Welcome to USMLE practice question #142! Today’s topic is cardiology.
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A 58-year-old man with a history of mitral valve prolapse presents to the hospital with fever, fatigue, and unintentional weight loss over the past 2 weeks. On examination, he has a new systolic murmur and splinter hemorrhages under his fingernails. Blood cultures grow Streptococcus mitis. Which of the following best explains the sequence of events leading to his condition?
A) Bacterial superantigen-induced T-cell activation
B) Hematogenous seeding
C) Endothelial invasion by bacteria
D) Immune complex deposition
E) Cytokine-mediated endothelial damage
Detailed Breakdown of Answers + Correct Answer Below ⏬
ANSWER + QUESTION BREAKDOWN
It’s important to adopt the correct MENTAL MODEL when answering USMLE questions; it saves time and increases accuracy. The mental model outlined below is a foundational component of our test-taking skills masterclass (check it out if you want to elevate your skills). Here’s how to think through this question:
Step 1. Read the last line to get to the heart of the question: “Which of the following best explains the sequence of events leading to his condition?”
Step 2: Is this a first-, second-, or third-order question?
Answer: 2nd order. 1st: Diagnose the problem, 2nd: Identify the underlying cause.
Step 3: Read the vignette carefully and ask yourself: “Based on my diagnosis, the most likely underlying cause is ______________.”
Step 4. Look at the answer choices and select the option most closely resembling your final thought from “Step 3” above.
GENERAL ANALYSIS
This 58-year-old man with a history of mitral valve prolapse (MVP) presents with fever, fatigue, weight loss, and findings suggestive of infective endocarditis (IE), including a new systolic murmur and splinter hemorrhages. Blood cultures grow Streptococcus mitis, a member of the viridans group streptococci (VGS), which is strongly associated with subacute IE, particularly in patients with underlying structural valve abnormalities such as MVP.
ANSWER CHOICES:
CHOICE A: Bacterial superantigen-induced T-cell activation
Explanation: Superantigens are exotoxins produced by certain bacteria (e.g., Staphylococcus aureus or Streptococcus pyogenes) that nonspecifically activate T cells, leading to massive cytokine release and systemic inflammation (e.g., toxic shock syndrome).
CHOICE B: Hematogenous seeding
Explanation: Hematogenous seeding refers to the spread of bacteria via the bloodstream to distant sites. In IE, transient bacteremia delivers bacteria to damaged or abnormal heart valves, where they adhere and form vegetations.
CHOICE C: Endothelial invasion by bacteria
Explanation: Some organisms (e.g., Staphylococcus aureus) can invade endothelial cells, leading to more aggressive forms of IE. However, S. mitis typically adheres to preexisting thrombi on damaged valves rather than directly invading endothelial cells.
CHOICE D: Immune complex deposition
Explanation: Immune complex deposition occurs in some complications of IE (e.g., glomerulonephritis or vasculitis) due to circulating antigen-antibody complexes. However, this is not part of the initial pathogenesis of IE.
CHOICE E: Cytokine-mediated endothelial damage
Explanation: Cytokine-mediated endothelial damage occurs in systemic inflammatory conditions but is not part of the pathogenesis of infective endocarditis caused by S. mitis.
FINAL VERDICT…
CORRECT ANSWER: B) Hematogenous seeding
The most likely sequence of events leading to this patient’s condition involves transient bacteremia delivering S. mitis to the damaged mitral valve caused by mitral valve prolapse. The bacteria adhere to preexisting fibrin-platelet thrombi on the valve surface, forming vegetations characteristic of infective endocarditis.
The pathogenesis of infective endocarditis involves a sequence of events:
Endothelial damage: MVP creates turbulent blood flow that damages the endothelium of the mitral valve.
Formation of nonbacterial thrombotic endocarditis: Platelets and fibrin adhere to the damaged endothelial surface, forming a sterile thrombus.
Bacteremia: Transient bacteremia (e.g., from dental procedures or poor oral hygiene) delivers bacteria to the thrombus.
Bacterial adherence and colonization: Bacteria such as S. mitis adhere to the thrombus and proliferate, forming vegetations.
Vegetation growth: Platelets and fibrin cover the bacteria, protecting them from host immune defenses and leading to persistent infection.
KEY CONCEPTS:
Pathogenesis of Infective Endocarditis (IE):
Endothelial damage (e.g., from MVP or turbulent flow).
Formation of nonbacterial thrombotic endocarditis (fibrin-platelet aggregates).
Transient bacteremia delivers organisms to the thrombus.
Bacterial adherence and colonization lead to vegetation formation.
Role of Mitral Valve Prolapse (MVP):
MVP is a common predisposing condition for IE due to turbulent blood flow causing endothelial injury.
Viridans group streptococci (e.g., S. mitis) are frequently implicated in MVP-associated IE.
Clinical Features of Subacute Infective Endocarditis:
Symptoms: Fever, fatigue, weight loss.
Signs: New murmur, splinter hemorrhages, Janeway lesions.
Blood cultures often grow alpha-hemolytic streptococci (e.g., S. mitis).
Diagnostic Tools for IE:
Blood cultures: Identify causative organism.
Echocardiography (transthoracic or transesophageal): Detect vegetations.
Duke criteria for definitive diagnosis.
Management of IE:
Antibiotics tailored to organism susceptibility (e.g., penicillin for VGS).
Valve surgery for complications such as heart failure or embolization.