens that cause Infective Endocarditis?
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Cocci (spheres)
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How do you do the Gram Stain? What do the results mean?
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1. Crystal Violet
2. Gram's Iodine 3. Decolorizer (alcohol or acetone) 4. Safranin Red (counter-stain) G+: purple = thick peptidoglycan G-: red = thin peptidoglycan |
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How does a laboratory delineate IE pathogens?
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1. Gram Stain: +
2. Shape: Cocci 3. Organization: - Chains: Streptococcus - Clusters: Staphylococcus |
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What is the most common cause of Infective Endocarditis?
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Staphylococcal organisms: especially S. aureus
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What are the characteristics of Staphylococcus aureus?
- Location? - Gram / catalase / coagulase / shape / organization? - Acute or Subacute? - Complications? - Mortality? - Associated with? |
- Anterior nares
- G+, catalase+, coagulase+, clustered cocci - Acute IE - Complicated by myocardial abscesses, purulent pericarditis, valve ring abscesses, or peripheral foci - High mortality (d/t fulminant infection) - Common in IV drug users (R-sided IE) |
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What complications can make treatment of Staphylococcus aureus Acute IE difficult?
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- Myocardial abscesses
- Purulent pericarditis - Valve ring abscesses - Peripheral foci |
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Which organism is associated with IV drug users?
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**Staphylococcus aureus
- Also Pseudomonas aeruginosa (other G- rods), but extremely rare |
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What are the characteristics of Staphylococcus epidermidis?
- Location? - Gram / catalase / coagulase / shape / organization? - Acute or Subacute? - Associated with? |
- Skin
- G+, catalase+, coagulase-, clustered cocci - Acute IE - Early prosthetic-valve endocarditis; increasing cause of native-valve endocarditis? |
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Which organism is associated with early prosthetic-valve endocarditis and increasingly native-valve endocarditis?
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Coagulase-negative Staphylococci (eg, S. epidermidis)
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Which organisms are associated with Acute IE?
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- Staphylococcus aureus
- Coagulase-negative staphylococci (Eg, S. epidermidis) |
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What are the characteristics of Viridans Streptococci (sanguis, bovis, mutans, mitis)?
- Location? - Gram / catalase / hemolytic / shape / organization? - Acute or Subacute? - Associated with? - Mortality rates? - Therapy? |
- Oral cavity
- G+, catalase-, α-hemolytic, cocci chains - Sub-acute - S. bovis prevalent among elderly, associated w/ pre-existing colonic lesions - High cure rate w/ appropriate therapy - Susceptible to penicillin generally |
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Which organism is associated with elderly and pre-existing colonic lesions?
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Viridans Streptococci bovis
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What are the Viridans Streptococci species susceptible to? How effective is treatment?
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- Penicillin
- High cure rate w/ appropriate therapy |
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What are the characteristics of Enterococci (faecalis and faecium)?
- Location? - Gram / catalase / shape / organization? - Acute or Subacute? - Associated with? - Mortality rates? - Therapy? |
- GI tract
- G+, catalase-, short chains of cocci or diplococci - Sub-acute - More common in elderly - High mortality (difficult to treat d/t resistance) - Need combos of aminoglycosides w/ either β-lactams or vancomycin; penicillin not bactericidal |
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Which organism is associated with elderly?
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- Enterococci (E. faecalis and E. faecium)
- Viridans Streptococci, specifically S. bovis |
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What are the Enterococci (E. faecalis and E. faecium) susceptible to? How effective is treatment?
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- Combinations of aminoglycosides w/ either β-lactams or vancomycin
- Penicillin is not bactericidal for enterococci - Widespread antibiotic resistance leads to high mortality |
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What are Abiotrophia? What is unique about them?
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- Nutritionally variant Streptococci
- More difficult to grow - need cofactors and longer incubation - Can be cause of "culture-negative" endocarditis - More likely to be penicillin resistant |
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What are the gram-negative bacteria that can cause Infective Endocarditis (rare)?
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HACEK group:
- Haemophilus - Actinobacillus - Cardiobacterium - Eikenella - Kingella |
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What are the characteristics of HACEK bacteria (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)?
- Location? - Gram / shape? - Acute or Subacute? - Associated with? - Unique characteristic? |
- Oropharynx
- G- rods - Subacute - Fastidious, requires special culture media and prolonged periods of culture for isolation |
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What G- rods do not fall under HACEK group? What are they associated with?
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- Pseudomonas aeruginosa
- Associated w/ IV drug use - Subacute IE |
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Which organisms are associated with Subacute IE?
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- Viridans Streptococci (sanguis, bovis, mutans, mitis)
- Enterococci (faecalis and faecium) - Abiotrophia - HACEK group - Other G- (Pseudomonas aeruginosa) |
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What can cause culture-negative endocarditis?
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- Fastidious organisms that require special or prolonged culture (eg, ABIOTROPHIA, HACEK group of bacteria, others)
- Also can be caused by administration of PRECEDING ANTIBIOTICS (single dose of oral antibiotic may be enough to decrease yield of blood cultures), for example if someone had left over antibiotics they self-medicated with - Non-infectious etiology (eg, Libman-Sacks, thrombotic/marantic type, cardiac tumors) - Coxiella burnetti (Q fever), psittacosis typhus, Bartonell (homeless, EtOH), Brucella, Tropheryma whipplei (Whipple's disease) |
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What are some non-infectious causes of endocarditis?
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- Libman-Sacks endocarditis associated with systemic lupus erythematosus
- Thrombotic/marantic endocarditis, associated with hypercoagulable state - Cardiac tumors (Atrial myxoma most common) |
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What is thrombotic / marantic endocarditis associated with?
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Hypercoagulable state
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What is Libman-Sacks endocarditis associated with?
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Systemic Lupus Erythematosus
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What is the most common cardiac tumor that may explain culture-negative endocarditis?
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Atrial myxoma
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What are the treatment strategies for Infective Endocarditis?
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- Surgery (debride or replace affected valves)
- Antibiotics |
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When is surgery used for Infective Endocarditis?
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- Debride (remove foreign material) affected valve
- Replace affected valve - Indicated when severe valvular failure occurs or when perivalvular abscess needs drainage - CHF, prosthetic valve endocarditis, valve perforation or rupture, new heart block, multiple embolic events, uncontrolled infection on appropriate tx, certain pathogens poorly treated w/ medical therapy alone |
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What is the regimen for a native valve infected by Staphylococci?
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- Nafcillin or Cefazolin if methicillin-susceptible
- Vancomycin or Daptomycin if methicillin-resistant or allergic |
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What is the regimen for a prosthetic valve infected by Staphylococci?
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- Nafcillin or Cefazolin if methicillin-susceptible
- Vancomycin or Daptomycin if methicillin-resistant or allergic - Add Rifampin for synergy |
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What is the regimen for IE d/t Streptococci?
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- Penicillin or Ceftriaxone if penicillin-suspceptible
- Vancomycin if penicillin-resistant |
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What is the regimen for IE d/t Enterococci?
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- Penicillin OR
- Ampicillin OR - Vancomycin - With Gentamicin (needs a cell-wall-active agent to increase penetrance) |
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When do you use Nafcillin?
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Staphylococcal infection of native valve that is methicillin-susceptible
(same as Cefazolin) |
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When do you use Cefazolin?
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Staphylococcal infection of native valve that is methicillin-susceptible
(same as Nafcillin) |
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When do you use Vancomycin?
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*β-lactam resistant infections or hyper-sensitivity (Staphylococcal or Streptococcal)
- Staphylococcal infection of native valve that is methicillin-resistant or if patient is allergic to penicillin - Streptococcal infection that is methicillin-resistant - Enterococci infection w/ Gentamicin (same as Ampicillin or Penicillin) |
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When do you use Daptomycin?
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Staphylococcal infection of native valve that is methicillin-resistant or if patient is allergic to penicillin
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When do you use Rifampin?
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Add for Staphylococcal infection of prosthetic valve for synergy (not usually as monotherapy)
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When do you use Penicillin?
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- Streptococcal infection that is penicillin-susceptible (same as Ceftriaxone)
- Enterococci infection w/ Gentamicin (same as Ampicillin or Vancomycin) |
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When do you use Ceftriaxone?
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Streptococcal infection that is penicillin-susceptible
(same for Penicillin) |
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When do you use Ampicillin?
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Enterococci infection w/ Gentamicin (same as Penicillin or Vancomycin)
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When do you use Gentamicin?
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Enterococci infection w/ either Ampicillin, Penicillin, or Vancomycin (need a cell-wall active agent to enhance penetration)
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When do you need to use prophylactic treatment for patients?
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Only for those w/ highest risk pre-existing conditions and undergoing highest risk procedures
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What is more important for prevention of infection than prophylactic antibiotic treatment?
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Maintenance of good oral hygiene
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What are the indications for prophylactic antibiotic treatment?
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Need to have a high risk condition and be undergoing a procedure:
Procedures (one of the following): - Manipulation of gingival mucosa or periapical teeth - Perforation of oral mucosa (not for any GI/GU procedures) High risk cardiac condition (one of the following): - Prosthetic valve - Previous infective endocarditis - Cardiac transplant w/ valvulopathy - Un-repaired cyanotic congenital heart defect |
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What is the most likely cause of a bacteremia or infective endocarditis?
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Much more likely to result from daily activities than from a procedure
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What is the regimen for prophylactic treatment for infective endocarditis?
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- Single dose amoxicillin 2g po
- Single dose clindamycin 600mg po |
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What are some other types of cardiac infections besides Infective Endocarditis?
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- Myocarditis
- Pericarditis - Cardiomyopathy (Many related to viral infections) |
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What is the most common cause of Myocarditis? Mechanism?
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Viruses - direct cytotoxicity via receptor-mediated entry of virus into cardiac myocytes
(also can be caused by bacteria, fungi, protozoa, and helminths, but less common) |
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What is the most common cause of Pericarditis? Other causes?
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- Most commonly: Idiopathic
- Many may be viral or post-viral (eg, coxsackievirus, echovirus, adenovirus, EBV, CMV, influenza, varicella, rubella, HIV, HepB, mumps, parvovirus B19, vaccinia - smallpox vaccine) - Also can be bacterial, mycoplasma, fungal, parasitic |
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What can an infective endocarditis with valve ring abscess lead to?
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Extension into pericardium (pericarditis)
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What are the cell wall antibiotics we need to know?
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- β-lactams: penicillin, nafcillin, cefazolin, ceftriaxone
- Vancomycin - Daptomycin |
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What are the β-lactams we need to know?
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- Penicillin
- Nafcillin - Cefazolin - Ceftriaxone |
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What are the protein synthesis inhibitors we need to know?
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Gentamicin
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What are the RNA synthesis inhibitors we need to know?
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Rifampicin
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What is the mechanism of β-lactam antibiotics?
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- Binds Penicillin Binding Proteins (PBPs)
- Blocks peptidoglycan cross-linking - Inhibits bacterial growth |
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What is a common problem with β-lactam antibiotics?
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Cause hypersensitivity (allergic reactions) in some cases, possibly severe
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How do bacteria develop resistance to β-lactam antibiotics?
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Mutations in PBPs prevent β-lactam antibiotics from binding (modification of antibiotic target)
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What is the mechanism of Vancomycin?
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- Glycopeptide that binds D-ala-D-ala at end of peptide side chain in peptidoglycan precursors
- Blocks PBPs from catalyzing transglycosylation / transpeptidation steps |
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What kind of bacteria does Vancomycin work on?
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- G+
- Not effective on G- because of permeability barrier of outer membrane |
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What is the mechanism of resistance to Vancomycin?
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- Modification of antibiotic target
- Bacteria acquires genes encoding machinery to produce altered peptidoglycan structure that lacks D-ala-D-ala groups - Contains D-ala-D-lac instead, which Vancomycin is unable to bind to - Usually encoded on plasmids or transposons - easily transferred to other bacteria |
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What is Vancomycin resistance associated with?
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Enterococci in hospital settings (VRE)
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What is the mechanism of Daptomycin?
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- Lipopeptide that binds to and disrupts cytoplasmic membrane
- Possibly causes loss of membrane potential, leading to death |
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What kind of bacteria does Daptomycin work on?
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- G+ bacteria
- Narrow spectrum and bactericidal - Used for infections caused by antibiotic-resistant bacteria |
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What is the mechanism of Rifampin?
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- Binds to and inhibits RNA polymerase to prevent gene expression
- Inhibits transcription of DNA into RNA |
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What is the mechanism of resistance to Rifampin?
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Point mutations in target of drug (RpoB subunit of RNA polymerase)
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What kind of bacteria does Rifampin work on?
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- G+
- Bactericidal and narrow spectrum - Used in combination for synergy |
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What is the mechanism of Gentamicin?
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- Aminoglycoside that binds irreversibly to 30S ribosomal subunit
- Causes misreading (incorporation of wrong AA into protein) and premature release of ribosome from mRNA |
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What kind of bacteria does Gentamicin work on?
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- Does not penetrate many G+ well (not good as monotherapy)
- Use with cell-wall-active agent to enhance penetration (synergy) |
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What are the adverse effects of Gentamicin?
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- Ototoxic
- Nephrotoxic |
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What is the mechanism of resistance to Gentamicin?
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- Enzymatic modification of antibiotic (transferases catalyze addition of adenyl, acetyl, or phosphoryl group)
- Prevents aminoglycoside binding to ribosome - Transferases usually found on mobile genetic elements that facilitate transfer to other bacteria |
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What are some procedures that may predispose to getting infective endocarditis?
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- Procedures that result in bacteremia w/ organism likely to cause endocarditis
- Dental work or poor hygiene (particularly if associated w/ bleeding) - Skin disruption - Hemodialysis - Injection drug use (especially R-sided) - Focal infection w/ typical organism |
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What makes a splinter hemorrhage more significant?
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- Proximal / mid-nail >> distal
- Red or purple >> brown |
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What are Osler nodes? Cause?
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- Tender, violaceous, subcutaneous lesions in fingers or toe pads
- Inflammatory / immune complex mediated |
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What are Janeway Lesions? Cause?
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- Nontender, erythematous or hemorrhagic macules or papules
- In fingertips, palms, or soles - Due to septic emboli |
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What are Roth spots? Cause?
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- Retinal lesions - hemorrhagic w/ white central spot
- Immunologic |
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What lab abnormalities are associated with Infective Endocarditis?
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- Anemia (70-90%)
- Leukocytosis (20-30%) - Microscopic hematuria (30-50%) - Elevated sed rate and C-reactive protein |
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What is the most common organism responsible for a early prosthetic valve endocarditis?
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Coagulase-negative Staphylococci (30-35%)
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What is the most common organism responsible for a late prosthetic valve endocarditis?
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Streptococci (30-40%)
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How do you treat HACEK Endocarditis?
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- Ceftriaxone
- Ampicillin - Ciprofloxacin |
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How long does it take to break the fever from Infective Endocarditis?
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- 50% afebrile w/in 3 days of starting tx
- 75% within 1 week |
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If a fever is prolonged despite treatment, what should you suspect?
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- IE d/t S aureus, GNR, fungi
- Associated w/ complications |
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What are some possible complications of Endocarditis?
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- Cardiac: CHF, heart block, valve failure, abscess or fistula
- Neuro: embolic stroke, mycotic aneurysm, meningitis - Systemic: septic emboli, abscesses |
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Where / under what circumstances are mycotic aneurysms most common? Symptoms?
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- Most commonly at peripheral MCA bifurcations
- Usually silent until bleed - More common w/ viridans Strep - May be d/t direct embolization / infection of wall or immune complex deposition |
