Anatomy/Heart
Microbiology
Diagnostics
Pharmacology
100

Where are vegetations most commonly located and why?

Most commonly on the mitral valve, followed by the aortic valve. This is because vegetations form at sites of highest turbulence and mechanical stress — like the atrial surface of the mitral valve (the side facing the low-pressure jet of regurgitant flow) and the ventricular surface of the aortic valve.

100

How is Viridans Streptococci transmitted?

bacteria is acquired from the patient's own endogenous oral flora via routine oral activities (brushing, flossing), dental procedures that involve gingival tissues, oral disease and poor dental hygiene.

the magnitude of bacteremia depends on tissue trauma and local inflammation. 

100

Why do we obtain a culture sample of 3 sites when  checking for IE? Why do we want to obtain our culture before starting antibiotics?

We get separate samples from 3 sites to increase the chance of detecting the organism - a single blood culture can miss bacteria. We also do this to distinguish true bacteremia from contamination. 


We take a culture sample BEFORE because antibiotics can kill or suppress bacteria in the blood-stream, giving us a false negative. 

100

What are the contraindications for vancomycin and ceftriaxone?

vancomycin: hypersensitivity, corn allergy, those with renal impairment, people who are pregnant or breastfeeding, do not administer via these routes: intramuscular, intrathecal, intraventricular, intraperitoneal, intracameral, or intravitreal. 


ceftriaxone: hypersensitivity, those allergic to beta lactams, premature neonates, those with severe renal and hepatic impairment, pregnant or lactating women, 

200

What are the cardiac findings in a person with infective endocarditis?

When doing an echocardiogram, we see:

​​​​- mobile valvular vegetation
- possible valve perforation, aneurysm, rupture
- new regurgitation​​​​


Generally: presence of a new murmur or change of an existing murmur.


200

What drugs are the viridans group streptococci susceptible and resistant to?

Commonly susceptible to vancomycin and advanced beta-lactams like ceftriaxone.

Show increasing resistance to penicillin (up to 40% of strains), macrolides (25-50%), tetracyclines, and TMP-SMX (can exceed 75%). 

Citation: Singh N, Poggensee L, Huang Y, Evans CT, Suda KJ, Bulman ZP. Antibiotic susceptibility patterns of viridans group streptococci isolates in the United States from 2010 to 2020. JAC Antimicrob Resist. 2022 May 19;4(3):dlac049. doi: 10.1093/jacamr/dlac049. PMID: 35599725; PMCID: PMC9117386.

200

Describe the purpose and process of antibiotic susceptibility studies. 

purpose: determine whether an isolated bacterium is susceptible, intermediate, or resistant to specific antibiotics. Results can be used to narrow empiric therapy, change to a more active antibiotic, or discontinue agents that are unnecessary or ineffective.

collect specimen → culture and identify organism → perform susceptibility testing via kirby bauer or MIC testing → interpret MIC or inhibition zone → report results.



200

What is the spectrum of ceftriaxone?

Works against gram positive and gram negative aerobes. Works against a few anaerobes. Does not cover fungi, viruses, MRSA, or C. Diff. 

300

Describe the etiology, composition, and pathologic effects of vegetations. 

  • Etiology: endothelial injury (from turbulent flow, prior valve damage, or direct trauma) exposes subendothelial tissue → platelets and fibrin deposit, forming a sterile thrombus → transient bacteremia allows circulating organisms to adhere to and colonize this thrombus, converting it into an infected vegetation.
  • Composition: platelets, fibrin, and colonies of the infecting organism, often with entrapped inflammatory cells.
  • Pathologic effects: valve leaflet destruction and perforation, new or worsening regurgitation, vegetation fragmentation leading to septic emboli (stroke, splenic infarct, etc.), and local extension causing abscess or conduction abnormalities if it invades adjacent cardiac tissue.
300

What are the virulence factors of Viridans Streptococci?

Dextran: promotes binding to fibrin-platelet aggregates on cardiac valves

FimA/Lral Adhesin facilitates attachment to fibrin-platelet matrix of sterile vegetations

Biofilm Formation supports adherence to dental surfaces and can protect bacteria from host clearance

lipotechicoic Acid contributes to adherence and stimulates inflammation througjh TLR2 signaling

300

What is the clinical presentation of infective endocarditis?

can depend on whether it is acute IE or subacute IE. for our patient: 

progression over weeks to months with fever, malaise, chills, night sweats, weight loss, dyspnea, back pain, myalgia, anthralgia

Osler's nodes, janeway lesions, splinter hemorrhages, roth spots (splinter hemorrhages), splenomegaly, acute confusional state

300

What is the spectrum of vancomycin?

Broad activity against gram-positive organisms, including MRSA, but no activity against gram-negative bacteria, mycobacteria, or fungi.

400

Compare and contrast congenital and new murmurs. How are they classified?

  • Congenital murmurs are present from birth or early childhood, caused by structural defects the person is born with . They're typically stable over time and often already known/documented.
  • New (acquired) murmurs arise later in life from an acquired change to a previously normal valve; things like infective endocarditis, rheumatic valve disease. A new murmur in someone with no prior cardiac history is a red flag.

How murmurs are classified:

  • Timing: systolic, diastolic, or continuous (relative to S1/S2)
  • Location/radiation: where it's loudest, where it travels
  • Grade: I–VI based on intensity (a II/VI, like Ms. Ng's, is soft but clearly audible)
  • Quality: blowing, harsh, rumbling, etc.
400

What are the features of Viridans Streptococci?

​​​- opportunistic pathogen, normally in oral flora
- gram-positive cocci arranged in chains
- catalase-negative 
- alpha hemolytic --> partial hemolysis and a green discoloration of blood agar
- facultative anaerobe
- optochin resistant, bile insoluble​​​
400

Reconcile the CBC and RF test results.

↑ WBC: Ongoing bacterial infection → inflammatory cytokines stimulate leukocyte production/release

↑ Neutrophils: Neutrophils are the major WBC response to bacterial infection

↑ Platelets: Inflammation can cause reactive thrombocytosis

↑ Rheumatoid factor: an autoantibody that targets IgG: caused by chronic infection → lots of antigen-antibody complexes and B-cell activation which can actually cause synthesis of autoantibodies.

↓ Hgb + ↓ Hct: Mild anemia related to her prolonged inflammatory illness (IL6 increases hepcidin production, this lowers circulating iron and iron absorption in order to starve bacteria, but with less circulating iron we get anemia. 


400

What are the adverse effects of vancomycin and ceftriaxone?

Vancomycin: MAINLY GIVEN VIA IV. nephrotoxicity, IV-related flushing reaction (occurs because IV infusion was too fast, NOT an IgE-mediated histamine reaction, ototoxicity, local toxicity and pain. 


Ceftriaxone: GIVEN PARENTERALLY, NOT ORALLY. adverse reactions include rash and other hypersensitivities, GI complications, hematologic effects, biliary and urinary precipitation, neurologic effects (confusion, encephalopathy).

500

Describe the overall structure and function of the valves and chambers of the heart. What order does blood flow?

  • Four chambers: atria receive blood; ventricles eject blood.
  • Right heart: sends deoxygenated blood to the lungs.
  • Left heart: sends oxygenated blood to the systemic circulation.
  • Four valves: maintain one-way blood flow.

Blood flow order:

  1. SVC/IVC → right atrium → tricuspid valve → right ventricle.
  2. Right ventricle → pulmonary valve → pulmonary trunk → lungs.
  3. Pulmonary veins → left atrium → mitral valve → left ventricle.
  4. Left ventricle → aortic valve → aorta → systemic circulation.
500

What is the pathophysiology/order in which viridans streptococci causes infective endocarditis?

  1. Oral colonization: viridans streptococci persist as commensals in the oropharynx and dental plaque.
  2. Transient bacteremia: mucosal trauma or inflammation allows organisms to enter the bloodstream.
  3. Endocardial injury: turbulent flow or an abnormal valve can injure the valvular endothelium and expose subendothelial matrix.
  4. Sterile vegetation formation: platelets and fibrin deposit on the injured surface, forming a sterile microthrombus.
  5. Bacterial adherence: dextran, FimA/LraI, and other adhesins allow viridans streptococci to bind to the fibrin–platelet matrix.
  6. Vegetation maturation: additional fibrin and platelets encase the organisms, creating a protected infected vegetation.
  7. Clinical complications: vegetation growth can cause valve destruction and regurgitation, while fragmentation can produce emboli and metastatic infection.
500

How do we formally diagnose infective endocarditis?

Patients must have 2 major criteria, 1major/3minor criteria, or 5 minor criteria of the "Duke Criteria" for diagnosis of IE.


500

What are the mechanisms of action of vancomycin and ceftriaxone?

Vancomycin binds the terminal D-Ala-D-Ala sequence of bacterial peptidoglycan precursors, blocks glycopeptide polymerization and inhibits peptidoglycan cell-wall synthesis, leading to cell wall damage and death. 

Ceftriaxone is a β-lactam antibiotic and is usually bactericidal. It binds penicillin-binding proteins and inhibits transpeptidase-mediated peptidoglycan cross-linking, preventing formation of a stable bacterial cell wall and leading to bacterial death.

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